痴呆症中神经递质的特异性改变：来自动物模型的见解

Neurotransmitter specific alterations in dementing disorders: insights from animal models.

作者信息

Coyle J T, Singer H, McKinney M, Price D

出版信息

J Psychiatr Res. 1984;18(4):501-12. doi: 10.1016/0022-3956(84)90037-2.

Abstract

Recent years have witnessed considerable change in the conceptualization of the pathophysiology of the cognitive impairments in dementing disorders, as a result of synaptic neurochemical analyses. Profound reductions in the forebrain cholinergic projections occur in Alzheimer's disease. In GM1 gangliosidosis, variable alterations in neurotransmitter related processes that are located in synaptic membranes have been described. Exploitation of animal models of human disorders resulting in dementia may further clarify the dynamic alterations in the biochemical processes required for effective neurotransmission in cortex.

摘要

近年来，由于突触神经化学分析，痴呆症认知障碍的病理生理学概念发生了相当大的变化。在阿尔茨海默病中，前脑胆碱能投射显著减少。在GM1神经节苷脂贮积症中，已描述了位于突触膜上的神经递质相关过程的各种改变。利用导致痴呆的人类疾病动物模型可能会进一步阐明皮质中有效神经传递所需生化过程的动态变化。