Aging-Related Calcium Dysregulation in Rat Entorhinal Neurons Homologous with the Human Entorhinal Neurons in which Alzheimer's Disease Neurofibrillary Tangles First Appear.
Aging-Related Calcium Dysregulation in Rat Entorhinal Neurons Homologous with the Human Entorhinal Neurons in which Alzheimer's Disease Neurofibrillary Tangles First Appear.
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DOI：
10.3233/jad-180618
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发表时间：
2018
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影响因子：
--
通讯作者：
Landfield PW
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文献类型：
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作者：
Gant JC;Kadish I;Chen KC;Thibault O;Blalock EM;Porter NM;Landfield PW
衰老是特发性阿尔茨海默病(AD)的主要危险因素，表明正常的衰老过程促进了AD的发生，并可能存在于AD发病的神经元中。在AD中，神经原纤维缠结(NFT)首先出现在内嗅皮层，提示内嗅神经元的衰老过程促进了NFT的发病。利用电生理学和免疫组织化学的方法，我们发现大鼠内嗅神经元中存在明显的与衰老相关的钙离子失调，与人类神经元中NFTs的起源具有同源性。考虑到人类概括了动物脑老化的许多方面，这些结果支持了这样的假设，即与衰老相关的钙离子失调发生在人的内嗅神经元中，并促进了NFT的发病。
Aging is the leading risk factor for idiopathic Alzheimer’s disease (AD), indicating that normal aging processes promote AD and likely are present in the neurons in which AD pathogenesis originates. In AD, neurofibrillary tangles (NFTs) appear first in entorhinal cortex, implying that aging processes in entorhinal neurons promote NFT pathogenesis. Using electrophysiology and immunohistochemistry, we find pronounced aging-related Ca2 + dysregulation in rat entorhinal neurons homologous with the human neurons in which NFTs originate. Considering that humans recapitulate many aspects of animal brain aging, these results support the hypothesis that aging-related Ca2 + dysregulation occurs in human entorhinal neurons and promotes NFT pathogenesis.