The calcium-sensing receptor: a novel Alzheimer's disease crucial target?

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DOIResolve DOI: http://doi.org/10.1016/j.jns.2012.07.031
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TypeArticle
Proceedings titleJournal of the Neurological Sciences
ConferenceSixth International Congress on Vascular Dementia, 2011, Riga, Latvia
ISSN0022-510X
Volume322
Issue1-2
Pages137140
SubjectAlzheimer's disease; Amyloid-β peptides; Calcium-sensing receptor; Human astrocytes
AbstractAlzheimer's disease (AD) is the most common human neurodegenerative ailment, the most prevalent (> 95%) late-onset type of which has a still uncertain etiology. The progressive decline of cognitive functions, dementia, and physical disabilities of AD is caused by synaptic losses that progressively disconnect key neuronal networks in crucial brain areas, like the hippocampus and temporoparietal cortex, and critically impair language, sensory processing, memory, and conscious thought. AD's two main hallmarks are fibrillar amyloid-β (fAβ) plaques in extracellular spaces and intracellular accumulation of fAβ peptides and neurofibrillary tangles (NFTs). It is still undecided whether either or both these AD hallmarks cause or result from the disease. Recently, the dysregulation of calcium homeostasis has been advanced as a novel cause of AD. In this case, a suitable candidate of AD driver would be the Aβ peptides–binding/activated calcium-sensing receptor (CaSR), whose intracellular signalling is triggered by Aβ peptides. In this review, we briefly discuss CaSR's roles in normal adult human astrocytes (NAHAs) and their possible impacts on AD.
Publication date
LanguageEnglish
AffiliationHuman Health Therapeutics; National Research Council Canada
Peer reviewedYes
IdentifierS0022510X12003656
NPARC number21268795
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Record identifier6a063edd-d2c0-4598-be7e-72df3bdaef01
Record created2013-11-13
Record modified2016-05-09
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