White Andrew J, Clark Karis A, Alexander Kellianne D, Ramalingam Nagendran, Young-Pearse Tracy L, Dettmer Ulf, Selkoe Dennis J, Ho Gary P H
Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.
NPJ Parkinsons Dis. 2024 May 21;10(1):107. doi: 10.1038/s41531-024-00725-y.
Alpha-synuclein (αS)-rich Lewy bodies and neurites in the cerebral cortex correlate with the presence of dementia in Parkinson disease (PD) and Dementia with Lewy bodies (DLB), but whether αS influences synaptic vesicle dynamics in human cortical neurons is unknown. Using a new iPSC-based assay platform for measuring synaptic vesicle cycling, we found that in human cortical glutamatergic neurons, increased αS from either transgenic expression or triplication of the endogenous locus in patient-derived neurons reduced synaptic vesicle cycling under both stimulated and spontaneous conditions. Thus, using a robust, easily adopted assay platform, we show for the first time αS-induced synaptic dysfunction in human cortical neurons, a key cellular substrate for PD dementia and DLB.
大脑皮层中富含α-突触核蛋白(αS)的路易小体和神经突与帕金森病(PD)和路易体痴呆(DLB)中的痴呆症存在相关,但αS是否影响人类皮层神经元中的突触小泡动力学尚不清楚。通过使用一种基于诱导多能干细胞(iPSC)的新检测平台来测量突触小泡循环,我们发现,在人类皮层谷氨酸能神经元中,无论是转基因表达还是患者来源神经元中内源性基因座的三倍体导致的αS增加,都会在刺激和自发条件下降低突触小泡循环。因此,通过使用一个强大且易于采用的检测平台,我们首次证明了αS在人类皮层神经元中诱导的突触功能障碍,这是PD痴呆和DLB的关键细胞底物。