Parkinson's Disease (cont.)
What Causes Parkinson's Disease?
Parkinson's disease occurs when nerve cells, or neurons,
in an area of the brain known as the substantia nigra die or become impaired. Normally, these
neurons produce an important brain chemical known as dopamine. Dopamine is a
chemical messenger responsible for transmitting signals between the substantia
nigra and the next "relay station" of the brain, the corpus striatum, to produce
smooth, purposeful movement. Loss of dopamine results in abnormal nerve firing
patterns within the brain that cause impaired movement. Studies have shown that
most Parkinson's patients have lost 60 to 80 percent or more of the
dopamine-producing cells in the substantia nigra by the time symptoms appear.
Recent studies have shown that people with Parkinson's disease also have loss of the nerve
endings that produce the neurotransmitter norepinephrine. Norepinephrine, which
is closely related to dopamine, is the main chemical messenger of the
sympathetic nervous system, the part of the nervous system that controls many
automatic functions of the body, such as pulse and blood pressure. The
loss of norepinephrine might help explain several of the non-motor features seen
in Parkinson's disease, including fatigue and abnormalities of blood pressure regulation.
Many brain cells of people with Parkinson's disease contain Lewy bodies –
unusual deposits or clumps of the protein alpha-synuclein, along with other proteins. Researchers
do not yet know why Lewy bodies form or what role they play in development of
the disease. The clumps may prevent the cell from functioning normally, or they may
actually be helpful, perhaps by keeping harmful proteins "locked up" so that the
cells can function.
Scientists have identified several genetic mutations associated with
Parkinson's disease, and
many more genes have been tentatively linked to the disorder. Studying the genes
responsible for inherited cases of Parkinson's disease can help researchers understand both
inherited and sporadic cases. The same genes and proteins that are altered in
inherited cases may also be altered in sporadic cases by environmental toxins or
other factors. Researchers also hope that discovering genes will help identify
new ways of treating Parkinson's disease.
Although the importance of genetics in
Parkinson's disease is increasingly recognized, most
researchers believe environmental exposures increase a person's risk of
developing the disease. Even in familial cases, exposure to toxins or other
environmental factors may influence when symptoms of the disease appear or how
the disease progresses. There are a number of toxins, such as
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, or MPTP (found in some kinds of
synthetic heroin), that can cause parkinsonian symptoms in humans. Other,
still-unidentified environmental factors also may cause Parkinson's disease in genetically
susceptible individuals.
Viruses are another
possible environmental trigger for Parkinson's disease. People who developed encephalopathy after
a 1918 influenza epidemic were later stricken with severe, progressive
Parkinson's-like symptoms. A group of Taiwanese women developed similar symptoms
after contracting herpes virus infections. In these women, the symptoms, which
later disappeared, were linked to a temporary inflammation of the substantia nigra.
Several lines of research suggest that mitochondria may play a role in the
development of Parkinson's disease. Mitochondria are the energy-producing components of the cell
and are major sources of free radicals — molecules that damage membranes,
proteins, DNA, and other parts of
the cell. This damage is often referred to as oxidative stress. Oxidative stress-related changes, including free radical
damage to DNA, proteins, and fats, have been detected in brains of
Parkinson's disease patients.
Other research suggests that the cell's protein disposal system may fail in
people with Parkinson's disease, causing proteins to build up to harmful levels and trigger cell
death. Additional studies have found evidence that clumps of protein that
develop inside brain cells of people with Parkinson's disease may contribute to the death of
neurons, and that inflammation or overstimulation of cells (because of toxins or
other factors) may play a role in the disease. However, the precise role of the
protein deposits remains unknown. Some researchers even speculate that the
protein buildup is part of an unsuccessful attempt to protect the cell. While
mitochondrial
dysfunction, oxidative stress, inflammation, and many other
cellular processes may contribute to Parkinson's disease, the actual cause of the dopamine cell
death is still undetermined.
Next: What Genes are Linked to Parkinson's Disease? »
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