Tag Archives: life

Driving Under the Influence of Parkinson’s

“Have you ever noticed that anybody driving slower than you is an idiot, and anyone going faster than you is a maniac?” George Carlin

“If all the cars in the United States were placed end to end, it would probably be Labor Day Weekend.” Doug Larson

The Dilemma: At some age in our life, maybe, just maybe, we could lose the privilege of driving our car/truck.  If you are living with Parkinson’s, depending on the individual, losing the legal right to drive your motor vehicle might/could happen at an even earlier age.  A discussion of driving under the influence of Parkinson’s is presented here.

“I love driving cars, looking at them, cleaning and washing and shining them. I clean ’em inside and outside. I’m very touchy about cars. I don’t want anybody leaning on them or closing the door too hard, know what I mean?” Scott Baio

The Michon model of normal driving behavior:  In 1985, Michon proposed that drivers need to conduct problem-solving while driving; he divided it  into three levels of skill and control. The model includes strategic (planning), tactical (maneuvering), and operational (control) levels.   When you think about it driving really is a complicated task.   The strategic level is basically the general route and planning needed to successfully navigate the motor vehicle.  The tactical and control levels involve the individual driving circumstances and how one responds and our responsiveness to the action of driving.   And of course, it’s quite obvious, that unsafe driving is operating a motor vehicle in an unsafe manner regardless of your health status. Driving safely is important for the individual as well as for the people around you; thus, it is a serious task to evaluate someone’s competency to drive a motor vehicle. Shown below is a schematic drawing of the Michon model of normal driving behavior.

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“The one thing that unites all human beings, regardless of age, gender, religion, economic status, or ethnic background, is that, deep down inside, we all believe that we are above-average drivers.” Dave Barry

Decision-making while driving:   Below are some traffic signs that we might encounter in our usual driving pattern depending on where we live. When you think about decision-making you’re in your lane you’re driving down the road and you see signs like this, then what?  You can see how it takes all three levels of driving competency to navigate successfully while driving a motor vehicle in a complex maneuver.  Now add the complications of someone with Parkinson’s, you may need to re-think the entire situation. What this says is that when you’re driving a motor vehicle you’re trying to integrate many levels of sensory, motor and cortical function to the process. In Parkinson’s, we may have some sort of motor skill/task impairment, potentially mixed with a minor cognitive disorder, and further clouded by traditional drug therapy. Who makes the decision for the patient with Parkinson’s about being able to continue to drive?  Not an easy answer.

“Some beautiful paths can’t be discovered without getting lost.” Erol Ozan

 Possible problems that could occur while driving with Parkinson’s: The control or operational level of driving a car can be influenced by motor defects experienced by many with Parkinson’s, including rigidity, tremor, bradykinesia and dyskinesia. Futhermore, non-motor deficits could impair both route planning, strategic and tactical levels, and these would include cognitive decline, neuropsychiatric symptoms and/or visual impairment. And on top of that in the elderly population, many people with Parkinson’s have additional co-morbidity that could also contribute to diminish our ability to drive a motor vehicle. Thinking about just one aspect, slowness in cognitive function, the inability to make a decision quickly could lead to poor performance time and might affect driving in someone with Parkinson’s. Alternatively, you may have none of these problems and will be driving for many more years. But as we all start to exhibit signs and symptoms of motor and non-motor deficits, this will eventually become an important issue for each of us to deal with at some point in time.

“Always focus on the front windshield and not the review mirror.” Colin Powell

 What are some criteria for determining our fitness to drive a motor vehicle when you have Parkinson’s? In a very nice review, Jitkritsadakul and Bhidayasiri suggest there are five different red flags that should tell our neurologist that we may have an impairment that should limit our driving of motor vehicles. First, these include our clinical history, which would be a history of accidents, sleeping attacks while driving and combined with the daily dose amount of levodopa. Next would be a questionnaire to determine our level of daily sleepiness. Third, a motor assessment skills test. Fourth, a cognitive assessment. And fifth would be a visual assessment.  Look above at the Michon driving schematic and think about the three levels of skill required for driving and substitute someone with Parkinson’s and how that could diminish one or more of the skill sets over time.  What this says to me is that through a combination of family and friends and carepartner,  along with the advice of our neurologist, one should be able to make a critical assessment of whether or not we should continue to drive.

“Driving your car through deep pools of flood water is a great way of making your car unreliable. Smart people turn around and avoid it.” Steven Magee

A love of motor vehicles (a personal expression):  I grew up loving automobiles; and living on Air Force Bases, I saw many different types of sports cars  (e.g., Corvette, Jaguar, Triumph, Porsche, Shelby Mustang, Ferrari- you just had to believe that Air Force pilots live for speed in the air and their cars showed it on the ground). I can remember in 1964 (I was 11 years old) going to the Ford dealership with my dad to see the very first Ford Mustang cars; thinking how beautiful they were and remembering my dad’s comment that was a lot of car for $2,400.   I still have vivid memories of riding with my dad (yes, he was a former pilot) in his ~1962 white Porsche. I can still remember in 1971 getting my first car, a 1968 Chevrolet Camaro (red interior and red exterior) with standard transmission (three on the floor) and powered by a 327 cubic inch V-8 engine. [Please note, the pictures below are representative images because I could not find any actual old photos of these cars]

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Over the decades, I can recall the weekly car-washing sessions, typically on Saturday mornings. With the exception of one car in the early 1980’s, I have loved and truly enjoyed the automobiles I’ve driven.  Like many people I’ve named all my cars; my two current automobiles are named Raven and Portia. I still enjoy driving a standard shift car using the clutch that requires both cognitive function and motor skills to navigate the automobile. I have always thought “It’s going to be a cold day in hell before they take my car away”; however, it’s a reality in the future I now face with Parkinson’s. In fact one of the very first people I ever told about my Parkinson’s several years ago, the very first question she asked me was “Are you still able to drive?”  In summary, driving under the influence of Parkinson’s is something we all will need to consider with time; I wish you well with your driving experiences.

“Driving a car provides a person with a rush of dopamine in the brain, which hormonal induced salience spurs modalities of creative and critical thinking regarding philosophical concepts such as truth, logical necessity, possibility, impossibility, chance, and contingency.” Kilroy J. Oldster

https://www.ncbi.nlm.nih.gov/pubmed/27729986

1.    Jitkritsadakul O, Bhidayasiri R. Physicians’ role in the determination of fitness to drive in patients with Parkinson’s disease: systematic review of the assessment tools and a call for national guidelines. Journal of Clinical Movement Disorders. 2016;3(1):14. doi: 10.1186/s40734-016-0043-x.

Cover photo credit: s-media-cache-ak0.pinimg.com/564x/22/d1/75/22d175ac53a0a5dbb04e77ae52a49c52.jpg

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Building Empathy for Parkinson’s

“When people talk, listen completely. Most people never listen.”  Ernest Hemingway

“To perceive is to suffer.”  Aristotle

Introduction: The loss of dopamine-producing neurons in the mid-brain leads to Parkinson’s disease, which usually presents with motor dysfunction of different degrees of progression from person-to-person.  This post explores the differences between empathy and sympathy, and describes a new device that allows one to actually experience a person-with-Parkinson’s tremor; surely providing much empathy from the experience.

“No one cares how much you know, until they know how much you care”  Theodore Roosevelt

A lesson learned from the classic rock opera “Tommy” by The Who: The plot of the 1969 rock opera “Tommy” begins with Tommy’s parents.  His father, Captain Walker, fought in World War II but it is assumed he died. However, Captain Walker is alive and returns home to his wife and Tommy. Believing her husband to be dead, Mrs. Walker has a new lover.  Captain Walker accidentally kills the lover, in the presence of Tommy. Tommy is traumatized by what he witnessed; he becomes catatonic.  Three musical examples: Go to the Mirror (listen here) Tommy sings “See me, me, feel me, touch me, heal me / See me, feel me, touch me, heal me.” Tommy’s father sings “I often wonder what he is feeling / Has he ever heard a word I’ve said? / Look at him in the mirror dreaming / What is happening in his head?” In Tommy Can You See Me? (listen here)  his mother sings “Tommy can you hear me? / Can you feel me near you? /  Tommy can you feel me / Can I help to cheer you.” In See Me, Feel Me (listen here) Tommy sings “See me, feel me, touch me, heal me / See me, feel me, touch me, heal me / See me, feel me, touch me, heal me / See me, feel me, touch me, heal me / Listening to you, I get the music / Gazing at you, I get the heat / Following you, I climb the mountain / I get excitement at your feet.” Hopefully, you can empathize, not sympathize, with Tommy and the life-struggles he encounters and overcomes in this rock opera.

“for there is nothing heavier than compassion. Not even one’s own pain weighs so heavy as the pain one feels with someone, for someone, a pain intensified by the imagination and prolonged by a hundred echoes.” Milan Kundera

*Empathy vs. sympathy: Empathy means you have the ability to understand and share the feelings of another.  By contrast, sympathy means feelings of pity and sorrow for someone else’s misfortune (https://en.oxforddictionaries.com/definition/empathy). Yes, it sucks to have a chronically-progressing neurodegenerative disorder like Parkinson’s. But it could be worse, really.

Empathy.  What a great word.  Try to be empathetic to me; you don’t have to become one with me, just strive to understand how I’m feeling.  Our bond will surely strengthen.  You may not be able to exactly feel what I’m feeling, but just trying says much to you, your inner processing, the soul of your humanity.

Please don’t pity me, that reduces the feelings between us.  Please don’t have sorrow or sadness for me, it weakens our ties. If you give me sympathy, you’ll never truly be able to grasp the extent and meaning of my Parkinson’s.  Parkinson’s is not my friend; however, having your friendship and understanding (empathy) instead of your pity (sympathy) will give me strength and help me deal on a more positive-front with this unrelenting disorder.

*This post is dedicated to the first-year medical students at the UNC School of Medicine. On Friday, May 5, I had the privilege and honor of being presented as a person-with-Parkinson’s in our Neurologic Block. They asked very specific questions in their attempt to understand Parkinson’s and to learn how I am living with this disorder. It was clear that they were trying to follow the advice of Dr. William Osler who said “It is much more important to know what sort of a patient has a disease than what sort of a disease a patient has.”

“Some people think only intellect counts: knowing how to solve problems, knowing how to get by, knowing how to identify an advantage and seize it. But the functions of intellect are insufficient without courage, love, friendship, compassion, and empathy.”  Dean Koontz

What is the life expectancy of someone diagnosed with Alzheimer’s, Parkinson’s, Amyotrophic Lateral Sclerosis (ALS), and Huntington’s disease? These neurodegenerative disorders are listed in ranked order of how many people are affected from most to least, respectively. Alzheimer’s typically progress over 2 to 20 years, and individuals live for 8 to 10 years after the diagnosis.  People who have Parkinson’s usually have the same average life expectancy as people without the disease.  Life expectancy from ALS is usually at least 3-4 years. The time from diagnosis  of Huntington’s to death is about 10 to 30 years.  Each of these disorders is uniquely different and unsettling to me; but your empathy, not your sympathy, will truly help me sail my boat along the shoreline for many more years.  Accept me with ‘my unique medical issues’, try to understand it. Your empathy will add stability to my battle; just watch.

“Resolve to be tender with the young, compassionate with the aged, sympathetic with the striving, and tolerant of the weak and the wrong. Sometime in life you will have been all of these.” Lloyd Shearer

A novel engineering device is empathy-producing to someone with Parkinson’s: The whole story is revealed from watching this video (click here). Klick Labs in Toronto, Canada, has created the SymPulse Tele-Empathy Device. This device is capable of mimicking and producing the tremors and involuntary movements of someone with Parkinson’s in people without Parkinson’s. The video is quite powerful, you immediately sense the empathy.

The SymPulse Tele-Empathy Device is based on digitized muscle activity from electromyograms of Parkinson’s patients. The signal is unique for each person with Parkinson’s. When the person without Parkinson’s receives this novel voltage pattern, their muscles will contract exactly as found in the person with Parkinson’s. Developing such a device shows the deviant nature of Parkinson’s to disrupt/distort normal neuro-muscular circuitry.

This device could be used to increase empathy in doctors and other caregivers. And it could enable family members and loved-ones the unique opportunity to experience the actual tremor/involuntary movements of their special person with Parkinson’s. Company officials note that most people wear the device for at most a couple of minutes; turn off the device and they return to normal. Remember, there is no off-on switch for the person with Parkinson’s.  I can only imagine empathy evolving from this device when used on someone without Parkinson’s.

“When we honestly ask ourselves which person in our lives mean the most to us, we often find that it is those who, instead of giving advice, solutions, or cures, have chosen rather to share our pain and touch our wounds with a warm and tender hand. The friend who can be silent with us in a moment of despair or confusion, who can stay with us in an hour of grief and bereavement, who can tolerate not knowing, not curing, not healing and face with us the reality of our powerlessness, that is a friend who cares.” Henri J.M. Nouwen

Cover photo credit: gsmnp.com/wp-content/uploads/View-of-Smoky-Mountains-from-Oconaluftee.jpg

Life-Journey with Parkinson’s Blog (2016-2017): Recap of Quotes, Service, and Research

“Give your life a destination.” Debasish Mridha

“We’re all a beautiful, wonderful work in progress….Embrace the process!” Nanette Mathews

Précis: This post is a review of my public journey and life-steps with Parkinson’s in the 2nd year of the blog: i) rationale for the blog; ii) quotes/highlights from selected posts between March 2016-March 2017; iii) overview of service activities/events; iv) research and the 4th World Parkinson Congress; v) some of the people that make a difference in my life, and vi) six favorite cover photos from the past year.

Update on I’m Still Here: Journey and Life with Parkinson’s

A thought from Day 01: On March 9, 2015, I began my journey and Parkinson’s-life-story with this blog.  The first blog post ended with the following comment: “I am trying to live life well and authentically, and not be defined by my PD. With the help of family, friends, colleagues, and personal physicians, my goals are to stay positive and strive to keep focused on what matters the most…I am still here!”

Foundational themes of the blog:  The overall goal of the blog is divided between these topics: (a) to describe living with Parkinson’s (“Life Lessons”); (b) to present emerging medical strategies for dealing with Parkinson’s (“Medical Education”); (c) to provide a support mechanism for anyone with Parkinson’s or another neurodegenerative disorder (“Strategy for Living”); and (d) to give an overview of the scientific aspects of Parkinson’s (“Translating Science”).  I really appreciate your continual support, feedback, critiques, and suggestions for future topics (here’s an example): “I enjoy reading your informative blog posts. I believe that addressing the many frustrations of living with Parkinson’s as you are doing with such “matter of factness” and then with a plan of action, must be inspiring to others dealing with the same.  All the while working so hard to maintain your positive outlook…the mental exercise! The other side of the overall challenge in this competition with Parkinson’s Disease to live your present life fully.” If there are some specific topics/life aspects of Parkinson’s you’d like for me to research and present here, please send me the topic(s).  If there is some format change in presentation you’d like to see to improve the readability of future posts, please send me a suggestion.

Quotes and highlights from selected posts from March 2016-March 2017:

  1. “As a long-time educator, I feel that my daily lesson plans are partly derived from my life-experiences and that my syllabus is the sum of my life’s journey.”  From Parkinson’s and the Positivity of Michael J. Fox (click here to read post).
  2. “A regular aerobic exercise program likely helps to promote the appropriate conditions for the injured brain to undergo neuroplasticity.”  From Déjà Vu and Neuroplasticity in Parkinson’s (click here to read post).
  3. We are identified by our characteristic symptoms of our unwanted companion named Parkinson’s. We are all in this together, united by our disorder; held together by those who love and care for us.” From Update on I’m Still Here: Life with Parkinson’s (click here to read post).
  4. While we wait for the potion that slows progression, we exercise and remain hopeful. While we live with a neurodegenerative disorder, we strive to remove the label and we stay positive.” From Parkinson’s Treatment With Dopamine Agonist, Complementary and Alternative Medicine (CAM), and Exercise(click here to read post).
  5. Living with Parkinson’s requires you to adapt to its subtle but progressive changes over a long period of time; you need to remain hopeful for many different things.” From Chapter 1: A Parkinson’s Reading Companion on Hope (click here to read post).
  6. “This disorder robs you physically of mobility and flexibility, so maintaining physical strength is really important. This disorder robs you emotionally and this deficit is bigger than the physical defects; thus, to thrive with Parkinson’s demands several character strengths.” From Chapter 3: A Parkinson’s Reading Companion on Strength (click here to read post).
  7. “Life with Parkinson’s is best lived in the current moment without dwelling on the past and dreading the future.”  From Chapter 8: A Parkinson’s Reading Companion on Mindfulness (click here to read post).
  8. “The journey with Parkinson’s requires effort, teamwork, awareness, and a heart-fueled positive attitude to keep going.”  From Chapter 9: A Parkinson’s Reading Companion on Journey (click here to read post).
  9. “Consider your disorder, you must be able to embrace this unexpected turn in your life and manage the best you can. Personalize your disorder and understand its nuances on you; then you will be able to successfully navigate life in its daily presence.” From 9 Life Lessons from 2016 Commencement Speeches (click here to read post).
  10. “I truly believe that the effort most people are using to handle their disorder puts them in a healthier and better lifestyle to manage their symptoms. An emerging predominate picture of Parkinson’s today is a person striving to live strongly.” From The Evolving Portrait of Parkinson’s (click here to read post).
  11. “Believe in Life in the Presence of Parkinson’s”: Every thought expressed here matters to me (click here to read post).
  12. “Your home may change many times over the coming years. Let your heart tell you where your home is.” From 2016 Whitehead Lecture: Advice, Life Stories and the Journey with Parkinson’s (click here to read post).
  13.  “Here’s a simple mindfulness experience/moment: simply be aware of the steam leaving your morning cup of coffee/tea, clear your immediate thoughts, then sip, focus and savor this moment.”  From 7 Healthy Habits For Your Brain (click here to read post).
  14. “You’ve played 17 holes of golf, and you approach the 18th hole to finish the round. This is a long par three with a lake between you on the tee box and the putting surface.  Your three golf buddies have already safely hit their balls over the lake;  you  launch the ball over the water and safely onto the green (this is a big deal).  Without Parkinson’s, your facial expression and your exuberance are so obvious.  With Parkinson’s, your joy and exuberance are still over-flowing inwardly yet it is displayed in a more muted manner.”  From The Mask of Parkinson’s (click here to read post).
  15. “We must remain hopeful that advances in Parkinson’s treatment are being made and that our understanding of the science of Parkinson’s is continuing to evolve.”  From 2016: The Year in Parkinson’s (click here to read post).
  16. “Since receiving my Parkinson’s diagnosis, my opinion of exercise has changed.  With Parkinson’s, I’m now exercising as if my life depends on it.”  From 9 Things to Know About Exercise-induced Neuroplasticity in Human Parkinson’s (click here to read post).

Service and research:
Service- I was most fortunate to be able to participate in 2 ways for the 4th World Parkinson Congress (WPC), first as a member of the Communications Committee, World Parkinson Coalition; second, as the Co-Editor, Daily Parkinson eNewspaper for the 4th WPC.  And it gave me an opportunity to work with the very talented Eli Pollard (Executive Director WPC).  A truly amazing Editorial Board was assembled of PD advocates, researchers, experts, PwP, and just a superb group of people devoted to Parkinson’s (click here to read the Editorial Board Biographical Sketches).   This was a meaningful experience to have worked with the Editorial Board, a real honor.

Being part of the Planning Committee, Moving Day NC Triangle, headed up by Jessica Shurer, was such fun.  This was my first year on the committee; however, it was my second year to organize a team for Moving Day.

PWR!Moves® Instructor Workshop Certificate. Spent a weekend in Greenville, SC to participate and get certified in PWR!Moves (PWR = Parkinson Wellness Recovery).  To sum it up is easy, truly an amazing event.  I was fortunate to have an experienced-talented instructor and a group of personal trainers committed to working with PwP (click here to read the blog post describing the PWR! experience). Although I was happy to contribute as the person-with-Parkinson’s and go through the exercise routines for everyone, it was even more fun getting trained and certified in PWR!Moves.

Research-  One of the new directions in my life is a shift in the focus of my research away from hematology and to Parkinson’s.  I keep asking myself, why? and keep answering why not!  The process is just like everything else related to research and grant applications; you read, plan, write, submit, and wait.  However, I am pleased to say that CJ’s fellowship entitled “Localization of Proteases and their Inhibitors in Parkinson’s Disease” was funded by UNC-CH.  It’s a start…we begin gathering data next month.  And I am so proud of CJ for seeking (and obtaining) funding to get us started in the science of Parkinson’s.

“Life is like a roller-coaster with thrills, chills, and a sigh of relief.” Susan Bennett

The people that make a difference in my life: Collectively, everyone here gives me strength each and every day of my journey with this disorder.

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Above- Barbara, the best care-partner/best friend/best everything; I can’t imagine being here and doing all of this without your never-ending love and support.

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Top and bottom right panels above- lab/research group [especially important are CJ (currently working in the lab) and Mac (a long-time collaborator) and Chantelle, Savannah, and Jasmine (no longer working in the lab but still are great friends and vital to our success)]; middle panel- nothing more valuable than family, with my sisters (Tina and Kitty), and bottom left panel- my all-important golf buddies [Walter, Kim, Nigel (not pictured) and John].

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Panels above- undergraduate classes from SP ’16, FA’ 16 and SP ’17 inspire me every day to keep teaching and fuel my inner-core to keep going another year.

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Above panels- medical students (all 180 students/class) enrich my life and challenge me to keep working hard and stay happy.

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Besides attending a Parkinson’s Congress, getting certified in PWR!, publishing a book, and walking for Parkinson’s; it was all made easier by my PWR! Physical Therapist and gifted teacher Jennifer (top right panel), expert medical guidance from my Neurologist Dr. Roque (middle panel), Parkinson’s-education-awareness from the best movement disorder center social-worker Jessica (bottom middle panel), perpetual energy and role model of a PwP-advocate Lisa (bottom right panel), and Johanna and Katie (not pictured above) who make my day-job such a joyful experience.  And I apologize to many others who are not pictured here because you do really matter to me.

6 favorite cover photos from the past year (links to photos at the end):

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Thank you! Thank you for your support during the second year of my journey with this blog. As always, live decisively, be positive, stay focused, remain persistent and stay you.

“I want to be in the arena. I want to be brave with my life. And when we make the choice to dare greatly, we sign up to get our asses kicked. We can choose courage or we can choose comfort, but we can’t have both. Not at the same time. Vulnerability is not winning or losing; it’s having the courage to show up and be seen when we have no control over the outcome. Vulnerability is not weakness; it’s our greatest measure of courage.”  Brené Brown, Rising Strong

Noted added in proof: For a day or so, a preliminary version of this post appeared in 200 Years Ago James Parkinson published “An Essay On The Shaking Palsy” (click here to view).  Together, this combined post was substantially longer than my usual blog post.  Therefore, I separated them and decided to present this year-end-review in an expanded format.

Cover photo credit: farm4.staticflickr.com/3953/15575910318_ec35ebb523_b.jpg

Photo credits for the 6 favorite cover photos for 2016-2017: top left http://epod.usra.edu/.a/6a0105371bb32c970b015438c5312a970c-pi;  top right: : http://vb3lk7eb4t.search.serialssolutions.com/?V=1.0&L=VB3LK7EB4T&S=JCs&C=TC0001578421&T=marc ; middle left wallpaper-crocus-flower-buds-violet-primrose-snow-spring-flowers.jpg; middle right : http://az616578.vo.msecnd.net/files/2016/03/19/635940149667803087959444186_6359344127228967891155060939_nature-grass-flowers-spring-2780.jpg ; bottom left : http://www.beaconhouseinnb-b.com/wp-content/uploads/dawn-at-spring-lake-beach-bill-mckim.jpg ; bottom right : http://www.rarewallpapers.com/beaches/lifeguard-station-10678

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Milestones in Parkinson’s Disease Research and Discovery

“The real voyage of discovery consists not in seeking new landscapes, but in having new eyes.” Marcel Proust

“The process of scientific discovery is, in effect, a continual flight from wonder.” Albert Einstein

Preface:  Happy birthday to James Parkinson (neurologist, geologist, scientist, activist),  born April 11, 1755 and died December 21, 1824.  World Parkinson’s Day April 11, 2017.

Introduction to the historical timeline on Parkinson’s disease: This historical description of Parkinson’s is a joint venture/adventure between Frank and Simon . The idea for this project started as a conversation during a recent North Carolina beach weekend for Frank and Barbara: “Wouldn’t it be cool to publish a Parkinson’s historical timeline for Parkinson’s awareness month?” However, to complete this project I needed a Parkinson’s expert. As a follower of his outstanding blog ‘Science of Parkinson’s’, I approached Simon about helping out on this timeline project; and to my delight he said yes. Therefore, we are happy to present the milestones in Parkinson’s disease research and discovery. We do apologize to the clinicians, scientists, health-care specialists, and their projects that were not cited here but we limited the timeline to ~50 notations.

The entire historical timeline can be downloaded (click here for the PowerPoint file) and we encourage you to view it in ‘presentation’ mode. Each individual page of the timeline is presented below along with a brief explanation for each of the highlighted events. And Simon and I will be sharing the historical timeline in our own individual blogs.

“I want to see books taken out of historical time and placed into a different timeline, such as evolutionary or geological time, as a means of putting the human experience in context.” Douglas Coupland

1817-1919, Milestones in Parkinson’s Disease Research and Discovery (Part 1a: Historical):
Slide1

First description of Parkinson’s disease:
In 1811, Mr James Parkinson of no. 1 Hoxton Square (London) published a 66 page booklet called an ‘An Essay on the Shaking Palsy’. At the date of printing, it sold for 3 shillings (approx. £9 or US$12). The booklet was the first complete description of a condition that James called ‘Paralysis agitans’ or shaking palsy. In his booklet, he discusses the history of tremor and distinguishes this new condition from other diseases. He then describes three of his own patients and three people who he saw in the street.

The naming of Parkinson’s disease:
Widely considered the ‘Father of modern neurology’, the importance of Jean-Martin Charcot’s contribution to modern medicine is rarely in doubt. From Sigmund Freud to William James (one of the founding fathers of Psychology), Charcot taught many of the great names in the early field of neurology. Between 1868 and 1881, Charcot focused much of his attention on the ‘paralysis agitans’. Charcot rejected the label ‘Paralysis agitans’, however, suggesting that it was misleading in that patients were not markedly weak and do not necessarily have tremor. Rather than Paralysis Agitans, Charcot suggested that Maladie de Parkinson (or Parkinson’s disease) would be a more appropriate name, bestowing credit to the man who first described the condition. And thus 70 years after passing away, James Parkinson was immortalized with the disease named after him.

The further clinical characterization of Parkinson’s disease:
British neurologist Sir William Gowers published a two-volume text called the Manual of Diseases of the Nervous System (1886, 1888). In this book he described his personal experience with 80 people with Parkinson’s disease in the 1880s. He also identified the subtle male predominance of the disorder and provided illustrations of the characteristic posture. In his treatment of Parkinson’s tremor, Gower used hyoscyamine, hemlock, and hemp (cannabis) as effective agents for temporary tremor abatement.

The discovery of the chemical dopamine:
In the Parkinsonian brain there is a severe reduction in the chemical dopamine. This chemical was first synthesized in 1910 by George Barger and James Ewens at the Wellcome labs in London, England.

The discovery of Lewy bodies:
One of the cardinal features of Parkinson’s disease in the brain is the presence of Lewy bodies – circular clusters of protein. In 1912, German neurologist Friedrich Lewy, just two years out of medical school and still in his first year as Director of the Neuropsychiatric Laboratory at the University of Breslau (now Wroclaw, Poland) Medical School discovered these ‘spherical inclusions’ in the brains of a people who had died with Parkinson’s disease.

The importance of the substantia nigra in Parkinson’s disease:
The first brain structure to be associated with Parkinson’s disease was the substantia nigra. This region lies in an area called the midbrain and contains the majority of the dopamine neurons in the human brain. It was in 1919 that a Russian graduate student working in Paris, named Konstantin Tretiakofirst demonstrated that the substantia nigra was associated with Parkinson’s disease. Tretiakoff also noticed circular clusters in the brains he examined and named them ‘corps de Lewy’ (or Lewy bodies) after the German neurologist Friedrich Lewy who first discovered them.

“Everyone wants answers and wants to know what the timeline is. Unfortunately, it’s a complex situation, and we don’t have the final answers yet.” Dennis Miller

1953-1968, Milestones in Parkinson’s Disease Research and Discovery (Part 1b: Historical):

Slide2

The first complete pathologic analysis of the Parkinsonian brain:
The most complete pathologic analysis of Parkinson’s disease with a description of the main sites of damage was performed in 1953 by Joseph Godwin Greenfield and Frances Bosanquet.

The discovery of a functional role for dopamine in the brain:
Until the late 1950s, the chemical dopamine was widely considered an intermediate in the production of another chemical called norepinephrine. That is to say, it had no function and was simply an ingredient in the recipe for norepinephrine. Then in 1958, Swedish scientist Arvid Carlsson discovered that dopamine acts as a neurotransmitter – a discovery that won Carlsson the 2000 Nobel prize for Physiology or Medicine.

The founding of the Parkinson’s Disease Foundation:
In 1957, a nonprofit organization called the Parkinson’s Disease Foundation was founded by William Black. It was committed to finding a cure for Parkinson’s Disease. Since its founding in 1957, PDF has funded more than $115 million worth of scientific research in Parkinson’s disease. The National Parkinson Foundation (NPF), was also founded in 1957 by Jeanne C. Levey. NPF is a national organization whose mission is to make life better for people with Parkinson’s through expert care and research. The foundation has funded more than $208 million in care, research and support services.

The discovery of the loss of dopamine in the brain of people with Parkinson’s disease:  In 1960, Herbert Ehringer and Oleh Hornykiewicz demonstrated that the chemical dopamine was severely reduced in brains of people who had died with Parkinson’s disease.

The first clinical trials of Levodopa:
Knowing that dopamine can not enter the brain and armed with the knowledge that the chemical L-dopa was the natural ingredient in the preoduction of dopamine, Oleh Hornykiewicz & Walther Birkmayer began injecting people with Parkinson’s disease with L-dopa in 1961. The short term response to the drug was dramatic: “Bed-ridden patients who were unable to sit up, patients who could not stand up when seated, and patients who when standing could not start walking performed all these activities with ease after L-dopa. They walked around with normal associated movements and they could even run and jump.” (Birkmayer and Hornykiewicz 1961).

The first internationally-used rating system for Parkinson’s disease:
In 1967, Melvin Yahr and Margaret Hoehn published a rating system for Parkinson’s disease in the journal Neurology. It involves 5 stages, ranging from unilateral symptoms but no functional disability (stage 1) to confinement to wheel chair (stage 5). Since then, a modified Hoehn and Yahr scale has been proposed with the addition of stages 1.5 and 2.5 in order to help better describe the intermediate periods of the disease.

Perfecting the use of L-dopa as a treatment for Parkinson’s disease:
In 1968, Greek-American scientist George Cotzias reported dramatic effects on people with Parkinson’s disease using oral L-dopa. The results were published in the New England Journal of Medicine. and L-dopa becomes a therapeutic reality with the Food and Drug Administration (FDA) approving the drug for use in Parkinson’s disease in 1970. Cotzias and his colleagues were also the first to describe L-dopa–induced dyskinesias.

“Nothing in life is to be feared, it is only to be understood. Now is the time to understand more, so that we may fear less.” Marie Curie

1972-1997, Milestones in Parkinson’s Disease Research and Discovery (Part 1c: Historical):

Levodopa + AADC inhibitors (carbidopa or benserazide:
 When given alone levodopa is broken down to dopamine in the bloodstream, which leads to some detrimental side effects.  By including an aromatic amino acid decarboxylase (AADC) inhibitor with levodopa allows the levodopa to get to the blood-brain barrier in greater amounts for better utilization by the neurons. In the U.S., the AADC inhibitor of choice is carbidopa and in other countries it’s benserazide.

The discovery of dopamine agonists:
Dopamine agonists are ‘mimics’ of dopamine that pass through the blood brain barrier to interact with target dopamine receptors. Since the mid-1970’s, dopamine agonists are often the first medication given most people to treat their Parkinson’s; furthermore, they can be used in conjunction with levodopa/carbidopa. The most commonly prescribed dopamine agonists in the U.S. are Ropinirole (Requip®), Pramipexole (Mirapex®), and Rotigotine (Neupro® patch). There are some challenging side effects of dopamine agonists including compulsive behavior (e.g., gambling and hypersexuality),  orthostatic hypotension, and hallucination.

The clinical use of MAO-B inhibitors:
In the late-1970’s, monoamine oxidase-B (MAO-B) inhibitors were created to block an enzyme in the brain that breaks down levodopa. MAO-B inhibitors have a modest effect in suppressing the symptoms of Parkinson’s.  Thus, one of the functions of MAO-B inhibitors is to prolong the half-life of levodopa to facilitate its use in the brain.  Very recently in clinical trials, it’s been shown that MAO-B inhibitors have some neuroprotective effect when used long-term.  The most widely used MAO-B inhibitors in the U.S. include Rasagiline (Azilect®) and Selegiline (Eldepryl® and Zelpar®); MAO-B inhibitors may reduce “off” time and extend “on” time of levodopa.

Fetal Cell transplantation:
After successful preclinical experiments in rodents, a team of researchers in Sweden, led by Anders Bjorklund and Olle Lindvall, began the first clinical trials of fetal cell transplantation for Parkinson’s disease. These studies involved taking embryonic dopamine cells and injecting them into the brains of people with Parkinson’s disease. The cells then matured and replaced the cells that had been lost during the progression of the disease.

The discovery of MPTP:
In July of 1982, Dr. J. William Langston of the Santa Clara Valley Medical Center in San Jose (California) was confronted with a group of heroin addicts who were completely immobile. A quick investigation demonstrated that the ‘frozen addicts’ had injected themselves with a synthetic heroin that had not been prepared correctly. The heroin contained a chemical called MPTP, which when injected into the body rapidly kills dopamine cells. This discovery provided the research community with a new tool for modeling Parkinson’s disease.

LSVT LOUD®:
LSVT stands for Lee Silverman Voice Treatment for use by speech pathologists; she was the first patient treated by this innovative therapeutic technique in 1985.   LSVT LOUD® was one of the first treatment strategies used for boosting the voice and sound levels of patients with Parkinson’s.   It is set up to be one hour per day for four days per week for four weeks of treatment, and it’s typically very effective in boosting volume and clarity of someone’s voice. LSVT LOUD® led to LSVT BIG®, developed by Dr. Becky Farley and others and it focused on improving movement, mobility, stiffness and stability in Parkinson’s.

Deep-brain stimulation (DBS) surgery becomes a treatment for Parkinson’s disease:
DBS is a surgical procedure used to treat some of the disabling neurological symptoms of Parkinson’s when drug therapy has failed to help the patient’s tremor, rigidity, stiffness, slowed movement, and walking problems.  There are three components in DBS surgery, the electrode, the extension from the electrode to the neurostimulator, which is also called the battery pack. The subthalamic nucleus and the globus pallidus are FDA-approved target sites in the brain for stimulation by the electrode. Although most patients still need to take medication after DBS, many patients experience considerable reduction of their  symptoms and are able to greatly reduce their medications.

“Imagination will often carry us to worlds that never were. But without it we go nowhere.” Carl Sagan

1997-2006, Milestones in Parkinson’s Disease Research and Discovery (Part 1d: Historical):

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Alpha synuclein becomes the first gene associated with familial cases of Parkinson’s disease and its protein is found in Lewy bodies:
In 1997, a group of researchers at the National institute of Health led by Robert Nussbaum reported the first genetic aberration linked to Parkinson’s disease. They had analyzed DNA from a large Italian family and some Greek familial cases of Parkinson’s disease.

The gene Parkin becomes the first gene associated with juvenile Parkinson’s disease:
The gene Parkin provides the instructions for producing a protein that is involved with removing rubbish from within a cell. In 1998, a group of Japanese scientists identified mutations in this gene that resulted in affected individuals being vulnerable to developing a very young onset (juvenile) version of Parkinson’s disease.

The first use of PET scan brain imaging for Parkinson’s disease:
Using the injection of a small amount of radioactive material (known as a tracer), the level of dopamine present in an area of the brain called the striatum could be determined in a live human being. Given that amount of dopamine in the striatum decreases over time in Parkinson’s disease, this method of brain scanning represented a useful diagnostic aid and method of potentially tracking the condition.

The launch of Michael J Fox Foundation:
In 1991, actor Michael J Fox was diagnosed with young-onset Parkinson’s disease at 29 years of age. Upon disclosing his condition in 1998, he committed himself to the campaign for increased Parkinson’s research. Founded on the 31st October, 2000, the Michael J Fox Foundation has funded more than $700 million in Parkinson’s disease research, representing one of the largest non-governmental sources of funding for Parkinson’s disease.

The Braak Staging of Parkinson’s pathology:
In 2003, German neuroanatomist Heiko Braak and colleagues presented a new theory of how Parkinson’s disease spreads based on the post mortem analysis of hundreds of brains from people who had died with Parkinson’s disease. Braak proposed a 6 stage theory, involving the disease spreading from the brain stem (at the top of the spinal cord) up into the brain and finally into the cortex.

The gene DJ1 is linked to early onset PD:
DJ1 (also known as PARK7) is a protein that inhibits the aggregation of Parkinson’s disease-associated protein alpha synuclein. In 2003, researchers discovered mutations in the DJ1 gene that made people vulnerable to a early-onset form of Parkinson’s disease.

The first GDNF clinical trial indicates neuroprotection in people with Parkinson’s disease:
A small open-label clinical study involving the direct delivery of the chemical Glial cell-derived neurotrophic factor (GDNF) into the brains of people with Parkinson’s disease indicated that neuroprotection. The subjects involved in the study exhibited positive responses to the treatment and postmortem analysis of one subjects brain indicated improvements in the brain.

The genes Pink1 and LRRK2 are associated with early onset PD:
Early onset Parkinson’s is defined by age of onset between 20 and 40 years of age, and it accounts for <10% of all patients with Parkinson’s.  Genetic studies are finding a causal association for Parkinson’s with five genes: α-synuclein (SNCA), parkin (PARK2), PTEN-induced putative kinase 1 (PINK1), DJ-1 (PARK7), and Leucine-rich repeat kinase 2 (LRRK2). However it happens, and at whatever age it occurs, there is no doubt that genetics and environment combine together to contribute to the development of Parkinson’s.

The discovery of induced pluripotent stem (IPS) cells:
In 2006, Japanese researchers demonstrated that it was possible to take skin cells and genetically reverse engineer them into a more primitive state – similar to that of a stem cell. This amazing achievement involved a fully mature cell being taken back to a more immature state, allowing it to be subsequently differentiated into any type of cell. This research resulted in the discoverer, Shinya Yamanaka being awarded the 2012 Nobel prize for Physiology or Medicine.

“Science is organized knowledge. Wisdom is organized life.” Immanuel Kant

2007-2016, Milestones in Parkinson’s Disease Research and Discovery (Part 1e: Historical):

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The introduction of the MDS-UPDRS revised rating scale:
The Movement Disorder Society (MDS) unified Parkinson’s disease rating scale (UPDRS) was introduced in 2007 to address two limitations of the previous scaling system, namely a lack of consistency among subscales and the low emphasis on the nonmotor features. It is now the most commonly used scale in the clinical study of Parkinson’s disease.

The discovery of Lewy bodies in transplanted dopamine cells:
Postmortem analysis of the brains of people with Parkinson’s disease who had fetal cell transplantation surgery in the 1980-1990s demonstrated that Lewy bodies are present in the transplanted dopamine cells. This discovery (made by three independent research groups) suggests that Parkinson’s disease can spread from unhealthy cells to healthy cells. This finding indicates a ‘prion-like’ spread of the condition.

SNCA, MAPT and LRRK2 are risk genes for idiopathic Parkinson’s disease:
Our understanding of the genetics of Parkinson’s is rapidly expanding. There is recent evidence of multiple genes linked to an increase the risk of idiopathic Parkinson’s. Interestingly, microtubule-associated protein tau (MAPT) is involved in microtubule assembly and stabilization, and it can complex with alpha-synuclein (SNCA).  Future therapies are focusing on  the reduction and clearance of alpha-synuclein and inhibition of Lrrk2 kinase activity.

 IPS derived dopamine neurons from people with Parkinson’s disease:
The ability to generate dopamine cells from skin cells derived from a person with Parkinson’s disease represents not only a tremendous research tool, but also opens the door to more personalized treatments of suffers. Induced pluripotent stem (IPS) cells have opened new doors for researchers and now that we can generate dopamine cells from people with Parkinson’s disease exciting opportunities are suddenly possible.

Neuroprotective effect of exercise in rodent Parkinson’s disease models:
Exercise has been shown to be both neuroprotective and neurorestorative in animal models of Parkinson’s. Exercise promotes an anti-inflammatory microenvironment in the mouse/rat brain (this is but one example of the physiological influence of exercise in the brain), which helps to reduce dopaminergic cell death.  Taking note of these extensive and convincing model system results, many human studies studying exercise in Parkinson’s are now also finding positive benefits from strenuous and regular exercise to better manage the complications of Parkinson’s.

Transeuro cell transplantation trial begins:
In 2010, a European research consortium began a clinical study with the principal objective of developing an efficient and safe treatment methodology fetal cell transplantation in people with Parkinson’s disease. The trial is ongoing and the subjects will be followed up long term to determine if the transplantation can slow or reverse the features of Parkinson’s disease.

Successful preclinical testing of dopamine neurons from embryonic stem cells:
Scientists in Sweden and New York have successfully generated dopamine neurons from human embryonic stem cells that can be successfully transplanted into animal models of Parkinson’s disease. Not only do the cells survive, but they also correct the motor deficits that the animals exhibit. Efforts are now being made to begin clinical trials in 2018.

Microbiome of the gut influences Parkinson’s disease:
Several research groups have found the Parkinson’s disease-associated protein alpha synuclein in the lining of the gut, suggesting that the intestinal system may be one of the starting points for Parkinson’s disease. In 2016, researchers found that the bacteria in the stomachs of people with Parkinson’s disease is different to normal healthy individuals. In addition, experiments in mice indicated that the bacteria in the gut can influence the healthy of the brain, providing further evidence supporting a role for the gut in the development of Parkinson’s disease.

“Any fool can know. The point is to understand.” Albert Einstein

2016-2017, Milestones in Parkinson’s Disease Research and Discovery (Part 2: Clinical trials either recently completed or in progress)

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Safety, Tolerability and Efficacy Assessment of Dynacirc (Isradipine) for PD (STEADY-PD) III trial:
Isradipine is a calcium-channel blocker approved for  treating high blood pressure; however, Isradipine is not approved for treating Parkinson’s. In animal models, Isradipine has been shown to slow the progression of PD by protecting dopaminergic neurons.  This study is enrolling newly diagnosed PD patients not yet in need of symptomatic therapy. Participants will be randomly assigned Isradipine or given a placebo.

Treatment of Parkinson’s Psychosis with Nuplazid:~50% of the people with Parkinson’s develop psychotic tendencies. Treatment of their psychosis can be relatively difficult. However, a new drug named Nuplazid™ was recently approved by the FDA specifically designed to treat Parkinson’s psychosis.

Opicapone (COMT Inhibitor) as Adjunct to Levodopa Therapy in Patients With Parkinson Disease and Motor Fluctuations:
Catechol-O-methyl transferase (COMT) inhibitors prolong the effect of levodopa by blocking its metabolism. COMT inhibitors are used primarily to help with the problem of the ‘wearing-off’ phenomenon associated with levodopa. Opicapone is a novel, once-daily, potent third-generation COMT inhibitor.  It appears to be safer than existing COMT drugs. If approved by the FDA, Opicapone is planned for use in patients with Parkinson’s taking with levodopa who experience wearing-off issues.

Nilotinib (Tasigna® by Novartis) indicates positive results in phase I trial:
Nilotinib is a drug used in the treatment of leukemia. In 2015, it demonstrated beneficial effects in a small phase I clinical trial of Parkinson’s disease. Researchers believe that the drug activates the disposal system of cells, thereby helping to make cells healthier. A phase II trial of this drug to determine how effective it is in Parkinson’s disease is now underway.

ISCO cell transplantation trial begins:
International Stem Cell Corporation is currently conducting a phase I clinical cell transplantation trial at a hospital in Melbourne, Australia. The company is transplanting human parthenogenetic stem cells-derived neural stem cells into the brains of people with Parkinson’s disease. The participants will be assessed over 12 months to determine whether the cells are safe for use in humans.

Neuropore’s alpha-synuclein stabilizer (NPT200-11) passes phase I trial:
Neuropore Therapies is a biotech company testing a compound (NPT200-11) that inhibits and stablises the activity of the Parkinson’s disease-associated protein alpha synuclein. This alpha-synuclein inhibitor has been shown to be safe and well tolerated in humans in a phase I clinical trial and the company is now developing a phase II trial.

mGluR4 PAM  (PXT002331) well tolerated in phase I trial:
Prexton Therapeutics recently announced positive phase I clinical trial results for their lead drug, PXT002331, which is the first drug of its kind to be tested in Parkinson’s disease. PXT002331 is a mGluR4 PAM – this is a class of drug that reduces the level of inhibition in the brain. In Parkinson’s disease there is an increase in inhibition in the brain, resulting in difficulties with initiating movements. Phase II clinical trials to determine efficacy are now underway.

Initial results of Bristol GDNF trial indicate no effect:
Following remarkable results in a small phase I clinical study, the recent history of the neuroprotective chemical GDNF has been less than stellar. A subsequent phase II trial demonstrated no difference between GDNF and a placebo control, and now a second phase II trial in the UK city of Bristol has reported initial results also indicating no effect. Given the initial excitement that surrounded GDNF, this result has been difficult to digest. Additional drugs that behave in a similar fashion to GDNF are now being tested in the clinic.

Immunotherapies proves safe in phase I trials (AFFiRis & Prothena):
Immunotherapy is a treatment approach which strengthens the body’s own immune system. Several companies (particularly ‘AFFiRis’ in Austria and ‘Prothena’ in the USA) are now conducting clinical trials using treatments that encourage the immune system to target the Parkinson’s disease-associated protein alpha synuclein. Both companies have reported positive phase I results indicating the treatments are well tolerable in humans, and phase II trials are now underway.

Living Cell Technologies Limited continue Phase II trial of NTCELLA New Zealand company called Living Cell Technologies Limited have been given permission to continue their phase II clincial trial of their product NTCELL, which is a tiny capsule that contains cells which release supportive nutrients when implanted in the brain. The implanted participants will be blindly assessed for 26 weeks, and if the study is successful, the company will “apply for provisional consent to treat paying patients in New Zealand…in 2017”.

MAO-B inhibitors shown to be neuroprotective:
MAO-B inhibitors block/slow the break down of the chemical dopamine. Their use in Parkinson’s disease allows for more dopamine to be present in the brain. Recently, several longitudinal studies have indicated that this class of drugs may also be having a neuroprotective effect.

Inhalable form of L-dopa:
Many people with Parkinson’s disease have issues with swallowing. This makes taking their medication in pill form problematic. Luckily, a new inhalable form of L-dopa will shortly become available following recent positive Phase III clinical trial results, which demonstrated a statistically significant improvements in motor function for people with Parkinson’s disease during OFF periods.

Exenatide trial results expected:
Exenatide is a drug that is used in the treatment of diabetes. It has also demonstrated beneficial effects in preclinical models of Parkinson’s disease, as well as an open-label clinical study over a 14 month period. Interestingly, in a two year follow-up study of that clinical trial – conducted 12 months after the patients stopped receiving Exenatide – the researchers found that patients previously exposed to Exenatide demonstrated significant improvements compared to how they were at the start of the study. There is currently a placebo-controlled, double blind phase II clinical trial being conducted and the results should be reported before the end of 2017.

“This is where it all begins. Everything starts here, today.” David Nicholls

A personal reflection:
In my adult life as a scientist, I’ve studied the world of hematology and how your blood clots.   And as a lifelong medical educator, I’ve taught the principles of biomedical science/hematology/oncology/immunology.   But this thing with Parkinson’s,  this for the rest of your life disorder is still relatively new in my life-line. Making this historical timeline was very educational for me; I learned a tremendous amount of information about this disease.  This timeline would not exist without the help and guidance of Simon my friend in Cambridge, England. He has his own blog entitled the Science of Parkinson’s.  Simon went out of his way to help plan and expedite this calendar of Parkinson’s history; I am most thankful for his participation.

“I’m going to be totally honest with you. Dealing with a diagnosis of Parkinson’s is not easy and there is no one, single technique that will ease the pain and no magic pill that will miraculously enable you to cope with it. However … I sincerely hope that you are able to come to terms with the diagnosis and perhaps even come to view it as a positive life-changing experience.” John Baxter

Cover photo credit: http://www.hoasaigon.com.vn/kcfinder/upload/images/tu-van-tang-hoa-chuc-mung-ngay-10-10-cho-nhung-nguoi-phu-nu-than-yeu-14.jp

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9 Things to Know About Exercise-induced Neuroplasticity in Human Parkinson’s

“A willing mind makes a hard journey easy.” Philip Massinger

“Lack of activity destroys the good condition of every human being.” Plato

Introduction: Much of my life has been spent exercising. Most of this exercise has been done with sheer delight.  Since receiving my Parkinson’s diagnosis, my opinion of exercise has changed.  With Parkinson’s, I’m now exercising as if my life depends on it.  Why?  Animal models (mouse and rat) of Parkinson’s have convincing shown the effect of exercise-induced neuroplasticity.  These animal studies demonstrated neuroprotection and even neurorestoration of Parkinson’s.  But we’re neither mice/rats nor are we an animal model of Parkinson’s disease; thus, this post is an update on exercise-induced neuroplasticity in human Parkinson’s.

“If you don’t do what’s best for your body, you’re the one who comes up on the short end.” Julius Erving

cartoon-brain-exercise

9 Things to Know About Exercise-induced Neuroplasticity in Human Parkinson’s: Neuroplasticity,  neuroprotection and neurorestoration are catchy words that populate a lot of publications, blogs from many of us with Parkinson’s and from professionals who study/work in the field of Parkinson’s.  It is important for you to develop your own opinion about exercise-induced neuroplasticity. My goal in this post is to provide the basic elements, concepts and key reference material to help you with this opinion. Here is a 1-page summary of “9 Things to Know About Exercise-induced Neuroplasticity in Human Parkinson’s” (click here to download page).

9_things_exercise_neuroplasticity_parkinsons

(1) Parkinson’s Disease (PD): Parkinson’s is a neurodegenerative disorder. Parkinson’s usually presents as a movement disorder, which is a slow progressive loss of motor coordination, gait disturbance, slowness of movement, rigidity, and tremor.  Parkinson’s can also include cognitive/psychological impairments. ~170 people/day are diagnosed with Parkinson’s in the USA; the average age of onset is ~60 years-old.

(2) Safety First: The benefit of an exercise routine/program will only work if you have (i) talked about it with your Neurologist and have his/her consent; (ii) you have received advice from a physical therapist/certified personal trainer about which exercises are ‘best’ for you; and (iii) you recognize that PD usually comes with gait and balance issues, and you are ready to begin. Safety first, always stay safe!

(3) Exercise: Exercise is activity requiring physical effort, carried out especially to sustain or improve health and fitness. Exercise is viewed by movement disorders clinicians, physical therapists, and certified personal trainers as a key medicinal ingredient in both treating and enabling patients at all stages of Parkinson’s.

(4) Brain Health: With or without Parkinson’s disease, taking care of your brain is all-important to your overall well-being, life-attitude, and health. For a balanced-healthy brain, strive for: proper nutrition and be cognitively fit; exercise; reduce stress; work and be mentally alert; practice mindfulness/meditation; sleep; and stay positive.

(5) Neuroplasticity: Neuroplasticity describes how neurons in the brain compensate for injury/disease and adjust their actions in response to environmental changes. “Forced-use exercise” of the more affected limb/side can be effective in driving neural network adaptation.  Ultimately, this can lead to improved function of the limb/side.

(6) Synapses are junctions between two nerve cells whereby neurotransmitters diffuse across small gaps to transmit and receive signals.

(7) Circuitry: A key result of neuroplasticity is the re-routing of neuronal pathways of the brain along which electrical and chemical signals travel in the central nervous system (CNS).

(8) Parkinson’s-specific Exercise Programs:
PWR!Moves (click here to learn more)
Rock Steady Boxing (click here to learn more)
LSVT BIG (click here to learn more)
Dance for PD (click here to learn more)
LIM Yoga (click here to learn more)
Tai Chi for PD (click here to learn more)

What types of exercise are best for people with Parkinson’s disease? Here is a nice overview of the benefits of exercise for those of us with Parkinson’s  (click here). Regarding the PD-specific exercise programs,  I am most familiar with PWR!Moves, Rock Steady Boxing and LSVT BIG (I’m certified to teach PWR!Moves, I’m a graduate of LSVT BIG, and I’ve participated in Rock Steady Boxing). A goal for you is to re-read ‘Safety First’ above and begin to decide which type of exercise you’d benefit from and would enjoy the most.

(9) Brain/Behavior Changes: The collective results found increase in corticomotor excitability, increase in brain grey matter volume, increase in serum BDNF levels, and decrease in serum tumor necrosis factor-alpha (TNFα) levels. These results imply that neuroplasticity from exercise may potentially either slow or halt progression of Parkinson’s.

What the terms mean: Corticomotor describes motor functions controlled by the cerebral cortex (people with Parkinson’s show reduced corticomotor excitability). Brain grey matter is a major component of the central nervous system consisting of neuronal cells, myelinated and unmyelinated axons, microglial cells, synapses, and capillaries. BDNF is brain-derived neurotrophic factor, which is a protein involved in brain plasticity and it is important for survival of dopaminergic neurons. Tumor necrosis factor-alpha (TNFα) is an inflammatory cytokine (protein) that is involved in systemic inflammation.  Some studies of exercise-induced neuroplasticity in human Parkinson’s found the above-mentioned changes, which would imply a positive impact of exercise to promote neuroplastic changes.

What can you do with all of the cited articles listed at the end? Compiled below are some comprehensive and outstanding reviews about exercise-induced neuroplasticity in Parkinson’s.  Looking through these papers, you’ll see years of work, but this work has all of the details to everything I’ve described.

“All life is an experiment. The more experiments you make the better.” Ralph Waldo Emerson

What I believe about neuroplasticity and exercise in Parkinson’s: [Please remember I am not a physician; definitely talk with your neurologist before beginning any exercise program.]  I think about exercising each day; I try to do it on a daily basis.  As a scientist, I’m impressed by the rodent Parkinson’s data and how exercise promotes neuroplasticity. The human studies are also believable; sustained aerobic exercise induces neuroplasticity to improve overall brain health. “Forced-use exercise” is an important concept; I try to work my right-side (arm and leg), which are slightly weaker and stiffer from Parkinson’s. Initially, I used my left arm more, now I ‘force’ myself on both sides with the hope my neural network is stabilized or even improving. If you enjoy exercising as I do, I view it as both an event and a reward; ultimately, I believe it can work and improve my response to Parkinson’s. If you don’t enjoy exercising, this may be more of a task and duty; however, the benefits over time can be better health. Exercise is good for you (heart and brain).  Begin slow, make progress, and see if you are living better with your disorder.  Remain hopeful and be both persistent and positive; try to enjoy your exercise.

“I am not afraid of storms for I am learning how to sail my ship.” Louisa May Alcott

Past blog posts: Both exercise itself and the benefit of exercise-induced neuroplasticity have been common themes for this blog, including (click on title to view blog posting):
Believe in Life in the Presence of Parkinson’s;
Déjà Vu and Neuroplasticity in Parkinson’s;
Golf And Parkinson’s: A Game For Life;
The Evolving Portrait of Parkinson’s;
Believe In Big Movements Of LSVT BIG Physical Therapy For Parkinson’s;
Meditation, Yoga, and Exercise in Parkinson’s;
Exercise and Parkinson’s.

“Do not let what you cannot do interfere with what you can do.” John Wooden

References on neuroplasticity and exercise in Parkinson’s:
Farley, B. G. and G. F. Koshland (2005). “Training BIG to move faster: the application of the speed-amplitude relation as a rehabilitation strategy for people with Parkinson’s disease.” Exp Brain Res 167(3): 462-467 (click here to view paper).

Fisher, B. E., et al. (2008). “The effect of exercise training in improving motor performance and corticomotor excitability in people with early Parkinson’s disease.” Arch Phys Med Rehabil 89(7): 1221-1229 (click here to view paper).

Hirsch, M. A. and B. G. Farley (2009). “Exercise and neuroplasticity in persons living with Parkinson’s disease.” Eur J Phys Rehabil Med 45(2): 215-229 (click here to view paper).

Petzinger, G. M., et al. (2010). “Enhancing neuroplasticity in the basal ganglia: the role of exercise in Parkinson’s disease.” Mov Disord 25 Suppl 1: S141-145 (click here to view paper).

Bassuk, S. S., et al. (2013). “Why Exercise Works Magic.” Scientific American 309(2): 74-79.

Lima, L. O., et al. (2013). “Progressive resistance exercise improves strength and physical performance in people with mild to moderate Parkinson’s disease: a systematic review.” Journal of Physiotherapy 59(1): 7-13 (click here to view paper).

Petzinger, G. M., et al. (2013). “Exercise-enhanced neuroplasticity targeting motor and cognitive circuitry in Parkinson’s disease.” Lancet Neurol 12(7): 716-726 (click here to view paper)..

Ebersbach, G., et al. (2015). “Amplitude-oriented exercise in Parkinson’s disease: a randomized study comparing LSVT-BIG and a short training protocol.” J Neural Transm (Vienna) 122(2): 253-256 (click here to view paper).

Petzinger, G. M., et al. (2015). “The Effects of Exercise on Dopamine Neurotransmission in Parkinson’s Disease: Targeting Neuroplasticity to Modulate Basal Ganglia Circuitry.” Brain Plast 1(1): 29-39 (click here to view paper).

Abbruzzese, G., et al. (2016). “Rehabilitation for Parkinson’s disease: Current outlook and future challenges.” Parkinsonism Relat Disord 22 Suppl 1: S60-64 (click here to view paper).

Hirsch, M. A., et al. (2016). “Exercise-induced neuroplasticity in human Parkinson’s disease: What is the evidence telling us?” Parkinsonism & Related Disorders 22, Supplement 1: S78-S81 (click here to view paper)

Tessitore, A., et al. (2016). “Structural connectivity in Parkinson’s disease.” Parkinsonism Relat Disord 22 Suppl 1: S56-59 (click here to view paper).

“If we could give every individual the right amount of nourishment and exercise, not too little and not too much, we would have found the safest way to health.” Hippocrates

“Life is complex. Each one of us must make his own path through life. There are no self-help manuals, no formulas, no easy answers. The right road for one is the wrong road for another…The journey of life is not paved in blacktop; it is not brightly lit, and it has no road signs. It is a rocky path through the wilderness.” M. Scott Peck

Cover photo credit: http://paper4pc.com/free-seascape.html#gal_post_55564_free-seascape-wallpaper-1.jpg

Brain exercising cartoon: http://tactustherapy.com/neuroplasticity-stroke-survivors/

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2016: The Year in Parkinson’s

“The most beautiful experience we can have is the mysterious. It is the fundamental emotion that stands at the cradle of true art and true science.” Albert Einstein

“Your assumptions are your windows on the world. Scrub them off every once in a while, or the light won’t come in.” Isaac Asimov

Summary: (Part 1) A brief review of my year with Parkinson’s. (Part 2) An overview of 12 scientific research studies on Parkinson’s from 2016.

Part 1. A personal Parkinson’s 2016 calendar review

Life with Parkinson’s: 706 days ago I started this blog ‘Journey with Parkinson’s’; and it’s been a remarkable journey through time since then.  Life is full, rarely a dull moment.  Dealing with a disorder like Parkinson’s is difficult because it slowly creeps around your body, somewhat stealth by nature but always ever present.  It requires a daily inventory of body movements, mental capacity and overall self-feelings compared to the day-week-month-year before.

Life is loving, fun, intellectually challenging, active, full, rarely a moment off; however, its best that way for me.  I close this paragraph by repeating two quotes from last year. They remind me to simply try to live as best as I am able for as long as I can.  My hope for you is likewise as well; keep going, keep working, stay active, stay the course.  Please make a manageable life-plan/contract with your care-partner, family and close friends; keep going, and please don’t give up.

“Never confuse a single defeat with a final defeat.” F. Scott Fitzgerald

“If you fell down yesterday, stand up today.” H.G. Wells

My year with Parkinson’s: To highlight my 2016, I’ve chosen 1 event/month to describe (not mentioned are the trips to the beach/vacation with Barbara, golf with the golf buddies, and other activities related to education, research and outreach for Parkinson’s.)  I am a very fortunate person.

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January-June, 2016:
(JAN) The 22nd year/class of undergraduates taking my spring semester course on ‘Biology of Blood Diseases’, great fun!
(FEB) An anniversary dinner with Barbara, a most loving person and the best care-partner.
(MAR) Started work on the WPC Parkinson Daily (eNewspaper) for the World Parkinson Congress).
(APR) Compiled all of the quotes from the students in class that led to the Kindle version (2016)/Paperback version (2017) of “A Parkinson’s Reading Companion”  (Click here to read about it).
(May) Graduation ceremonies are always on Mother’s Day weekend; it is filled with joy and regalia, promise and the future ahead for all of the graduates (typically, I attend the medical school ceremony on Saturday and as many undergraduate ceremonies on SAT-SUN my schedule permits (picture above is from the Dept. Biology commencement).
(JUN) A weekend in the Smoky Mountains in Asheville, NC: to attend a Parkinson’s retreat, to relax-renew-play golf, and to get a second Parkinson’s-related tattoo.

“Be happy for this moment. This moment is your life.” Omar Khayyam

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July-December, 2016:
(JUL) A weekend in Greenville, SC to participate and get certified in PWR! (Parkinson Wellness Recovery); an amazing experience (click here to read blog post about it).
(AUG) Truly a professional highlight of my career being chosen by the medical students to deliver the 2016 Richard H. Whitehead Lecture (click here to read blog post about it).
(SEP) Attended and presented a poster at the 4th World Parkinson Congress (WPC) in Portland, OR (click here to read about the WPC).
(OCT) Moving Day® NC Triangle, National Parkinson Foundation; great team and such a fun day/experience (click here to read about NC Triangle Moving Day).
(NOV) Research proposal submitted on the role of proteases and their inhibitors, alpha-synuclein and exercise in Parkinson’s. It is something I’ve been thinking about all of last year (click here to read about the funding program).
(DEC) Finished teaching the 3rd class of the Honor’s-version and fall semester of the undergraduate ‘Biology of Blood Diseases’ course; a great honor for me.

“Success is not the key to happiness. Happiness is the key to success. If you love what you are doing, you will be successful.” Albert Schweitzer

Part 2. The year (2016) in Parkinson’s science

Parkinson’s with a hopeful future: To live successfully with a chronic and progressing neurodegenerative disorder like Parkinson’s requires much, but in the least it takes hope.  We must remain hopeful that advances in Parkinson’s treatment are being made and that our understanding of the science of Parkinson’s is continuing to evolve.

Parkinson’s research: Parkinson’s is the most prevalent neurodegenerative movement disorder.  According to PubMed, there were 6,782 publications in 2016 that used “Parkinson’s disease” in the Title/Abstract.  Likewise in 2016, PubMed had 9,869 and 1,711 citations on Alzheimer’s disease and on Amyotrophic Lateral Sclerosis (ALS), respectively. Most research studies move in incremental steps; we describe a hypothesis and collect the data to hopefully advance us forward.

2016, the year in Parkinson’s: To remind us of some of these forward steps in Parkinson’s research, and to add to our base-level of hope, here are 12 projects from 2016 regarding Parkinson’s (there are several studies, not mentioned here, that I’m currently working on for individual blog posts because they seemed super-relevant and in need of more thorough presentation/explanation).  Although 12 is a minuscule list of citations/work reported from last year, it reinforces a simple notion that our trajectory is both positive and hopeful.

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January, 2016: Dipraglurant FDA-approved to treat dyskinesia. After ~5 years of treatment with the ‘gold-standard’ Levodopa/Carbidopa, many people-with-Parkinson’s develop drug-induced involuntary movement (also called dyskinesia).  This can be a serious side-effect of levodopa, and it can lead to numerous detrimental consequences.  The pharmaceutical company, Addex Therapeutics, has received orphan drug status for their drug named Dipraglurant, which will be used for the treatment of levodopa-induced dyskinesia.  Click here to read about the putative molecular mechanism of Dipraglurant, what advantages Addex gains from the designated orphan-drug status, and for more information about Addex.

“January is here, with eyes that keenly glow, A frost-mailed warrior striding a shadowy steed of snow.” Edgar Fawcett

February, 2016: Early detection of Parkinson’s from mouth salivary gland biopsy.   There is no definitive test to identify Parkinson’s in its early stages.  Finding an easily accessible tissue for  biopsy  to help with the diagnosis would be of value.  From autopsy samples, the submandibular saliva glands in the mouth seemed to be a relevant and easily accessible site to study.  The test involved inserting a needle into the submandibular salivary gland under the jaw,  staining for modified-a-synuclein.   The results revealed  that Parkinson’s patients had  increased level of a-synuclein  compared to patients  without Parkinson’s.  Click here to view this paper: Adler, Charles H. et al. “Peripheral Synucleinopathy in Early Parkinson’s Disease: Submandibular Gland Needle Biopsy Findings.” Movement disorders : official journal of the Movement Disorder Society 31.2 (2016): 250–256. PMC. Web. 13 Feb. 2017.

“Even though February was the shortest month of the year, sometimes it seemed like the longest.” Lorraine Snelling

March, 2016:  Three-dimensional scaffold used  to grow neuronal cells for transplant to brain.  Scientists have been able to convert adult stem cells into neuronal cells by culturing the stem cells in three-dimensional  scaffolding.   There are many obstacles successfully using stem cells to treat Parkinson’s disease; one of them is converting the stem cells into dopamine-producing-neuronal cells to replace the dead brain cells of the patient.   The three-dimensional scaffolding facilitated which allowed the neuronal cells to be injected into mice. Hopefully, this approach will eventually be ready for testing in humans; however, this is a potential glimpse to the future. To read this research paper, click here: “Generation and transplantation of reprogrammed human neurons in the brain using 3D microtopographic scaffolds” by Aaron L. Carlson et al., in Nature Communications. Published online March 17 2016 doi:10.1038/ncomms10862

“It was one of those March days when the sun shines hot and the wind blows cold: when it is summer in the light, and winter in the shade.” Charles Dickens, Great Expectations

April, 2016: Role of Mer and Axl in immune clearance of neurons in Parkinson’s.
TAM receptors are found on immune system cells and they help clear out dead cells  generated by out bodies.  Two of the TAM receptors, dubbed Mer and Axl, help immune cells called macrophages act as garbage collectors. This study asked whether or not the brain microglial cells (brain macrophages) had such activity through Mer and Axl.  Interestingly, in mice lacking Mer and Axl, neurons regenerated much more rapidly in certain areas of the brain. Furthermore, microglial expression of Axl was upregulated in the inflammatory environment in a mouse model of Parkinson’s.  These results identify TAM receptors as controllers of microglial scavenger activity and also as potential therapeutic targets for Parkinson’s.  Click here to view this article: Fourgeaud, L., et al. (2016). “TAM receptors regulate multiple features of microglial physiology.” Nature 532(7598): 240-244.

“April hath put a spirit of youth in everything. (Sonnet XCVIII)”  William Shakespeare, Shakespeare’s Sonnets

May, 2016:  Complex genetics found in the study of Parkinson’s in human brain tissue.  Genetic changes were found in Parkinson’s disease and Parkinson’s disease dementia.  A team of scientists used RNA sequencing to illuminate two phenomena linked with the onset of Parkinson’s disease: specifically, differential gene expression and alternative splicing of genes. The study describes 20 differentially expressed genes in Parkinson’s and Parkinson’s dementia, comparing these with healthy controls. Genes showing over-expression included those involved with cell movement, receptor binding, cell signaling and ion homeostasis. Under-expressed genes had an involvement with hormone signaling.  These results increase our understanding of Parkinson’s; furthermore, the complexity of their results suggest we may be able to achieve a more detailed diagnosis .  Click here to view paper: Henderson-Smith, Adrienne et al. “Next-Generation Profiling to Identify the Molecular Etiology of Parkinson Dementia.” Neurology: Genetics 2.3 (2016): e75.

“May, more than any other month of the year, wants us to feel most alive.” Fennel Hudson

June, 2016: Mutations in a gene called TMEM230 causes Parkinson’s. The role of TMEM230  was found to be in packaging the neurotransmitter dopamine in neurons.  Interestingly, TMEM230 bridges membranes in synaptic vesicles; these vesicles are storage reservoirs for neurotransmitters. Since the loss of dopamine-producing neurons defines Parkinson’s, a defect in TMEM230 implies a new link to a genetic cause of Parkinson’s.  The research team identified this mutation in Parkinson’s patients in North America and Asia. Click here to view paper: Deng, H-X, et al., “Identification of TMEM230 mutations in familial Parkinson’s disease”. Nature Genetics 48, 733–739 (2016).

“I wonder what it would be like to live in a world where it was always June.”  L.M. Montgomery

July, 2016: Improving deep brain stimulation (DBS), one patient at a time.  Instead of one-size-fits-all, these researchers are pioneering a novel strategy for fine-tuning DBS on each person’s individual physiology.  Their DBS platform, termed Phasic Burst Stimulation, has the potential to (i) enhance therapeutic efficacy, (ii) extend battery lifespan; (iii) reduce detrimental side effects, and (iv)  adjust as each person’s motor symptoms change.  This tuning-based DBS approach has real promise.  Click here to view paper: “Phasic Burst Stimulation: A Closed-Loop Approach to Tuning Deep Brain Stimulation Parameters for Parkinson’s Disease.” by A.B. Holt et al., PLOS Computational Biology, http://dx.doi.org/10.1371/journal.pcbi.100501

“My life, I realize suddenly, is July. Childhood is June, and old age is August, but here it is, July, and my life, this year, is July inside of July.” Rick Bass

August, 2016: Comparison of different movement disorders to better understand Parkinson’s.  These researchers compared multiple system atrophy (MSA) and progressive supranuclear palsy (PSP) to Parkinson’s.  MSA and PSP are progressive disorders that also cause changes in balance and walking.  The study consisted of  functional magnetic resonance imaging (fMRI) brain scans with each person using a grip strength exercise, which showed changes in the regions of brain that control muscle movement. Parkinson’s patients showed changes in the putamen and the primary motor cortex;  MSA patients had changes in the primary motor cortex, the supplementary motor area and the superior cerebellum. PSP patients showed a change in all four areas.  Normal healthy controls had no changes. These detailed results (i) show the progression of each movement disorder and (ii) indicate that biomarkers for these specific-regions of the brain might be useful for not only monitoring disease progression but also response to therapy. Click here to view article: Burciu et al., “Functional MRI of disease progression in Parkinson disease and atypical parkinsonian syndromes.”, Burciu, Chung, Shukla, Ofori, McFarland, Okun, Vaillancourt, Neurology, 016 Aug 16;87(7):709-17. doi: 10.1212/WNL.0000000000002985

“The month of August had turned into a griddle where the days just lay there and sizzled.” Sue Monk Kidd, The Secret Life of Bees

September, 2016: Preventing falls by combining virtual reality and treadmill training.   Falling down is one of the most common and most detrimental problems in the elderly  with Parkinson’s. This research team combined treadmill use with virtual reality training. They tested a large group of older adults at high risk for falls; they found that treadmill training with virtual reality led to reduced fall rates compared to treadmill training alone.Click here to view article: Mirelman et al.,  “Addition of a non-immersive virtual reality component to treadmill training to reduce fall risk in older adults (V-TIME): a randomised controlled trial”, The Lancet, 2016 Sep 17;388(10050):1170-82. doi: 10.1016/S0140-6736(16)31325-3

“By all these lovely tokens September days are here, With summer’s best of weather And autumn’s best of cheer.”  Helen Hunt Jackson

October, 2016: Caffeine-based compounds stop alpha (a)-synuclein misfolding in a yeast model of Parkinson’s. The aggregation (misfolding) of the protein a-synuclein is thought to be a key contributing factor in neuronal cell death that leads to Parkinson’s.  The misfolded a-synuclein ultimately forms what are termed Lewy bodies, which produce much neuronal cell morbidity and mortality. Caffeine has been shown to be  somewhat protective against Parkinson’s. The study here made double-headed constructs of compounds using caffeine and nicotine and other chemicals and asked whether or not they could stop a-synuclein misfolding.  Possibly a far-fetched  idea, 2 of the caffeine-double-headed compounds worked.  These studies used a novel a-synuclein-fluorescent-green substance expressed in yeast.  Expression of the green-a-synuclein misfolded and killed the yeast; however, in the presence of the caffeine-adducts, the green-a-synuclein folded properly and the yeast stayed alive.  Such cool science.  To read this paper, click here) “Novel dimer compounds that bind α-synuclein can rescue cell growth in a yeast model overexpressing α-synuclein. a possible prevention strategy for Parkinson’s disease”, Jeremy Lee et al., ACS Chem Neurosci. Epub 2016 Oct 7. 2016 Dec 21;7(12):1671-1680. doi: 10.1021/acschemneuro.6b00209.

“Autumn is my favourite season of all. It is a transitory period that allows the earth to rest before it sees the harshness of winter and hears the promise of spring.”  Kamand Kojouri

November, 2016: PINK1 gene mutation linked to early onset of Parkinson’s.  A single mutation in the PTEN-induced putative kinase 1 (PINK1) gene has been found to promote  the development of early-onset Parkinson’s. There is growing evidence that PINK1 collaborates with the protein named PARKIN; together they help regulate neuronal cell mitochondria. This interaction to regulate mitochondria (the cell’s power plant) by  PINK1 and PARKIN is important because many brain disorders are known to have issues with energy production (mitochondria) besides Parkinson’s. Click here to view paper: Puschmann, A., et al. Heterozygous PINK1 p.G411S increases risk of Parkinson’s disease via a dominant-negative mechanism. Brain 2016; 140 (1): 98-117. doi: 10.1093/brain/aww261.

“October extinguished itself in a rush of howling winds and driving rain and November arrived, cold as frozen iron, with hard frosts every morning and icy drafts that bit at exposed hands and faces.”  J.K. Rowling, Harry Potter and the Order of the Phoenix

December, 2016:  President Obama signed the 21st Century Cures Act. Not a paper but a National Institute of Health (NIH) federally-supported research initiative. The Cures Act is focused on  cancer, brain disease, drug addiction and other diseases/processes for the next  decade. The 21st Century Cures Act contains $4.8 billion in new NIH (National Institutes of Health) funds, including the BRAIN Initiative for the comprehensive mapping of  the brain.  It is anticipated that we will achieve an even better understanding of Parkinson’s than we have today.  Recently, a commentary about the Cures Act from the viewpoint of the NIH was published in the New England Journal of Medicine. Click here to read this article: Hudson, K. L. and F. S. Collins (2017). “The 21st Century Cures Act — A View from the NIH.” New England Journal of Medicine 376(2): 111-113.

“December’s wintery breath is already clouding the pond, frosting the pane, obscuring summer’s memory…” John Geddes

“I like the scientific spirit—the holding off, the being sure but not too sure, the willingness to surrender ideas when the evidence is against them: this is ultimately fine—it always keeps the way beyond open—always gives life, thought, affection, the whole man, a chance to try over again after a mistake—after a wrong guess.”  Walt Whitman, Walt Whitman’s Camden Conversations

Useful Parkinson’s disease News/Health Information/Reference Sites (click on links below):
Google Scholar- Parkinson’s disease
Parkinson’s News Today Weekly Digest
Medical News Today (MNT)
Science News- Mind & Brain News
Harvard Medical School- Harvard Healthbeat
The Science of Parkinson’s disease
STAT
NY Times- Well
Neurology Advisor

Cover photo credit: winter smoky mts- http://holicoffee.com/wp-content/uploads/2015/05/great-smoky-mountains-national-park-usa-extreme-out-door-hiking-trail-adventure-37.jpg

PD word cloud- http://us.123rf.com/450wm/lculig/lculig1612/lculig161200292/66735623-parkinson-disease-word-cloud.jpg?ver=6

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Journey with Parkinson’s Blog in Feedspot Top 50 Parkinson Blogs

“Every day is a journey, and the journey itself is home.” Matsuo Basho

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Award: The Journey with Parkinson’s blog has been recognized by FeedSpot as a top 50 blog on Parkinson’s Disease! “Top 50 Parkinson Blogs & Websites For People Living With Parkinson’s Disease” (Click here to see the list).

“‘Thank you’ is the best prayer that anyone could say.” Alice Walker

Acknowledgment and thank you: We thank FeedSpot for adding this blog to this very distinguished group of blog sites; this is indeed an honor.

Thank you to the readers and followers of the blog; your continued presence, comments and suggestions truly help sustain the time and energy needed to compose these blog posts.

“The measure of achievement is not winning awards. It’s doing something that you appreciate, something you believe is worthwhile.” Julia Child

The future: It is my hope that the Journey with Parkinson’s blog will continue to educate, to bolster and to offer support to anyone with Parkinson’s (or any other neurodegenerative disorder).

“Each day we wear a cape on our back labeled with the letters PD (Parkinson’s Disease).  Each day we bring a positive reaction to handle our symptoms, I am convinced we begin to fade those letters; we begin to gain control of our symptoms. While it is not easy to remain positive with such a somber disorder, staying positive can help you cope. Thus, we should strive to live positively as we try to shed our cape named Parkinson’s.” Frank C. Church (Excerpt from “Hope, Courage, Persistence, Positivity, Mindfulness, and the Journey“; click here to read this blog post).

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