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Aberrant Excitatory–Inhibitory Synaptic Mechanisms in Entorhinal Cortex Microcircuits During the Pathogenesis of Alzheimer’s Disease

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

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Alexandra L Petrache; Aarib Rajulawalla; Anqi Shi; Andrea Wetzel; Takashi Saito; Takaomi C Saido; Kirsten Harvey; Afia B Ali;
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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. Adenosine Differentially Modulates Synaptic Transmission of Excitatory and Inhibitory Microcircuits in Layer 4 of Rat Barrel Cortex [J] . Qi Guanxiao, van Aerde Karlijn, Abel Ted, Cerebral cortex . 2017,第9期

机译：腺苷差异地调节大鼠桶皮层三层兴奋剂和抑制微电路的突触传递
3. Synaptic Depression and Aberrant Excitatory Network Activity in Alzheimer’s Disease: Two Faces of the Same Coin? [J] . Jorge J. Palop, Lennart Mucke NeuroMolecular Medicine . 2010,第1期

机译：阿尔茨海默氏病的突触抑制和异常兴奋性网络活动：同一枚硬币的两个面孔？
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. Synaptic Plasticity and Excitatory-Inhibitory Balance in the Auditory Cortex. [D] . D'Amour, James Arthur. 2016

机译：听觉皮层中的突触可塑性和兴奋抑制性平衡。
6. Aberrant Excitatory–Inhibitory Synaptic Mechanisms in Entorhinal Cortex Microcircuits During the Pathogenesis of Alzheimer’s Disease [O] . Alexandra L Petrache, Aarib Rajulawalla, Anqi Shi, -1

机译：阿尔茨海默氏病发病机理中内嗅皮层微回路中异常的兴奋抑制性突触机制
7. Molecular mechanisms of neurodegeneration in the entorhinal cortex that underlie its selective vulnerability during the pathogenesis of Alzheimer's 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

Aberrant Excitatory–Inhibitory Synaptic Mechanisms in Entorhinal Cortex Microcircuits During the Pathogenesis of Alzheimer’s Disease

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