Rock Steady Boxing

Rock Steady Boxing improves the quality of life for people battling Parkinson’s disease through non-contact, boxing inspired fitness training.

We are learning everyday that there are ways in which people with Parkinson’s disease can enhance their daily quality of life and even build impressive power,
strength, flexibility and speed! By exercising with Coaches who know the ropes, you can fight your way out of the corner and start to feel and function better.

Boxing works by moving your body in all planes of motion while continuously changing the routine as you progress through the workout. These classes have proven that anyone, at any level of Parkinson’s, can actually lessen their symptoms and lead a healthier/happier life.

To see individuals in the ring click here

Fruit flies study identifies gene that could help treat Parkinson’s

King’s College London (KCL) researchers have identified a gene that regulates nerve function, and could be switched off as part of a new Parkinson’s treatment. The breakthrough was made by studying the disease in fruit flies, and significantly furthers our understanding of the degenerative condition.

Parkinson’s is a wide-spread condition, affecting more than seven million people across the globe. It causes a progressive loss of motor function, as well as cognitive impairment and psychiatric issues, and current treatments only deal with the symptoms of the disease, rather than tackling the route of the problem.

In an attempt to change that, the KCL team turned to fruit flies. They’re interesting creatures, and in the past we’ve tweaked their genes to extend their lifespan, observed their ability to detect cancerous cells, and much more. Now researchers have looked to the little insects to help in the fight against Parkinson’s.

Closely studying insects with the disease, the team discovered that damaged mitochondria emit a signal that stop the function of nerve cells – themselves regulated by a gene known as HIFalpha. They then found that when the gene was deactivated, the nerve function – normally disabled by the damaged mitchondria – was restored, and further failure of nerve cells was prevent. The same effect was observed when turning off the gene in fruit flies with Leigh syndrome, suggesting the method may be useful in treating numerous neurodegenerative diseases.

As the HIFalpha gene is found in humans, the research could lead to new treatments. Based on the results from the fruit fly testing, it could be a big breakthrough.

“Like their human counterparts, flies with Parkinson’s disease progressively lose motor function, which includes negative impact on their ability to climb,” says KCL’s Dr. Joseph Bateman. “Remarkably, we found that switching off a particular gene dramatically improved their motor function and climbing ability.”

According to the team, the study has significantly improved our understanding of Parkinson’s disease. We now know that the damaged mitochondria are responsible for loss of nerve function, and have identified a strong avenue of research for treating the disease.

The study was carried out in conjunction with the University of York, and Imperial College London. The researchers published their findings in the journal Proceedings of the National Academy of Sciences of the United States of America.

Chris Wood October 21, 2015

The Bright Side of Parkinson’s

The New York Times Feb.21,2015

EUGENE, Ore. — FOUR years ago, I was told I had Parkinson’s disease, a condition that affects about one million Americans. The disease is relentlessly progressive; often starting with a tremor in one limb on one side of the body, it spreads. The patient’s muscles become more rigid, frequently leading to a stooped posture, and movements slow down and get smaller and less fluid. As the disease advances — usually over a number of years — the patient becomes more and more disabled, experiencing symptoms from constipation to sleep disorders to cognitive impairment.
Can Parkinson’s be slowed, stopped or even reversed? Can the disease be prevented before it starts, like polio and smallpox? More than at any time in history, success seems possible.

Having sequenced the human genome, biomedical researchers have now set their sights on the ultimate frontier — the human brain. The formidable puzzle is to figure out how a three-pound lump of mostly fatty matter enables us to perform a seemingly endless number of tasks, like walking, seeing, hearing, smelling, tasting, touching, thinking, loving, hating, speaking and writing … and why those awesome abilities break down with neurological disease. Many scientists view Parkinson’s as a so-called pathfinder. If they can figure out what causes Parkinson’s, it may open the door to understanding a host of other neurodegenerative diseases — and to making sense of an organ of incredible complexity.

In Parkinson’s, the circuitry in a tiny region of the brain called the basal ganglia becomes dysfunctional. Along with the cerebellum, the basal ganglia normally acts as a kind of adviser that helps people learn adaptive skills by classic conditioning — rewarding good results with dopamine bursts and punishing errors by withholding the chemical. Babies rely on the basal ganglia to learn how to deploy their muscles to reach, grab, babble and crawl, and later to accomplish many complex tasks without thinking. For example, when a tennis player practices a stroke over and over again, the basal ganglia circuitry both rewards and “learns” the correct sequence of activities to produce, say, a good backhand drive automatically.

But this brain circuit has a vulnerability: It depends on dopamine. When the production of dopamine is interrupted, as it is with Parkinson’s, the signals passing through the basal ganglia are garbled, and it ends up giving poor advice. Corrupted signals pass to other brain regions such as the thalamus (which relays sensory and motor data) and the cortex (which is responsible for many higher functions such as language and consciousness). These bad signals disrupt communication between the brain and the muscles. This is one reason people with Parkinson’s have trouble picking up small objects and moving around fluently: Their motions are too hesitant, too small, too slow, too rigid, too shaky, too feeble and badly timed. These are symptoms of a brain in conflict with itself.

Having Parkinson’s feels a bit like going on vacation in another country and having to drive on the “wrong” side of the road. Driving is one of those activities that we outsource, in large part, to the basal ganglia. When an American, who has spent thousands of hours driving on the right side of the street, tries to drive in England, his learned habits are a liability. To compensate, he must invoke the deliberate and goal-directed part of his brain — the cortex — to override the basal ganglia. The driving will be difficult, partly because the conscious brain is now doing all the work, but mainly because it’s having to compensate for signals from the basal ganglia that are inappropriate for the situation at hand.

But why is the production of dopamine interrupted in the first place?

That may come down to the behavior of a common protein called alpha-synuclein. This molecule’s importance for Parkinson’s was discovered over 20 years ago, when the New Jersey neuroscientist Lawrence Golbe stumbled across two patients who were descendants of an extended family originally from the Italian village of Contursi. This family was cursed with a very rare genetic form of Parkinson’s; family members had a 50 percent chance of inheriting the disease. Subsequent research found that those affected carried a mutated gene on Chromosome 4 that coded for alpha-synuclein.

While Parkinson’s disease is not usually inherited like this, the discovery provided a vital clue about the way Parkinson’s typically worked. Most patients do not have this mutation, but they do, it turned out, have sticky deposits of alpha-synuclein inside their brains, found when they were examined post-mortem. This protein seems to be an integral part of the disease that affects all Parkinson’s patients.

Here’s the theory scientists have come up with: Sometimes good proteins go bad. For multiple reasons (like genes, environment and age) proteins can “misfold” and stick to other proteins. When proteins do this, they can become toxic, capable of jumping from cell to cell, causing other alpha-synuclein proteins to do the same and potentially killing neurons (especially dopamine-producing ones) in their wake. This process is not confined to Parkinson’s disease. Misfolded proteins appear to be implicated in other devastating neurological disorders such as Alzheimer’s disease, Huntington’s disease, Lou Gehrig’s disease and Creutzfeldt-Jakob disease — a human variant of mad cow.

What can be done about such badly behaving proteins? Cells possess an elaborate series of control mechanisms to help proteins behave correctly and to destroy and recycle them if they don’t. But these controls are not perfect. As human life spans increase so, too, does the likelihood of protein malfunctioning that could lead to neurological disease.

SO patients like me are looking to neuroscience research to lend nature a helping hand. And remarkably, some researchers foresee the possibility that one day in the not too distant future they may be able to develop drugs to target these rogue proteins, potentially combating several neurological diseases in one go.

An American biotech company, NeuroPhage, for example, plans to enroll Alzheimer’s and Parkinson’s patients in 2016 and 2017 in Phase 1 trials of its new product, a genetically engineered compound derived from a naturally occurring virus called M13. Researchers have demonstrated that this compound can enter rodents’ brains and neutralize toxic clumps of alpha-synuclein and the corresponding targets for Alzheimer’s (the proteins amyloid beta and tau). The question is, will it work as well in people’s brains? And will it arrest or reverse patients’ symptoms?

People with Parkinson’s progressively lose core pieces of themselves. We forget how to walk. Our arm muscles get weaker. Our movements slow down. Our hands fumble simple tasks like buttoning a shirt or balancing spaghetti on a fork. Our faces no longer express emotions. Our voices lose volume and clarity. Our minds, in time, may lose their sharpness and more. But unlike many cancer victims, people with Parkinson’s tend to survive for a long time. And unlike Alzheimer’s or Huntington’s patients, many of us can report lucidly on our condition until the end. Parkinson’s patients like me take comfort from the idea that our insights can help unpack these diseases and assist in the scientific pursuit of better therapies and ultimate cures.

Jon Palfreman is a professor of broadcast journalism at the University of Oregon and the author of the forthcoming book “Brain Storms: The Race to Unlock the Mysteries of Parkinson’s Disease.”

Yoga for Movement Disorders CONTINUES!

Mondays at 2pm at Project Yoga Richmond, 6517 Dickens Place, Richmond, VA 23230
Contact Sarah Humphries at (804)840-4881 or email:
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June 30th will be final Monday this is offered.

However, Sarah offers a Genle EnJoYoga class most Saturdays at 10:30am at the same location and $10 recommended donation. This class is appropriate for people with PD. Contact her for details.

Gentle Yoga for PD – April 2014

Do you have Parkinson’s Disease, ET, dystonia, MS or another neurological condition?
Have you been curious about trying yoga?

PROJECT YOGA RICHMOND (PYR) is offering a 4 week gentle yoga class for people with movement disorders. Try one class or come to them all!

Dates: Mondays: April 7, April 14, April 21, and April 28, 2014
Time: 2:00 – 3:00 pm
Location: Project Yoga Richmond (PYR) studio is located at 6517 Dickens Place, Richmond, VA 23230
Audience: Anyone with a movement disorder and their spouse or care partner
Cost: All on-site classes are donation-based. On-site suggested donation is $10 per class or pay what you can. (Cash and check only, please.)
Instructor: PYR Ambassador, Sarah Humphries, ERYT – 200

Questions? contact Lynn Klanchar (804) 675-6952 at PADRECC, MCGuire VAMC

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