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Parkinson's Disease

PARKINSON'S DISEASE (PD) first described by James Parkinson in 1817, is a disorder of the central nervous system (CNS). It is marked by the presence of Lewy bodies (abnormal protein aggregates) and, more importantly, by a progressive loss of dopamine—producing neurons in the substantia nigra region of the brain. Although uncommon in people under age 40 years, the incidence of PD greatly increases with age, affecting approximately 1 percent of individuals older than 60 years.

As of yet, PD is incurable, and current therapies focus only on alleviating symptoms rather than on treating the underlying disease. However, because of the nature of its development, PD is a prime beneficiary candidate of stem cell research.

Traditionally, PD has been regarded as a motor system disorder, with four cardinal characteristics: resting tremor, muscular rigidity, bradykinesia (abnormally slow movements and difficulty initiating motion), and postural instability. Although nonmotor manifestations such as dementia and face recognition impairment are strongly associated with PD, diagnosis requires presence of these motor deficiencies.

Pathophysiology

It is believed that PD arises from a partial genetic predisposition, as it is more common in Caucasians than in Africans or Asians. This is supported by evidence that links the development of Parkinson's dementia with alterations in chromosome 4 at the gene that codes for the protein, alpha—synuclein.

Little is known about this protein, but major theories hold that overproduction or mutations of alpha—synuclein makes it more liable to gather into fiber clusters, forming Lewy bodies that are potentially toxic. These protein aggregations are also seen with dementia arising from other disorders such as Alzheimer's disease or diffuse Lewy body disease.

However, the change that appears to be most responsible for PD—induced motor déficits in patients is the deterioration of dopamine—producing neurons within the substantia nigra region of the brain. Insufficient amounts of dopamine, a chemical messenger of the CNS, results in diminished activation of the striatum—the control center for planning and modulation of movement. This causes problems with motor coordination. Research has shown that 70–80 percent of these neurons are lost before motor symptoms appear. In patients with PD, 9–13 percent of dopamine—producing neurons are lost every decade of life for reasons unknown, bringing the average age of diagnosis to 70.5 years.

Current Therapies

Because current therapies are still unable to halt the continual decline of dopamine—producing neurons, treatment methods focus on symptom improvement. The most common and effective approach is with oral administration of levodopa (or L—DOPA), an intermediate in dopamine synthesis. After L—DOPA crosses the blood—brain barrier (which dopamine cannot), it is converted to supplement the preexisting dopamine of the substantia nigra and putamen. Unfortunately, chronic administration, especially with higher doses, causes most patients to develop motor complications including dyskinesia (involuntary movements) and motor fluctuations. As a consequence, this renders levodopa an inappropriate agent for long—term treatment.

As other therapies similarly lose their efficacy, the need for a cure has opened the door to non—pharmacological remedies, including stem cell research. Of all advancements that have been made in potential treatments of PD, cell transplantation is the course that has shown the most promise of full recovery and restoration of functional capacity.

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