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Updated: Jul 9, 2025

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices
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Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

Published on: July 14, 2010

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氨基酸β1-42寡合体通过NMDAR激活增强mGlu5R-依赖的突触削弱,并补充C5aR1信号传递

Ai Na Ng1, Eric W Salter2,3, John Georgiou2,4

  • 1School of Physiology, Pharmacology and Neuroscience, University of Bristol, Biomedical Sciences Building, University Walk, Bristol BS8 1TD, UK.

iScience
|December 6, 2023
PubMed
概括

寡合性粉样β通过激活补充路径触发阿尔茨海默病的突触损失. 这项研究揭示了metabotropic谷氨酸受体和N-甲基-D-酸盐受体如何与补充系统相互作用,驱动异常突触衰弱.

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卫生科学 卫生科学分子神经科学分子神经科学神经科学是一个神经科学.病理生理学 病理生理学

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Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining,...
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