Histology and Embryology Unit, Department of Life and Reproduction Sciences, University of Verona Medical School, Verona, Venetia, Italy.
J Neurol Sci. 2012 Nov 15;322(1-2):137-40. doi: 10.1016/j.jns.2012.07.031. Epub 2012 Jul 28.
Alzheimer's disease (AD) is the most common human neurodegenerative ailment, the most prevalent (>95%) late-onset type of which has a still uncertain etiology. The progressive decline of cognitive functions, dementia, and physical disabilities of AD is caused by synaptic losses that progressively disconnect key neuronal networks in crucial brain areas, like the hippocampus and temporoparietal cortex, and critically impair language, sensory processing, memory, and conscious thought. AD's two main hallmarks are fibrillar amyloid-β (fAβ) plaques in extracellular spaces and intracellular accumulation of fAβ peptides and neurofibrillary tangles (NFTs). It is still undecided whether either or both these AD hallmarks cause or result from the disease. Recently, the dysregulation of calcium homeostasis has been advanced as a novel cause of AD. In this case, a suitable candidate of AD driver would be the Aβ peptides-binding/activated calcium-sensing receptor (CaSR), whose intracellular signalling is triggered by Aβ peptides. In this review, we briefly discuss CaSR's roles in normal adult human astrocytes (NAHAs) and their possible impacts on AD.
阿尔茨海默病（AD）是最常见的人类神经退行性疾病，其中最常见（>95%）的是发病较晚的类型，其病因仍不确定。AD 患者认知功能的逐渐下降、痴呆和身体残疾是由突触丧失引起的，这些突触逐渐使关键的神经元网络在关键的大脑区域（如海马体和颞顶叶皮层）断开，严重损害语言、感觉处理、记忆和有意识的思维。AD 的两个主要特征是细胞外空间中的纤维状淀粉样β（fAβ）斑块和细胞内聚集的 fAβ肽和神经原纤维缠结（NFTs）。目前仍不确定是这两个 AD 特征中的一个或两个导致了这种疾病，还是由疾病引起的。最近，钙稳态失调被认为是 AD 的一个新的病因。在这种情况下，AD 的一个合适的驱动候选物可能是 Aβ肽结合/激活的钙敏感受体（CaSR），其细胞内信号由 Aβ肽触发。在这篇综述中，我们简要讨论了 CaSR 在正常成人星形胶质细胞（NAHAs）中的作用及其对 AD 的可能影响。
