The underlying cause of Parkinson's disease is still enigma. Several mechanisms have been implicated in the etiopathogenesis of PD including oxidative damage, environmental toxins, genetic predisposition, and accelerated aging. Recent research suggests that salsolinol, a derivate of dopamine, is an important contributing factor. In the presence of acetaldehyde dopamine is converted into salsolinol, a neurotoxin involved in apoptosis of dopaminergic neurons. Increased production of acetaldehyde is associated with chronic polysystemic candidiasis (CPC). Chronically elevated levels of acetaldehyde in patients with CPC might participate in the formation of salsolinol and its metabolites in the brain contributing to the destruction of dopaminergic cells in substantia nigra. Clinical mental symptoms of PD often correspond with the mental manifestations of CPC. This hypothesis may constitute basis for further scientific and clinical research of PD etiopathogenesis (Fig. 1, Ref. 29).