Therapeutic targets in the biology of Alzheimer's disease


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Abstract

The cause of Alzheimer's disease is closely associated with the accumulation of β-amyloid in the neocortex. The neurochemical factors responsible for precipitating this otherwise normal, soluble protein are contentious. Nevertheless, in the absence of any other curative treatment for Alzheimer's disease, the majority of the research effort has focussed on inhibiting the production of β-amyloid (using secretase inhibitors) or destroying the protein (vaccination with synthetic peptide). Both approaches assume that the protein serves no purposive function. In contrast, a new alternative has recently emerged employing small metal complexing agents that inhibit the neurotoxic hydrogen peroxide produced by β-amyloid, and which facilitate the dissolution of brain amyloid deposits in vivo in transgenic mice. Currently in clinical trials, this class of agent may interdict the Alzheimer disease process at its most generic biochemical level.

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