title: Calcium/calmodulin-dependent kinase II and Alzheimer's disease.
abstract: 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.
authors.affiliation: Maurice Wohl Clinical Neuroscience Institute, King's College London, 5 Cutcombe Road, London, SE5 9RT, UK. anshua.ghosh@kcl.ac.uk.
authors.forename: Anshua
authors.initials: A
authors.lastname: Ghosh
authors.affiliation: Maurice Wohl Clinical Neuroscience Institute, King's College London, 5 Cutcombe Road, London, SE5 9RT, UK. karl.giese@kcl.ac.uk.
authors.forename: Karl Peter
authors.initials: KP
authors.lastname: Giese
mesh_terms: D000544:Alzheimer Disease / Q000201:enzymology* / Q000473:pathology*; D000818:Animals; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000378:metabolism*; D004195:Disease Models, Animal; D006801:Humans; D008954:Models, Biological
chemical_list: D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2