Brain and Spine Institute - ICM, Center for NeuroImaging Research - CENIR, Paris, France.
Sorbonne Université, University Pierre and Marie Curie Paris 06, Inserm U1127, Centre National de la Recherche Scientifique (CNRS) Unité Mixte de Recherche (UMR) 7225, Paris, France.
Mov Disord. 2019 Apr;34(4):516-525. doi: 10.1002/mds.27561. Epub 2018 Dec 10.
Cognitive deficits in Parkinson's disease (PD) may result from damage in the cortex as well as in the dopaminergic, noradrenergic, and cholinergic inputs to the cortex. Cholinergic inputs to the cortex mainly originate from the basal forebrain and are clustered in several regions, called Ch1 to Ch4, that project to the hippocampus (Ch1-2), the olfactory bulb (Ch3), and the cortex and amygdala (Ch4).
We investigated changes in basal forebrain and their role in cognitive deficits in PD.
We studied 52 nondemented patients with PD (Hoehn & Yahr 1-2) and 25 age-matched healthy controls using diffusion and resting state functional MRI.
PD patients had a loss of structural integrity within the Ch1-2 and Ch3-4 nuclei of the basal forebrain as well as in the fornix. Tractography showed that the probability of anatomical connection was decreased in PD between Ch3-4 and the associative prefrontal cortex, occipital cortex, and peri-insular regions. There was a reduction in functional connectivity between Ch1-2 and the bilateral hippocampi and parahippocampal gyri, the left middle and superior temporal gyri, and the left fusiform gyrus and between Ch3-4 and the right inferior frontal gyrus and the right and left thalamus. In Ch1-2, loss of structural integrity and connectivity correlated with scores at the memory tests, whereas changes in Ch3-4 correlated with scores of global cognition and executive functions.
This study highlights the association between deficits of different cholinergic nuclei of the basal forebrain and the extent of cognitive impairments in nondemented PD patients. © 2018 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.
帕金森病(PD)的认知缺陷可能源于皮质以及皮质中的多巴胺能、去甲肾上腺素能和胆碱能传入的损伤。皮质中的胆碱能传入主要来源于基底前脑,并聚集在几个区域,称为 Ch1 到 Ch4,投射到海马体(Ch1-2)、嗅球(Ch3)以及皮质和杏仁核(Ch4)。
我们研究基底前脑的变化及其在 PD 认知缺陷中的作用。
我们使用弥散张量成像和静息态功能磁共振成像研究了 52 名非痴呆 PD 患者(Hoehn & Yahr 1-2 期)和 25 名年龄匹配的健康对照者。
PD 患者基底前脑的 Ch1-2 和 Ch3-4 核以及穹窿的结构完整性丧失。示踪研究显示,PD 患者 Ch3-4 与额下回、顶叶皮质和岛周区之间的解剖连接概率降低。Ch1-2 与双侧海马体和海马旁回、左侧中颞和上回以及左侧梭状回之间以及 Ch3-4 与右侧额下回和右侧、左侧丘脑之间的功能连接减少。在 Ch1-2 中,结构完整性和连接的丧失与记忆测试评分相关,而 Ch3-4 的变化与整体认知和执行功能评分相关。
本研究强调了基底前脑不同胆碱能核团的缺陷与非痴呆 PD 患者认知障碍程度之间的关联。© 2018 作者。运动障碍由 Wiley 期刊出版公司代表国际帕金森和运动障碍协会出版。