Zinc and its effects on oxidative stress in Alzheimer’s disease

Alzheimer’s disease (AD) is a progressive age-related neurodegenerative disorder. The patho-physiological characteristic of AD is abnormal deposition of fibrillar amyloid β protein, intracellular neurofibrillary tangles, oxidative damage and neuronal death in the brain. Zinc is an important trace element in human body regulating many physiological processes. Increasing evidence suggests that the etiology of AD may involve disruptions of zinc homeostasis, and oxidative stress facilitating reactive oxygen species production is an early and sustained event in AD disease progression. Both Zn deficiency and Zn overload may affect cellular Zn distribution and be linked to neurodegeneration in AD. Meanwhile, Zn may play paradoxical roles in initiating and inhibiting oxidative stress and neurotoxicity. This review will focus on aspects of the role of zinc in AD, which includes a large body of research regarding zinc dyshomeostasis and its relation with oxidative stress.