Free radical damage, iron, and Alzheimer's disease.
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.
Smith
M A
MA
Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA.
Perry
G
G
D000544:Alzheimer Disease / Q000473:pathology*; D005609:Free Radicals; D006801:Humans; D007501:Iron / Q000502:physiology*; D009410:Nerve Degeneration / Q000502:physiology
D005609:Free Radicals; D007501:Iron