What are the causes of Parkinson’s disease (PD for short)? PD occurs when nerve cells and neurons in the substantia nigra die or are damaged. Under normal circumstances, these neurons produce an important chemical called dopamine. Dopamine is a chemical messenger responsible for transmitting signals between the substantia nigra and the next intracerebral relay station (striatum), enabling the body to produce stable random movements through signal transduction. Loss of dopamine leads to abnormalities in neuroelectrical transmission in the brain, which can cause movement disorders. Studies have shown that by the time patients become symptomatic, at least 60-80% or more of the dopaminergic cells have been lost in the substantia nigra. Recent studies have shown that loss of noradrenergic neurotransmitters also occurs in PD patients. Norepinephrine is structurally similar to dopamine, which is the main chemical transmitter of the sympathetic nervous system. The sympathetic nervous system controls many of the autonomic functions of the body, such as pulse and blood pressure. The loss of norepinephrine may help explain the non-motor symptoms of PD patients, including fatigue and abnormalities in blood pressure regulation. Patients’ brain cells contain Lewy vesicles, which are abnormal deposits and clumps of alpha and other proteins. Researchers do not yet understand the structure of lewy vesicles and their role in the development of the disease. These protein clumps may inhibit normal cell function, or they may be beneficial proteins – proteins that “lock in” harmful proteins so that the cell can maintain normal function. A number of mutated genes associated with PD have been identified, many of which have possible relevance to the disease. Genetic studies of familial PD cases can help to understand heritability and sporadicity. Genes and proteins that are altered in hereditary cases may be similarly altered in sporadic cases under the influence of environmental toxicity factors and other factors. It is expected that related studies will identify new treatments for Parkinson’s disease from the perspective of the studied genes. Despite the growing importance of genomics regarding PD, many researchers believe that environmental exposures also increase the risk of developing the disease. Even in familial cases, exposure to toxic and other environmental factors can influence the timing of disease symptoms and the course of disease progression. 1-methyl-4 phenyl-1, 2, 3, 6-tetrahydropyridine and other toxic substances can all cause Parkinson’s syndrome in humans. In addition, there are still more uncertain environmental factors that can cause Parkinson’s disease in genetically susceptible people. Viruses are another environmental trigger for Parkinson’s disease, and many patients who developed encephalitis during the influenza outbreak in 1918 developed severe progressive Parkinson’s-like symptoms later in life. Similar symptoms occurred in another group of Taiwanese women infected with the herpes virus, and these women’s symptoms faded away at a later stage, and are now thought to be related to a temporary infection with the substantia nigra. Multicenter studies have shown that mitochondria play an important role in the development of Parkinson’s disease. Mitochondria are an important source of energy production in the cell and a source of free radicals. Free radicals are molecules that can damage membrane structures, protein substances, DNA, and other cellular constituents in cells. It is also believed that the protein processing system of PD patients is impaired, which leads to the accumulation of proteins to harmful levels that trigger cell death. Evidence has also found an important association between protein clumps in brain cells of PD patients and neuronal death, cellular inflammation and hyperstimulation (toxic substances and other factors), which may play an important role in the development of the disease, however, the exact role of protein deposits remains unknown. Some researchers have even suggested that protein aggregation is a phenomenon of cellular protection against “self-abortion”. While mitochondrial dysfunction, oxidation, inflammation, and other cellular processes play an important role in the pathogenesis of PD, the actual cause of dopamine cell death remains uncertain.