Níveis da secretase ADAM10 em idosos com diabetes mellitus tipo 2 e doença de Alzheimer
Ano de defesa: | 2022 |
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Autor(a) principal: | |
Orientador(a): | |
Banca de defesa: | |
Tipo de documento: | Dissertação |
Tipo de acesso: | Acesso aberto |
Idioma: | por |
Instituição de defesa: |
Universidade Federal de São Carlos
Câmpus São Carlos |
Programa de Pós-Graduação: |
Programa de Pós-Graduação em Gerontologia - PPGGero
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Departamento: |
Não Informado pela instituição
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País: |
Não Informado pela instituição
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Palavras-chave em Português: | |
Palavras-chave em Inglês: | |
Área do conhecimento CNPq: | |
Link de acesso: | https://repositorio.ufscar.br/handle/ufscar/15746 |
Resumo: | Alzheimer's disease (AD) is a gradual and progressive neurodegenerative disease characterized by predominant cortical atrophy in the medial temporal lobe and microscopically extensive neuronal losses and deposits called neurofibrillary tangles and senile plaques. From the results of the Rotterdam study in 1992, it is known that type 2 diabetes mellitus (T2DM) increases the risk of dementia. Patients with T2DM have structural brain changes and cognitive impairment, with a high risk of developing AD. These data suggest that insulin may play a key role in brain activity and memory formation. Our group has been studying peripheral AD biomarkers since 2010. Our results indicate that ADAM10 (A Disintegrin And Metalloprotease), the α-secretase that inhibits the formation of senile plaques and, therefore, is protective against AD, is active and decreased on platelets. Conversely, ADAM10 is inactive and increased in older adults with this dementia than cognitively healthy older adults. In this sense, this study aimed to verify the plasma ADAM10 levels among cognitively healthy older adults without glycemic alteration, older adults with AD, older adults with T2DM and older adults with the concomitant presence of AD and T2DM. The results showed a significant difference between plasma ADAM10 levels between all groups compared to older adults with AD+T2DM. Therefore, alterations in the insulin pathway can cause changes in ADAM10 levels and contribute to the worsening of AD. |