Parkinson's disease may be due to failure of melanin in the Substantia Nigra to produce molecular hydrogen from dissociation of water, to protect the brain from oxidative stress.

Abstract

This hypothesis paper proposes that neuromelanin in the Substantia Nigra, functioning as a hybrid electronic/ionic conductor, may be capable of dissociating water molecules into molecular hydrogen and oxygen. The resulting hydrogen could act as an endogenous antioxidant, limiting excessive oxidative damage to dopaminergic neurons. In Parkinson's disease, progressive melanin degeneration would reduce this hydrogen-generating capacity, thereby permitting unchecked oxidative stress. Additionally, because melanin acts as a chelator, it may accumulate environmental toxins that further impair its water-splitting function, accelerating neuronal loss. The paper suggests that restoring melanin activity or supplying exogenous molecular hydrogen could represent strategies for reducing oxidative burden in this condition.

Mechanism

Neuromelanin in the Substantia Nigra is proposed to split water into molecular hydrogen and oxygen; the hydrogen suppresses oxidative stress. Melanin degeneration—potentially accelerated by chelated environmental toxins—abolishes this protective hydrogen production, allowing oxidative neuronal damage to progress.