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Research Foundation: Brochure 7

PARKINSON’S DISEASE

What Causes Parkinson’s?

While scientists don’t yet know what triggers Parkinson’s disease, they do know that the symptoms are the result of the progressive death or impairment of a discrete group of nerve cells in an area of the brain called the substantia nigra. Normally, these neurons produce dopamine, a neurotransmitter that acts as a chemical messenger to relay signals between the substantia nigra and another part of the brain called the striatum, which is part of the basal ganglia (see right). As the dopamine neurons die, the level of dopamine decreases, which causes nerve cells to fire abnormally and excessively. This disrupts the brain┼ís ability to initiate and control muscle movements, causing the classic symptoms of Parkinson’s disease.

Dopamine neurons die gradually, sometimes over the course of many years. Parkinson’s symptoms begin when the loss of dopamine reaches a critical point – typically when between 50 percent and 80 percent of dopamine neurons have died.

The question of why dopamine neurons begin to degenerate is being intensely investigated by scientists around the world. It is widely accepted that there is no single “cause” that triggers the disease; rather Parkinson’s likely results from a confluence of inherited (genetic) and environmental factors that interact in complex, poorly understood ways to set disease processes in motion. While Parkinson’s is not hereditary in the classic sense – that if one of your parents has it, you too will get it – individuals may inherit a degree of susceptibility to the disease.

This may not be enough to cause Parkinson’s, but if a genetically predisposed individual is also exposed to certain toxic environmental substances or possibly to a particular virus or bacteria, that individual may then develop the disease.

Current Theories on the Cause of Parkinson’s

In recent years, science has made great strides in understanding the potential triggers for Parkinson’s disease and there are a number of interrelated hypotheses about the mechanisms and pathways that lead to the disease. These include, but are not limited to:

* abnormalities in the way certain proteins (e.g., alpha-synuclein) are processed in the brain;
* cellular damage resulting from oxidative stress, which is sometimes described as the biological equivalent of metal rusting;
* impairments in mitochondria, the tiny vesicles inside cells that act as energy factories to fuel cellular functions;
* excitotoxicity, toxicity to neurons caused by neurotransmitters that get out of balance;
* loss of so-called trophic factors, naturally occurring chemicals in the brain that nurture and support nerve cells;
* inflammatory processes that may result when a subset of brain cells called microglial cells become inappropriately activated and release toxic substances that can damage nerve cells;
* overactive or misdirected apoptosis (programmed cell death), a natural process in which neurons in effect commit suicide.