Journal
NEUROCHEMICAL RESEARCH
Volume 36, Issue 7, Pages 1149-1156Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-010-0371-4
Keywords
Alzheimer's disease; Calcium; Inositol trisphosphate; Amyloid metabolism
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Funding
- Biotechnology and Biological Sciences Research Council [BBS/E/B/0000C134] Funding Source: Medline
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New insights into how Ca2+ regulates learning and memory have begun to provide clues as to how the amyloid-dependent remodelling of neuronal Ca2+ signalling pathways can disrupt the mechanisms of learning and memory in Alzheimer's disease (AD). The calcium hypothesis of AD proposes that activation of the amyloidogenic pathway remodels the neuronal Ca2+ signalling pathways responsible for cognition by enhancing the entry of Ca2+ and/or the release of internal Ca2+ by ryanodine receptors or InsP(3) receptors. The specific proposal is that Ca2+ signalling remodelling results in a persistent elevation in the level of Ca2+ that constantly erases newly acquired memories by enhancing the mechanism of long-term depression (LTD). Neurons can still form memories through the process of LTP, but this stored information is rapidly removed by the persistent activation of LTD. Further dysregulation in Ca2+ signalling will then go on to induce the neurodegeneration that characterizes the later stages of dementia.
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