Abstract
While much of the focus on Alzheimers disease therapeutics has been directed at beta-amyloid peptide or at cholinergic synaptic transmission, recent data suggest that targeting signal transduction by the amyloid precursor protein (APP) itself may be an alternative approach with significant potential [1]. Here we discuss the possibility that APPmediated signal transduction, downstream from amyloid-beta peptide production itself, may be an appropriate therapeutic target in Alzheimers disease.
Keywords: amyloid precursor protein interactors, Alzheimers disease, degenerating neuron, misfolded proteins, caspase