Parkinson’s Disease and Mercury

Parkinson’s disease (PD) secondary to heavy metal poisoning is well known. Heavy metals, such as iron, mercury, manganese, copper, and lead, have been linked to PD and contribute to its progression. A well-known mass poisoning named Minimata’s disease was reported in 1956 in Japan due to the consumption of fish contaminated by methyl mercury discharge in the river. Chronic exposure to heavy metals can cause the activation of cytokines, resulting in neuronal loss through neuroinflammation. Metals can also induce free radical production there by reducing antioxidant levels in the substantia nigra, leading to cell death. Mitochondrial dysfunction, DNA damage, and apoptosis can potentially cause dopaminergic neurodegeneration.[1,2] Pathological hallmarks are the disturbance of the dopamine circuit in the substantia nigra and the presence of Lewy bodies in the dopaminergic neurons.[3] Classic symptoms triad of the disease is bradykinesia, tremors, and rigidity, which are motor symptoms. However, nonmotor symptoms, like autonomic disturbances, may precede the clinical symptoms. Several genes have been linked to the risk of developing the disease (e.g., the GBA gene). Some genes have been associated with autosomal dominant (LRRK2, VPS35, SNCA) and autosomal recessive PD (PINK1, PRKN, DJ-1) inheritance. Genes with recessive forms manifest as early onset, greater severity, and atypical characteristics.[4] Hence, it is clear that interaction between genetic factors and environmental factors plays an important role in the pathogenesis of the disease. PD commonly starts in fifth to sixth decade. However, young onset PD can occur in autosomal recessive PD. In the case report cited above, the patient was in the sixth decade. Also, the authors describe that he was working in a factory that used to make batteries for treadmill. It is pertinent to note that use of mercury has declined considerably in the last two decades. Mercury is used sometimes in the making of only small button batteries. Treadmill runs on AC or DC motors. Hence, it is doubtful whether it was an occupational hazard. There is no clinical difference between idiopathic PD and heavy metal-induced PD. Should heavy metal screening be done in all cases of PD? The answer is no. If there is suspicion of exposure to heavy metals, then only it should be done. The title of the article is—“Neurological Manifestations of Mercury Toxicity: A Clinical and Toxicological Perspective” should have been “Parkinson’s Disease Secondary To Mercury Toxicity” since there were no other neurological symptoms described apart from Parkinsonism symptoms. Other neurological symptoms are the involvement of the somatosensory cortex, cognitive impairment, and cerebellar ataxia due to the involvement of granule cell neurons of the cerebellum.[5] 2,3-dimercaptosuccinic acid (DMSA) and N-acetyl-D, L-penicillamine have been used as chelating agents in the treatment of mercury toxicity. The authors have not mentioned in the article whether chelating agents were used or not. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.