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Molecular mechanisms of neurodegeneration in the entorhinal cortex that underlie its selective vulnerability during the pathogenesis of Alzheimer's disease

机译：在Entorhinal皮层中神经变性的分子机制，在阿尔茨海默病的发病机制中提出了其选择性脆弱性

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Olayemi Joseph Olajide; Marcus E. Suvanto; Clifton Andrew Chapman;
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1. Aberrant Excitatory-Inhibitory Synaptic Mechanisms in Entorhinal Cortex Microcircuits During the Pathogenesis of Alzheimer's Disease [J] . Petrache Alexandra L., Rajulawalla Aarib, Shi Anqi, Cerebral cortex . 2019,第4期

机译：阿尔茨海默病发病机制期间兴奋性皮层微电路异常兴奋性抑制突触机制
2. Selective Vulnerability of Neurons in Layer II of the Entorhinal Cortex during Aging and Alzheimer's Disease [J] . Alexis M.Stranahan, Mark P.Mattson Journal of Neural Transplantation and Plasticity: Neural Plasticity . 2010,第4期

机译：衰老和阿尔茨海默病期间，在Entorhinal Cortex三层神经元的选择性脆弱性
3. Cellular and molecular mechanisms implicated in pathogenesis of selective neurodegeneration in Huntington＇s disease [J] . Jeffrey R CANTLE, Xiao-Hong LU, Xiaofeng GU, 物理学前沿：英文版 . 2012,第005期

机译：亨廷顿舞蹈病选择性神经退行性疾病发病机制中涉及的细胞和分子机制
4. Hippocampal and entorhinal cortex volume changes in Alzheimer's disease patients and mild cognitive impairment subjects [C] . S. Leandrou, I. Mamais, S. Petroudi, IEEE EMBS International Conference on Biomedical and Health Informatics . 2018

机译：阿尔茨海默氏病患者和轻度认知障碍患者的海马和内嗅皮质体积变化
5. Molecular mechanism of Alzheimer's disease pathogenesis in Down Syndrome. [D] . Sun, Xiulian. 2007

机译：唐氏综合症阿尔茨海默氏病发病机理的分子机制。
6. Molecular mechanisms of neurodegeneration in the entorhinal cortex that underlie its selective vulnerability during the pathogenesis of Alzheimers disease [O] . Olayemi Joseph Olajide, Marcus E. Suvanto, Clifton Andrew Chapman 2021

机译：在Entorhinal皮层中神经变性的分子机制在阿尔茨海默病的发病机制中提出了其选择性脆弱性
7. Aberrant Excitatory–Inhibitory Synaptic Mechanisms in Entorhinal Cortex Microcircuits During the Pathogenesis of Alzheimer’s Disease [O] . Alexandra L Petrache, Aarib Rajulawalla, Anqi Shi, 2019

机译：阿尔茨海默病发病机制期间兴奋性皮层微电路异常兴奋性抑制突触机制

Molecular mechanisms of neurodegeneration in the entorhinal cortex that underlie its selective vulnerability during the pathogenesis of Alzheimer's disease

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