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Molecular Brain

, 8:78

Molecules of Neural Disorders

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.

KeywordsCaMKII Alzheimer’s disease Post-mortem brain Autophosphorylation Memory Tau AbbreviationsAβAmyloid-β

ADAlzheimer’s disease

AηAmyloid-η

AMPARα-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptor

APPAmyloid precursor protein

CA1-3Cornu Ammonis areas 1-3

CaMKIICalcium-calmodulin binding protein kinase II

cdk5cyclin-dependent kinase 5

DGDentate gyrus

GluA1AMPAR subunit

GSK3-βGlycogen synthase kinase 3-β

LTD-LTPLong-term depression-potentiation

MCIMild cognitive impairment

MMSEMini-mental state examination

NFTNeurofibrillary tangle

NMDARN-methyl-D-aspartic acid receptor

NR2A-BNMDAR subunits

PHFPaired helical filament

PS1Presenilin-1

PSD-95Post-synaptic density protein 95

SPSenile plaque

VGCCVoltage-gated calcium channel

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Autor: Anshua Ghosh - Karl Peter Giese

Fuente: https://link.springer.com/



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