The onset of Parkinson’s disease is slow, and the initial symptoms often go unnoticed. However, Parkinson’s disease can be diagnosed clinically when the following symptoms occur. The disease is mainly caused by pathological changes in the cells located in the “substantia nigra” of the midbrain, resulting in a decrease in dopamine synthesis, a decrease in acetylcholine inhibition, and a relative increase in acetylcholine excitation. The result of the imbalance between the two is “tremor palsy. The cause of nigrostriatal cell degeneration and necrosis is still unknown and may be related to genetic and environmental factors. It has been suggested that inadequate intake of protein, fruit, dairy products, alcohol, trauma, overexertion, and certain psychological factors may be risk factors for the disease. Tremor palsy caused by an unexplained decrease in dopamine is medically known as primary tremor palsy, or Parkinson’s disease. The pathogenesis of PD is associated with a significant decrease in dopamine (DA) levels in the striatum. The more recognized theories are the “dopamine theory” and the “oxidative stress theory”. The former suggests that a decrease in DA synthesis leads to a decrease in striatal DA content, an imbalance between dopaminergic and cholinergic nerve function in the substantia nigra-striatal pathway, and a relative increase in cholinergic neuronal activity, resulting in extrapyramidal hyperfunction and tremor paralysis. The latter explains the degeneration of nigrostriatal dopaminergic neurons, i.e., during oxidative stress, the oxidative metabolism of DA in PD patients generates large amounts of H2O2 and superoxide anions, which are catalyzed by Fe2+ in the nigrostriatal sites, further generating more toxic hydroxyl radicals, when the activity of complex I of the nigrostriatal mitochondrial respiratory chain is reduced and antioxidants (especially glutathione) disappear, preventing the scavenging of free radicals. Thus, free radicals eventually lead to neuronal degeneration by oxidizing neural membrane lipids, disrupting DA neuronal membrane function, or directly damaging cellular DNA.