期刊
MOLECULAR BRAIN
卷 8, 期 -, 页码 -出版社
BIOMED CENTRAL LTD
DOI: 10.1186/s13041-015-0166-2
关键词
CaMKII; Alzheimer's disease; Post-mortem brain; Autophosphorylation; Memory; Tau
资金
- Medical Research Council
- Medical Research Council [G0800393, 1523477] Funding Source: researchfish
- MRC [G0800393] Funding Source: UKRI
CaMKII is a remarkably complex protein kinase, known to have a fundamental role in synaptic plasticity and memory formation. Further, CaMKII has also been suggested to be a tau kinase. CaMKII dysregulation may therefore be a modulator of toxicity in Alzheimer's disease, a dementia characterised by aberrant calcium signalling, synapse and neuronal loss, and impaired memory. Here, we first examine the evidence for CaMKII dysregulation in Alzheimer's patients and draw parallels to findings in disease models which recapitulate key aspects of the disease. We then put forward the hypothesis that these changes critically contribute to neurodegeneration and memory impairment in Alzheimer's disease.
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