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帕金森病认知功能障碍的功能脑影像学研究。

Functional brain imaging of cognitive dysfunction in Parkinson's disease.

机构信息

Department of Neurology, Chiba University School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba-shi, Chiba 260-8670, Japan.

出版信息

J Neurol Neurosurg Psychiatry. 2012 Oct;83(10):963-9. doi: 10.1136/jnnp-2011-301818. Epub 2012 Jul 17.

Abstract

Multiple factors are involved in the development of cognitive impairment in Parkinson's disease (PD) and related disorders. Notably, several underlying factors, such as monoaminergic dysfunction, Lewy body pathology, Alzheimer disease-like pathology and cerebrovascular disease are implied in the PD pathophysiology of cognitive impairment. The mesocortical dopaminergic system is associated with executive functions which are frequently affected in PD and are influenced by local levodopa concentration, dopamine metabolism and baseline performance status. The ventral striatum and frontal cortex are associated with impulse control disorders reported in PD patients treated with dopamine replacement therapy. Cholinergic impairment in PD plays a cardinal role in the development of dementia. Acetylcholinesterase positron emission tomography demonstrates that posterior brain areas are related to cognitive decline in PD patients. Amyloid radiotracer illustrates that patients with PD with severe cognitive impairment were prone to accompanied cortical amyloid deposition. Metabolism/perfusion change associated with cognitive impairment in PD, so-called PD related cognitive pattern, is characterised by reduced frontoparietal activity and is an effective way to differentiate and monitor cognitive function of individual PD patients. Cognitive impairment in PD cannot be explained by a single mechanism and is entangled by multiple factors. Imaging studies can unravel each pathological domain, further shed light on the interrelation between different pathomechanisms, not only in PD but also in other dementia related disorders, and thereby integrate its interpretation to apply to therapeutics in individual patients.

摘要

多种因素参与了帕金森病(PD)和相关疾病认知障碍的发展。值得注意的是,几种潜在的因素,如单胺能功能障碍、路易体病理、阿尔茨海默病样病理和脑血管病,都暗示了 PD 认知障碍的病理生理学。中皮质多巴胺能系统与执行功能有关,执行功能在 PD 中经常受到影响,并受到局部左旋多巴浓度、多巴胺代谢和基线表现状态的影响。腹侧纹状体和额叶皮层与 PD 患者接受多巴胺替代治疗时出现的冲动控制障碍有关。PD 中的胆碱能损伤在痴呆的发展中起着关键作用。乙酰胆碱酯酶正电子发射断层扫描表明,后脑部区域与 PD 患者的认知下降有关。淀粉样蛋白示踪剂表明,认知障碍严重的 PD 患者容易伴有皮质淀粉样蛋白沉积。与 PD 认知障碍相关的代谢/灌注变化,即所谓的 PD 相关认知模式,其特征是额顶叶活动减少,是区分和监测个体 PD 患者认知功能的有效方法。PD 中的认知障碍不能用单一机制来解释,而是被多种因素所纠缠。影像学研究可以揭示每个病理领域,进一步阐明不同病理机制之间的相互关系,不仅在 PD 中,而且在其他与痴呆相关的疾病中,从而将其解释整合到对个体患者的治疗中。

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