Alzheimer´s disease (AD) is a neurodegenerative disorder with no known cure and rapid rise in incidence. The
predominant cognitive impairment is currently treated using cognitive enhancers like cholinesterase inhibitors. The two
molecular hallmarks of AD are amyloid plaques created from an amyloid precursor protein and hyperphosphorylated tau
protein that is deposited as neurofibrillary tangles inside neurons. A number of pathological mechanisms follow or precede
these formations. Alteration in mitochondrial function and deposition of heavy metals are reported. The disease progression
is enhanced by oxidative stress. However, the role of oxidative stress is not universally accepted. The current review
covers and discusses the basic evidence and role of oxidative stress in AD development.
Keywords: Alzheimer disease, amyloid plaque, tau, antioxidants, Fenton reaction, heavy metals, mitochondria, parkinson´s
disease, reactive oxygen species.
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