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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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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