Ca PARKINSON’S DISEASE No doubt shout it The tremor in his right hand was geting worse. Mark had first noticed it almost a year ago, but because itscemed to happen only after working out atthe gym, he ateib- uted the shaking wo his advancing years and to his new routine with fre weights. Ater all, he ws nearly sixt-eight yeare old, and how many men his age sill exercised regulary? ‘No pain, no gain,” Mark told himself) and so he kept up this workouts, hoping to improve the muscle fatigue overtime 'omever, lately be felt ted all dhe time. His wife was always ftself—was that hi skin seemed oiler, almost ike when he wat in hie teens Mark, who had celebrated his sixtfith bitay and retire ‘by purchasing the set ‘ar of bis dreams, trated another eight months to se his plysian By then, ane of his hands shook xo badly he could hardly read the newpaper. His handwriting looked like a spider had ran acros the page. And he felt initable and deprested for 80 reason atl “T just want to feel better,” he told his doctor. “This isthe time in my life when T should really be taking advantage of my freedom and enjoying ie. What's wrong with me?” Parkinson's Disease 83 When his doctor diagnosed Parkinson's disease, Mark Felt as if the floor had dropped out from under him. "So what do ¥ do now?” he asked. Parkinson's Disease: An Overview Like most of us, Mark attibuted his muscle fatigue and tremor to the normal aging process. However in Mark's case—a with fone out of every forty people—these were early symptoms of Parkinson's disease, ‘A neurological disease of late middle age, Parkinson's disease alfects more than a million Americans. Up to 50,000 new cases fare diagnosed each year Some experts maintain that the diease isincreasng in the population and predict it will soon affect one fut of every twenty Americans overage Bly This slow degenerative nervous disorder most frequently attacks people in ther late ites orsicties However, more phys clans are nov reporting cases of Parkinson's in younger patients, Some estimate that up w 10 percent of Parkinson's patents are ‘now diagnosed before they tum forty. First described in 1817 by James ParknSom, British physician ‘who published a medical report on "the shaking palsy,” Parkin son's divease is characterized by tremor, slownew of movement, and rigidity. Although itis rarely a cause of death, Parkinson's ‘an weaken sufferers enough to fall prey to other diseaes. ‘While researchers have not yet fully defined its causes, range of symptoms, or a cure we now know that Parkiason’s symptoms are clearly linked wo the progressive deterioration of dopamine> producing cells inthe brain. ‘Normally, nature ereates so many ofthese neurons that we're ble to lose them every day without noticing, as these brain cells “isiotegrate owing to head injures, toxins, air pollutants, and aging, In fact, we have to lose over 75 percent of our dopamine rheurons before our body shows the telltale symptoms of Parki- ‘Some people suffering from Parkinson’s may end up severely handicapped after a decade ot less Others experience few mp toms even twenty-five years postdiagnosis: Recent popular Figures84 THE BRAIN WELLNESS PLAN 1 bring Parkinson's to the public eye include the actress Katha ne Hepburn and fighter Muhammad Al Society pays an enormous price for Parkinion’s disease, According to the National Parkitwon's Foundation, medications cost the average patient upward of 2.500 annually. When office ‘ints, social security payments, nursing home expenditures, and Tout income are totaled for Parkinson's patients, experts estimate that the disease costs the United States more than $5.6 billion a ear “That economic cost pales in comparison othe emotional wll the disease exacts on patients, for who wants to spend thet ‘golden years trapped in a body that shakes uncontrollably or freeres in place, behind a face devoid of expression owing 10 inactive maces? "The good newsis this Advances in treating Parkinson's repre= sent one of the major neurological research success stories of the past decade. Ie is now hailed as one of the few chronic neurological diseases for which we have found effective teat From the onset of symptoms to diagnosis from treatment to hope on the horizon, in this chapter we dicts Parkinson's di cise in light of what we know about the diveae' effects om the bralinimmune system connection on its mostinrcate, biochem® cal level At the end of the chapter, you will find an aggressive treatment plan baved! on the most current information available ‘on medications and nutritional therapies, What Goes Wrong in Parkinson's Disease, and Why? Although no speciic genes have been identified for Parkin- son's the disease mos likely results from an imeraction between genetics and envirome “A Genetic Predisposition While there vill more work to-doin unraveling the genetic bas for Parkinson's disease, scientists today believe that genet Patkiaon’s Disease 85 ‘ally impaired cellular detoxification mechaniams are the key freawn why certain individuals are at risk, When neurone are “unable wo naturally neutralize environmental toxins, the immune ‘stem mounts is forces against those invaders—and may end Lup killing off the body's own neurons inthe process “Exposure to Environmental Toxins Although all of us are exposed to environmental toxins, cur rent epidemiological studies demonstrate that Parkinson's di ‘care is much more prevalent in areas where individuals are more kel to be exposed to toxins like pesticides, carbon monoxide, ‘atbon disulfide, and other environmental contaminants. mn fact, clinical researchers have identified antibodies specific cally targeted to brain cells in the cerebrospinal flak of Parkin son's patients. When the immune system is activated by a combination of impaired cellular detoxification systems high exposure to toxins, the resul i cascade of responses that dam ages neurons in certain areas of the brain—in this case, the ‘neurone responsible for producing dopamine, the neurotrans- ie hat eee meses rm he ra 1 con mc ‘The Death of Dopamine-Producing Neurons at the Hands of MPTP and Other Neurotoxins Just about sixty yeas after James Parkinson first linked such syptomsas git disorder, postural eaning, and wemorasasingle ‘onic disease, Parkinson's pations were Weated by medications developed by French neurologist and hypaodist Jean-Martin Char- ‘cot, Charcot, known asthe "father of clinical neurology.” used potions derived from jimsonweed, a North American plant. The herbal remedy brought reliet from tremor and righty During the next century, patients with Parkinson's were treated with extracts from the belladonna plant, cousin of Jjmsonweed, and following World War I, with extracts of bella- ddonnatike drags. Real progress was finally made in the 1950s, when scientists began experimenting with tranquilizers to control high blood86 THE BRAIN WELLNESS PLAN pressure. These investigations yielded new information about ‘neurotransmitters, the chemical substances that wansfer informa: between nerve cells in the brain. By 1960, University of Vienna scientists had conducted autop: ies of the brains of Parkinson's patients and found those brains, strikingly short on the dopamine neurotransmiter. ‘Another piece of the Parkinson's puzzle fell nwo place in the 1980s, when illicit drug dealers made a designer drug to sell as asgyntheticheroin, [nan effort to boos their profits and the speed. ff the manufacturing process, these drug dealers inadvertently created a toxic substance known as MPTP. As reported in Science bby neurologistsat Stanford University School of Medicine, people ‘sho took the drug developed symptoms of Parkinson's within a ‘week, puzzling physicians unaccustomed w secing the disease in ‘young people Inwestigators eventually linked their common use of the MPTP- containing drug tothe Parkinson's symptoms Subsequent studies ‘wlaslalear austen abbas wale th AS ao meow, RE. the prevalence of Parkinson's is highest Recall that dopamine isa neurotransmitter that helps activate adrenaline to noradrenaline, thus gearing us up for “fight” oF “flight” at times of stress, Dopamine alo helps regulate our daily _moods—as we explain later in our chapter on depression. More relevant for Parkinson’s patients, however, i the fact that dopa ‘mine levels are directly related to our ability to move our muscles and keep our balance. "The brain cells that produce dopamine are located deep in ‘the brain stem, Most ofthese are in an area called the “substant nigra.” The name, which means “black substance" in Latin, ‘describes darkly pigmented area ofthe brain which isconnected, Parkinson's Disease 87 to other parts of the basal ganglia by a network of long, twisting nerve fibers. ‘Once dopamine is manufactured i the substantia nigra, it travels along those nerve fibers, acting as a messenger for the ‘neurological impulses that help regulate our muscular responses ‘and overall motor functions ‘Since discovering the link between Parkinson's and low brain levels of dopamine, scientists in several laboratories have been ‘examining the distribution of dopamine receptors. the chemistry fof that particular neurotransmitter, and texininduced damage ‘specifically to dopamine-containing neurons. ‘Mitochondrial Damage and Neuron Death Recently, Japanese investigators who published their findings Jn a 1995 issue of Biochimica et Biophysica Aca have concluded that MPTP selectively destroys neurons in the region ofthe brain function within cells to convert glucose into energy. In neurons, which require large amounts of protein to per~ {form their functional activites, the mitochondria are stall sen der rods and spheres located randomly throughout the cell body, boat typically near nerve terminals Fach mitochondria organelle is hounded by two membranes: smooth outer membrane and an inner membrane, which has ‘numerous infoldings. The matrix, the area enclosed by the inner ‘membrane, isabout half protein and contains the mitochonetia's DNA. or genetic blueprint. “The mitochondrial inner membrane is where oxidative phos: phorylation takes place—the chemical process so fundamental