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Parkinson’s Disease

Parkinson’s disease: New medical information

Parkinson’s disease affects about 100,000 Canadians each year. It is relentlessly progressive; often starting with a tremor in one limb (finger or arm), it gradually spreads. The patient’s muscles become more rigid, frequently leading to stooped posture, and movements slow down and get smaller and less fluid. Over years, as the disease advances, the patient becomes more and more disabled, experiencing symptoms from constipation to sleep disorders to cognitive impairment.
When you consider the list of debilitating diseases, Parkinson’s is way down the list. However, scientists feel that if they can unlock the mysterious causes of this disease it will open the door to understanding other neurodegenerative diseases and a better understanding of how the brain works.
Parkinson’s disease eventually affects your walking, seeing, hearing, smelling, tasting, touching, thinking, loving, hating, speaking and writing. Therefore finding a cure or a way to control this disease would open new areas of research into all of your brain’s activities.
In Parkinson’s, the circuitry in a tiny region of the brain called basal ganglia becomes dysfunctional. Along with the cerebellum, the basal ganglia normally act as a kind of advisor that helps people learn adaptive skills by classic conditioning; rewarding good results with dopamine outbursts and punishing errors by withholding the chemical. Babies rely on the basal ganglia to learn how to use 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 of both circuitry both “rewards “and learns the correct sequence of activities to produce, say, a good serve automatically.
But this brain circuit has 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 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 fluidly: Their motions are too hesitant, too small, too slow, too rigid, too shaky, too feeble and badly timed. The brain is in conflict with itself.
To imagine what Parkinson’s is like, imagine you went on vacation to the Cayman Islands, a British colony where everyone drives on the left and intersections have these strange roundabouts. Our basal ganglia lets us drive automatically but now, in order to compensate, the deliberate and goal-directed part of the brain, the cortex, must be used to override the basal ganglia. The driving will be difficult, partly because the conscious brain is doing all the work, but mainly because it has to compensate for signals from the basal ganglia that do not work for driving on the opposite side of the road. May be the reason why I had a little fender-bender when I was there last year.
But what strange thing in your brain stops the production of dopamine in the first place?
Scientists are looking at the behaviour of a common protein called alpha-synuclein.This molecule 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 per cent chance of inheriting the disease. It was later found that all those affected carried a mutated gene on Chromosome 4 that coded for the protein, alpha-synuclein.
It is very important to note that Parkinson’s is not usually inherited but this discovery provided a vital clue about its mechanism of action. Most patients do not have this genetic mutation, but they do have sticky deposits of alpha-synuclein inside their brains, found when they were examined after death. This protein seems to be an integral part of the disease that affects all Parkinson’s patients.
The theory is that as we age, some proteins just go bad. When proteins do this due to age, environment, or susceptible genes, they become toxic, capable of jumping from cell to cell, causing other alpha-synucelin proteins to do the same and eventually killing neurons (especially dopamine-producing ones) in their wake. This process appears to be implicated, not only in Parkinson’s, but in other neurological diseases such as Alzheimer’s disease, Huntingdon’s disease, Lou Gehrig’s disease (ALS) and Creutzfeldt-Jacob disease(mad cow disease).
Proteins that behave badly are supposed to be kept in check through an elaborate series of control mechanisms in your body. But sometimes they do not work, especially as we get older and this leads to neurological disease.
Researchers feel that in the near future they will develop drugs to target these rogue proteins. An American biotech company, NeuroPhage, for example, plans to enroll Alzheimer’s and Parkinson’s patients in 2016 and 2017 in Phase 1 human trials of its new product, a genetically engineered compound derived from a naturally occurring virus M13. Researchers have demonstrated that this compound can enter rodent’s brains and neutralize toxic clumps of alpha-synuclein and the corresponding target for Alzheimer’s (beta amyloid proteins). The question is will it work on human brains? And will it stop or reverse the patient’s symptoms.
People with Parkinson’s progressively lose core pieces of themselves. They forget how to walk, their arm muscles get weaker and movements slow down. Their hands fumble at simple tasks like buttoning a shirt or balancing spaghetti on a fork. Their faces no longer express emotions and their voices lose volume and clarity. Their minds may lose sharpness but unlike people with heart disease or cancer, they tend to survive for a very long time. This allows them to report their symptoms and assist in the scientific pursuit of better therapies and ultimate cures.
At the present time, we only have the prescription drug laradopa which is a drug that restores the missing dopamine to the body. Unfortunately, as time goes on the patient requires higher and higher doses until a second drug is needed. It is usually used in a combination of carbidopa and levodopa known as Sinemet. When this does not work anymore, some physicians add selegiline which tries to keep the body from losing dopamine and finally we have the drug Cogentin which just tries to limit the involuntary movements of the limbs. In rare cases, brain surgeons perform operations that sometimes halt the condition for six months but eventually it comes back.
Natural health supplements used for Parkinson’s include Coenzyme Q10 in doses of 1200mg three times a day along with other brain neurotransmitters such as phosphatidyl serine and phosphatidyl choline. Also the use of NADH (nicotinamide adenine dinucleotide) helps stop those bad proteins from jumping from one cell to another.
As I said earlier, at least the disease does not affect your life span so if you have this condition, hang in there; a cure may be just around the corner and hopefully you will live long enough to eventually get rid of this disease.