α -突触核蛋白在大鼠帕金森病模型中的过度表达表明肠道神经系统和肠道微生物组的改变

Sarah M O'Donovan, Erin K. Crowley, J. Brown, Ó. O’Sullivan, O. O'Leary, Suzanne Timmons, Y. Nolan, D. Clarke, N. Hyland, S. Joyce, A. Sullivan, C. O'Neill
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引用次数: 53

摘要

帕金森病(PD)的一个显著特征是α -突触核蛋白聚集体在整个大脑中积聚;然而,α‐突触核蛋白也在肠神经元中表达。胃肠(GI)症状和病理在PD中经常被报道,包括便秘、肠通透性增加、神经胶质病理和肠道微生物群组成的改变。α -突触核蛋白可以通过神经系统传播,但α -突触核蛋白病理的起源部位,是肠道还是大脑,尚不清楚。体育锻炼与缓解PD症状和改变肠道微生物群组成有关。
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Nigral overexpression of α‐synuclein in a rat Parkinson’s disease model indicates alterations in the enteric nervous system and the gut microbiome
A hallmark feature of Parkinson's disease (PD) is the build‐up of α‐synuclein protein aggregates throughout the brain; however α‐synuclein is also expressed in enteric neurons. Gastrointestinal (GI) symptoms and pathology are frequently reported in PD, including constipation, increased intestinal permeability, glial pathology, and alterations to gut microbiota composition. α‐synuclein can propagate through neuronal systems but the site of origin of α‐synuclein pathology, whether it be the gut or the brain, is still unknown. Physical exercise is associated with alleviating symptoms of PD and with altering the composition of the gut microbiota.
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