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Neurotransmitter Receptor—G-Protein-Mediated Signal Transduction in Alzheimer’s Disease

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Part of the book series: Contemporary Neuroscience ((CNEURO))

Abstract

Alzheimer’s disease is the most frequent cause of dementia in the elderly and is characterized clinically by a progressive loss of memory, intellect, and personality. The characteristic neuropathological hallmarks of Alzheimer’ s disease are the extracellular deposition of a 39–43 amino acid protein termed β-amyloid (or Aβ), in the cerebrovasculature (1) and cores of senile plaques (2), as well as the formation of paired helical filaments (PHFs) that com­prise intracellular neurofibrillary tangles (NFTs) (3), neuropil threads, and senile plaque neurites. The principal component of PHFs is an abnormally hyperphosphorylated form of the microtubule-associated protein tau (4). Other features of Alzheimer’s disease pathology include neuronal and syn­aptic fallout that disrupts neurotransmission via the ascending cholinergic, noradrenergic, and serotonergic projections to the neocortex, as well as corti­cal excitatory amino acidergic pyramidal neurones.

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© 2000 Humana Press Inc., Totowa, NJ

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Cowburn, R.F. (2000). Neurotransmitter Receptor—G-Protein-Mediated Signal Transduction in Alzheimer’s Disease. In: Reith, M.E.A. (eds) Cerebral Signal Transduction. Contemporary Neuroscience. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-019-3_5

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  • DOI: https://doi.org/10.1007/978-1-59259-019-3_5

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