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Neurochem Res. 2011 Jul;36(7):1149-56. doi: 10.1007/s11064-010-0371-4. Epub 2010 Dec 24.

Calcium signalling and Alzheimer's disease.

Author information

1
The Babraham Institute, Babraham, Cambridge, CB22 3AT, UK. michael.berridge@bbsrc.ac.uk

Abstract

New insights into how Ca(2+) regulates learning and memory have begun to provide clues as to how the amyloid-dependent remodelling of neuronal Ca(2+) 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 Ca(2+) signalling pathways responsible for cognition by enhancing the entry of Ca(2+) and/or the release of internal Ca(2+) by ryanodine receptors or InsP(3) receptors. The specific proposal is that Ca(2+) signalling remodelling results in a persistent elevation in the level of Ca(2+) 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 Ca(2+) signalling will then go on to induce the neurodegeneration that characterizes the later stages of dementia.

PMID:
21184278
DOI:
10.1007/s11064-010-0371-4
[Indexed for MEDLINE]

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