Lymphocyte Activation Gene 3 (Lag3) Contributes to α-Synucleinopathy in α-Synuclein Transgenic Mice

• DOI: 10.3389/fncel.2021.656426
• Publication Date: 2021-03-10T04:40:24Z
• Authors: Hao Gu; Xiuli Yang; Xiaobo Mao; Enquan Xu; Chen Qi; Haibo Wang; Saurav Brahmachari; Bethany York; Manjari Sriparna; Amanda Li; Michael Chang; Pavan Patel; Valina L. Dawson; Ted M. Dawson
• Keywords: Cellular and Molecular Neuroscience; 0303 health sciences; 03 medical and health sciences; α-synuclein; aggregation; Neurosciences. Biological psychiatry. Neuropsychiatry; Lag3; Parkinson’ disease; α-synucleinopathy; RC321-571; Neuroscience

Aggregation of misfolded α-synuclein (α-syn) is the major component Lewy bodies and neurites in Parkinson's disease (PD) related α-synucleinopathies. Some α-syn mutations (e.g., A53T) familial PD recapitulate pathology transgenic mice, which supports importance pathologic driving pathogenesis Lymphocyte activation gene 3 (Lag3) a receptor fibrils facilitating spread; however, role Lag3 mediating mice not clear. Here, we report that depletion human A53T (hA53T) significantly reduces level detergent-insoluble aggregates phosphorylated ser129 α-syn, inhibits microglia astrocytes. The absence delays progression behavioral deficits hA53T leading to prolonged survival. Taken together, these results show contributes mouse model.