Journal
SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
Volume 22, Issue 5, Pages 530-535Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.semcdb.2011.07.014
Keywords
Calcium; Calcium sensors; Synaptic plasticity; Alzheimer's disease; Neurodegenerative disease
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Funding
- Biotechnology and Biological Sciences Research Council [BB/G003963/1] Funding Source: Medline
- Medical Research Council [MC_G1000734] Funding Source: Medline
- Wellcome Trust [089703] Funding Source: Medline
- BBSRC [BB/G003963/1] Funding Source: UKRI
- MRC [MC_G1000734] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/G003963/1] Funding Source: researchfish
- Medical Research Council [MC_G1000734, 983724] Funding Source: researchfish
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Calcium (Ca2+) is a fundamental intracellular signalling molecule in neurons. Therefore, significant interest has been expressed in understanding how the dysregulation of Ca2+ signals might impact on neuronal function and the progression of different disease states. Many previous studies have examined the role of Ca2+ in neuronal excitotoxicity and some have started to understand how Ca2+ dysregulation might be a cause or consequence of neurodegeneration. This review will therefore focus on the significance of Ca2+ sensors, proteins that transduce Ca2+ signals, in neuronal function and dysfunction. Finally, we will assess their potential role in neurodegenerative processes, such as Alzheimer's disease (AD), arguing that they could serve as potential therapeutic targets. (C) 2011 Elsevier Ltd. All rights reserved.
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