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The pathogenesis of sporadic Alzheimers disease (AD) is intimately related to brain aging.Thus, the aged brain especially when metabolically manipulated can be employed as a useful tool to study AD pathogenesis.In the present study we have attempted to explore how iron dysregulation is involved in enhanced amyloid precursor protein (APP) and amyloid beta peptide (A β 42) synthesis and accumulation in the aged brain.