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Part of the book series: Current Clinical Neurology ((CCNEU))

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Abstract

Cognitive impairment and psychiatric disturbances in Alzheimer’s disease (AD) result from the dysfunction and degeneration of synapses, and consequent death of neurons, in the limbic system and associated regions of the cerebral cortex. A major molecular alteration in AD is increased amyloidogenic processing of the amyloid precursor protein (APP) resulting in increased production and accumulation of amyloid b-peptide (Ab) in the brain. Ab may promote synaptic dysfunction and can render neurons vulnerable to excitotoxicity and apoptosis by a mechanism involving oxidative stress and disruption of cellular calcium homeostasis. Some cases of inherited AD are caused by mutations in presenilins (PS)1 and PS2, which perturb cellular calcium homeostasis. Abnormalities in astrocytes, oligodendrocytes, and microglia have also been documented in studies of experimental models of AD, suggesting contributions of these alterations to neuronal dysfunction and cell death.

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Mattson, M.P. (2005). Alzheimer’s Disease. In: Tarazi, F.I., Schetz, J.A. (eds) Neurological and Psychiatric Disorders. Current Clinical Neurology. Humana Press. https://doi.org/10.1385/1-59259-856-0:051

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