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血管性痴呆的神经化学

The neurochemistry of vascular dementia.

作者信息

Gottfries C G, Blennow K, Karlsson I, Wallin A

机构信息

University of Göteborg, Department of Clinical Neuroscience, Mölndal Hospital, Sweden.

出版信息

Dementia. 1994 May-Aug;5(3-4):163-7. doi: 10.1159/000106715.

Abstract

Vascular dementia (VAD) is cognitive impairment caused by changes in the blood circulation of the brain. It is not synonymous with multi-infarct dementia. The latter is a subgroup of VAD. Neurochemical investigations of noninfarcted brain tissue from patients with VAD show general changes in VAD brains. The serotonin metabolism is severely reduced and so is the activity of choline acetyltransferase. Monamine oxidase B is significantly increased in the white matter. A severe decrease in myelin components indicates white matter disturbances of such a degree that they must be considered to be of pathogenetic importance. The levels of some neuropeptides in the hypothalamus are increased. This is a finding which is in agreement with clinical findings of a high activity in the hypothalamic-pituitary-adrenal axis in patients with VAD. This high activity is possibly due to a loss of serotonergic inhibitory tone on the hypothalamus in VAD brains.

摘要

血管性痴呆(VAD)是由大脑血液循环变化引起的认知障碍。它与多发性梗死性痴呆不同义。后者是VAD的一个亚组。对VAD患者非梗死脑组织的神经化学研究显示,VAD大脑存在一般性变化。血清素代谢严重降低,胆碱乙酰转移酶的活性也是如此。单胺氧化酶B在白质中显著增加。髓鞘成分的严重减少表明白质紊乱程度已达到必须被视为具有致病重要性的程度。下丘脑中一些神经肽的水平升高。这一发现与VAD患者下丘脑 - 垂体 - 肾上腺轴高活性的临床发现一致。这种高活性可能是由于VAD大脑中下丘脑的血清素能抑制性张力丧失所致。

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