@article{oai:shiga-med.repo.nii.ac.jp:00003231,
 author = {漆谷, 真 and Kaji, Seiji and Maki, Takakuni and Kinoshita, Hisanori and Uemura, Norihito and Ayaki, Takashi and Kawamoto, Yasuhiro and Furuta, Takahiro and URUSHITANI, Makoto and Hasegawa, Masato and Kinoshita, Yusuke and Ono, Yuichi and Mao, Xiaobo and Quach, Tran H and Iwai, Kazuhiro and Dawson, Valina L and Dawson, Ted M and Takahashi, Ryosuke},
 issue = {2},
 journal = {Stem Cell Reports},
 month = {Jan},
 note = {Glial cytoplasmic inclusions (GCIs), commonly observed as α-synuclein (α-syn)-positive 
aggregates within oligodendrocytes, are the pathological hallmark of multiple system atrophy. The origin of α-syn in GCIs is uncertain; there is little evidence of endogenous
α-syn expression in oligodendrocyte lineage cells, oligodendrocyte precursor cells (OPCs),
and mature oligodendrocytes (OLGs). Here, based on in vitro analysis using primary rat 
cell cultures, we elucidated that preformed fibrils (PFFs) generated from recombinant 
human α-syn trigger multimerization and an upsurge of endogenous α-syn in OPCs, 
which is attributable to insufficient autophagic proteolysis. RNA-seq analysis of OPCs 
revealed that α-syn PFFs interfered with the expression of proteins associated with 
neuromodulation and myelination. Furthermore, we detected cytoplasmic α-syn 
inclusions in OLGs through differentiation of OPCs pre-incubated with PFFs. Overall, our 
findings suggest the possibility of endogenous α-syn accumulation in OPCs that 
contributes to GCI formation and perturbation of neuronal/glial support in multiple 
system atrophy brains., Journal Article},
 pages = {356--365},
 title = {Pathological Endogenous α-Synuclein Accumulation in Oligodendrocyte Precursor Cells Potentially Induces Inclusions in Multiple System Atrophy.},
 volume = {10},
 year = {2018}
}