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β淀粉样蛋白在体外可增强海马神经元的存活率。

Amyloid beta protein enhances the survival of hippocampal neurons in vitro.

作者信息

Whitson J S, Selkoe D J, Cotman C W

机构信息

Department of Psychobiology, University of California, Irvine 92717.

出版信息

Science. 1989 Mar 17;243(4897):1488-90. doi: 10.1126/science.2928783.

Abstract

The beta-amyloid protein is progressively deposited in Alzheimer's disease as vascular amyloid and as the amyloid cores of neuritic plaques. Contrary to its metabolically inert appearance, this peptide may have biological activity. To evaluate this possibility, a peptide ligand homologous to the first 28 residues of the beta-amyloid protein (beta 1-28) was tested in cultures of hippocampal pyramidal neurons for neurotrophic or neurotoxic effects. The beta 1-28 appeared to have neurotrophic activity because it enhanced neuronal survival under the culture conditions examined. This finding may help elucidate the sequence of events leading to plaque formation and neuronal damage in Alzheimer's disease.

摘要

β-淀粉样蛋白在阿尔茨海默病中会逐渐沉积为血管淀粉样蛋白以及神经炎性斑块的淀粉样核心。与其代谢惰性外观相反,这种肽可能具有生物活性。为评估这种可能性,在海马锥体神经元培养物中测试了一种与β-淀粉样蛋白前28个残基同源的肽配体(β1-28)的神经营养或神经毒性作用。β1-28似乎具有神经营养活性,因为在所检测的培养条件下它能提高神经元的存活率。这一发现可能有助于阐明阿尔茨海默病中导致斑块形成和神经元损伤的事件顺序。

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