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阿尔茨海默病中的递质缺陷

Transmitter deficits in Alzheimer's disease.

作者信息

Hardy J, Adolfsson R, Alafuzoff I, Bucht G, Marcusson J, Nyberg P, Perdahl E, Wester P, Winblad B

机构信息

Umeå Dementia Research Group, Departments of Pathology, Psychiatry and Geriatric Medicine, University of Umeå, Umeå Sweden.

出版信息

Neurochem Int. 1985;7(4):545-63. doi: 10.1016/0197-0186(85)90050-6.

Abstract

The pattern of neurotransmitter pathway losses in Alzheimer's disease are reviewed. Deficits of the cholinergic pathway from the nucleus basalis, the noradrenergic pathway from the locus coeruleus and the serotoninergic pathway from the raphe nuclei are established. Cortical somatostatin interneurons are affected and dopaminergic neurons may be affected although these may be late or secondary phenomena in the disease process. Other neuronal systems, particularly in the hippocampus and temporal cortex, are also damaged. However, the disease is not one of generalised neuronal atrophy since some neurons are selectively spared. The established pathway-specific losses are discussed in relation to the clinical symptomatology and the pathology of the disorder. The biochemical and histological findings are compared with similar measurements made on tissues from other dementing disorders in an attempt to trace features common to dementias. Finally, as an addendum, a hypothesis is briefly outlined which attempts to explain the common features of the affected neurons and the pathogenesis of the disorder.

摘要

本文综述了阿尔茨海默病中神经递质通路缺失的模式。基底核胆碱能通路、蓝斑去甲肾上腺素能通路和中缝核5-羟色胺能通路的缺失已得到证实。皮质生长抑素中间神经元受到影响,多巴胺能神经元可能也会受到影响,尽管这可能是疾病过程中的晚期或继发现象。其他神经元系统,特别是海马体和颞叶皮质中的神经元系统,也会受损。然而,该疾病并非全身性神经元萎缩,因为一些神经元可选择性地幸免。文中讨论了已确定的特定通路缺失与该疾病的临床症状和病理学之间的关系。将生化和组织学研究结果与其他痴呆症组织的类似测量结果进行比较,试图找出痴呆症的共同特征。最后,作为附录,简要概述了一个假说,该假说试图解释受影响神经元的共同特征以及该疾病的发病机制。

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