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% 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 the 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.
what causes parkinson's disease?