Free radical damage, iron, and Alzheimer's disease

Abstract

We present evidence to support the premise that many of the pathological correlates of Alzheimer's disease are precipitated by free radical- and oxidative stress-induced mechanisms. We propose that amyloid-beta deposition in senile plaques, intracellular accumulation of protein in neurofibrillary tangles, and the degeneration of specific neuronal populations can be attributed to specific oxidative stress-type mechanisms. Free radicals in disease pathogenesis, generated in part as a result of Fenton-type reactions, suggest that lowering the level of available iron, intervention with antioxidants, or the administration of free radical scavengers could provide a therapeutic inroad in the fight against Alzheimer's disease.