作者: He-Jin Lee , Ji-Eun Suk , Christina Patrick , Eun-Jin Bae , Ji-Hoon Cho
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摘要: Abnormal neuronal aggregation of α-synuclein is implicated in the development many neurological disorders, including Parkinson disease and dementia with Lewy bodies. Glial cells also show extensive pathology may contribute to progression. However, mechanism that produces glial interaction between neurons glia disease-inflicted microenvironment remain unknown. Here, we proteins released from are taken up by astrocytes through endocytosis form inclusion The accumulation transmission protein was demonstrated a transgenic mouse model expressing human α-synuclein. Furthermore, were exposed underwent changes gene expression profile reflecting an inflammatory response. Induction pro-inflammatory cytokines chemokines correlated extent Together, these results suggest astroglial produced direct aggregates, causing responses. This step thus important mediator pathogenic responses could qualify as new therapeutic target.