作者: Oliveira da Silva , Gerhardt , Castillo , Outeiro , Babcock
DOI: 10.1101/2021.02.02.425931
关键词:
摘要: Abstract Cognitive dysfunction and dementia are presently recognized as major complications in α-synucleinopathies, namely Dementia with Lewy Bodies (DLB) Parkinson’s disease (PDD). In these disorders, α-Synuclein (αSyn) accumulation affects severely the hippocampus by inducing synaptic which culminates cognitive impairment. To characterize mechanisms underlying αSyn-induced neuronal we analysed effect of overexpression or extracellular administration αSyn on hippocampal neurons. We observed that induces dysregulation actin-binding protein cofilin its assembly into rod structures a mechanism mediated cellular prion (PrPC). Moreover, unraveled pathology mediator dendritic spine impairment Importantly, synucleinopathy mouse model validated at same age when deficits were observed. Our data supports novel player triggered Body dementias.