Cause of Parkinson's Disease
Genetic Factor Theory
A relatively new theory explores the role of genetic factors in the development of Parkinson's disease. Approximately 15 to 20 percent of people with the condition have a close relative who has experienced parkinsonian symptoms, such as a tremor.
Several causative genes have been identified, usually causing young-onset parkinsonism. Mutations in the gene for the protein alpha-synuclein, located on chromosome 4, results in autosomal dominant parkinsonism. The function of this protein is not known.
The most commonly occurring genetic defect affects the gene for the protein called parkin on chromosome 6. Mutations in this gene result in autosomal recessive parkinsonism that is slowly progressive and begins before the age of 40.
After studies in animals showed that MPTP interferes with the function of mitochondria within nerve cells, investigators became interested in the possibility that impairment in mitochondrial DNA may be the cause of Parkinson's disease. Mitochondria are essential organelles found in all animal cells that convert the energy in food into fuel for the cells. Families with maternal inheritance of parkinsonism, suggesting defects in the mitochondrial DNA, are being actively investigated.
Free Radical Theory
Another theory for the nerve death that happens with Parkinson's disease holds that free radicals -- unstable and potentially damaging molecules generated by normal chemical reactions in the body -- may contribute to nerve cell death, thereby leading to Parkinson's disease.
Free radicals are unstable because they lack one electron. In an attempt to replace this missing electron, free radicals react with neighboring molecules, especially metals such as iron, in a process called oxidation. Oxidation is thought to cause damage to tissues, including neurons.
Normally, free radical damage is kept under control by antioxidants, chemicals that protect cells from this damage. Evidence that oxidation may cause or contribute to Parkinson's includes the finding that people with the disease have increased brain levels of iron, especially in the substantia nigra, and decreased levels of ferritin, which serves as a protective mechanism by forming a ring around the iron and isolating it.