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One of the key features of Alzheimer's disease is the build-up of amyloid plaques between neurons in the brain. These peptides are proteolytic fragments of the transmembrane amyloid precursor protein. In a salutary brain, these protein scraps are broken down and eliminated, but these remnants accumulate to form insoluble plaques in diseased conditions leading to neural toxicity, which results in the damage and destruction of synapses that mediate memory and cognition. This chapter elaborates the underlying genetic etiology of these plaques along with other participating factors and their profound influence that in return controls the overall homeostasis resulting from gene expression to the biochemical basis of the disease. A complete understanding of the mechanistic aspects related to these ailments can contribute to accurate detection and development of targeted therapies.

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