Calcium Signalling and Alzheimer’s Disease |
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Authors: | Michael J Berridge |
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Institution: | (1) The Babraham Institute, Babraham, Cambridge, CB22 3AT, UK |
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Abstract: | 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 InsP3 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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