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12/11/2019 - Tiago Fleming Outeiro

No próximo dia 12 de novembro, às 12h, acontece mais uma edição do Seminário INBEB. O Instituto Nacional de Ciência e Tecnologia de Biologia Estrutural e Bioimagem (INBEB) recebe Tiago Fleming Outeiro, diretor do Departamento de Experimental Neurodegeneration da University Medical Center Goettingen, Alemanha, para falar sobre as bases moleculares da doença de Parkinson. O evento acontece no Auditório Leopoldo de Meis, no Instituto de Bioquímica Médica (IBqM) da UFRJ.

O pesquisador irá apresentar os resultados do estudo Disruption of synaptic proteostasis and function: insights into the molecular basis of Parkinson’s disease. O resumo do trabalho pode ser lido abaixo, em inglês.

O seminário será em português.

Disruption of synaptic proteostasis and function: insights into the molecular basis of Parkinson’s disease
Abstract: The aggregation of alpha-synuclein (ASYN) in Lewy bodies and Lewy neurites is the typical pathological hallmark of Parkinson’s disease (PD) and other synucleinopathies. Furthermore, mutations in the gene encoding for ASYN are associated with familial and sporadic forms of PD, suggesting this protein plays a central role in the disease. However, the precise contribution of ASYN to neuronal dysfunction and death is still unclear. By taking advantage of studies in model organisms, we are investigating the molecular underpinnings of PD, and found that prefibrillar soluble aSyn oligomers are crucial associated with synaptic dysfunction. We identified the 10 kDa heat shock protein (HSP10) as a mediator of aSyn-induced mitochondrial impairments in striatal synaptosomes. Overexpression of HSP10 ameliorateed aSyn-associated mitochondrial dysfunction and delayed aSyn pathology in vitro and in vivo. Altogether, our data indicate that increased levels of aSyn induce mitochondrial deficits, at least partially, by sequestering HSP10 in the cytosol and preventing it from acting in mitochondria. Importantly, these alterations manifest first at presynaptic terminals. Our study not only provides mechanistic insight into synucleinopathies but opens new avenues for targeting underlying cellular pathologies.

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