Calcium/calmodulin-dependent kinase II and Alzheimer's disease.
Calcium/calmodulin-dependent kinase II and Alzheimer's disease.
复制标题
DOI：
10.1186/s13041-015-0166-2
复制
发表时间：
2015-11-24
期刊：
影响因子：
3.6
通讯作者：
Giese KP
中科院分区：
文献类型：
--
作者：
Ghosh A;Giese KP
CaMKII是一种非常复杂的蛋白激酶，已知在突触可塑性和记忆形成中具有重要作用。此外，CaMKII也被认为是tau激酶。因此，CaMKII失调可能是阿尔茨海默病毒性的调节剂，阿尔茨海默病是一种以异常钙信号传导、突触和神经元损失以及记忆受损为特征的痴呆。在这里，我们首先研究了阿尔茨海默病患者CaMKII失调的证据，并与疾病模型中的发现进行了比较，这些发现概括了疾病的关键方面。然后，我们提出了这样的假设，即这些变化对阿尔茨海默病的神经变性和记忆障碍有重要作用。
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.