Alzheimer’s disease (AD) is associated with the cause of dementia in the elderly. The cause of AD is generally related to the aggregation of a normal protein, β-amyloid (Ab), within the neocortex. Aβ, a low molecular weight protein, that is a proteolytic product derived from the larger amyloid precursor protein (APP) by normal proteolytic processing, is the major component of neocortical amyloid collections in AD. In healthy individuals, most of the Ab is membrane associated, but in individuals with AD the aggregated (diffuse and plaque amyloid) and soluble fractions increase markedly. There have been an increasing number of studies which is now indicating a very interesting role played by transition metals in AD. Aβ has been shown to bind redox active metals like Fe and Cu. These metals are gradually reduced by Aβ which then react with O2 producing partially reduced oxygen species (PROS) e.g. H2O2 which are freely diffusing molecules that can lead to degeneration of neural cell walls. Furthermore H2O2 can generate toxic reactive oxygen species (OH.) in the presence of Fe2+ and Cu+, causing oxidative damages. This process of oxidative degradation is now proposed to precede plaque formation. Thus there is a vital need for understanding the interactions of key transition metals which are present in the brain with Aβ peptides. The talk will discuss recent developments of structure-function correlations of these metal active sites.

Redox active metals In Alzheimer's disease

254th National Meeting (2017)

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