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路易体痴呆中的胆碱能递质与神经营养活性:与帕金森病的相似性及与阿尔茨海默病的区别

Cholinergic transmitter and neurotrophic activities in Lewy body dementia: similarity to Parkinson's and distinction from Alzheimer disease.

作者信息

Perry E K, Irving D, Kerwin J M, McKeith I G, Thompson P, Collerton D, Fairbairn A F, Ince P G, Morris C M, Cheng A V

机构信息

MRC Neurochemical Pathology Unit, Newcastle General Hospital, Newcastle upon Tyne, England.

出版信息

Alzheimer Dis Assoc Disord. 1993 Summer;7(2):69-79. doi: 10.1097/00002093-199307020-00002.

DOI:10.1097/00002093-199307020-00002
PMID:8347330
Abstract

Senile dementia of Lewy body type or Lewy body dementia (LBD), characterized neuropathologically by the presence of Lewy bodies in the brainstem and cortex, and in most cases neocortical senile plaques (but few or no tangles), bears a closer resemblance to Parkinson's (PD) than to Alzheimer disease (AD) in its cholinergic neurochemical pathology. Thus, reductions in the biochemical activity of choline acetyltransferase were generally more extensive in neo- as opposed to archicortical regions in LBD (especially hallucinating cases) and in PD, whereas muscarinic receptor binding was significantly increased in LBD and PD but not in AD. Nerve growth factor receptor (P75) assessed immunocytochemically in the archicortex were decreased in PD and, to a lesser extent, in LBD in conjunction with reductions of neuronal numbers in the nucleus of Meynert (Ch4), but were relatively spared in AD. These observations indicate that although AD is primarily associated with dysfunction of cholinergic axonal input to the cortex, LBD and PD are more likely to involve degeneration of the basal forebrain cholinergic system. Relevance of the findings in terms of aetiopathology and cholinergic treatment strategies is discussed.

摘要

路易体痴呆症(LBD),其病理特征为脑干和皮质中存在路易体,且在大多数情况下新皮质有老年斑(但神经缠结很少或没有),在胆碱能神经化学病理学方面,与帕金森病(PD)的相似性高于阿尔茨海默病(AD)。因此,在LBD(尤其是有幻觉症状的病例)和PD中,胆碱乙酰转移酶的生化活性降低在新皮质区域比在旧皮质区域通常更广泛,而毒蕈碱受体结合在LBD和PD中显著增加,但在AD中没有增加。通过免疫细胞化学方法评估的旧皮质中的神经生长因子受体(P75)在PD中减少,在LBD中也有一定程度的减少,同时Meynert核(Ch4)中的神经元数量减少,但在AD中相对保留。这些观察结果表明,虽然AD主要与皮质胆碱能轴突输入功能障碍有关,但LBD和PD更可能涉及基底前脑胆碱能系统的退化。本文讨论了这些发现病因病理学及胆碱能治疗策略方面的相关性。

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