Synaptic dysfunction induced by Aβ oligomers in Alzheimer's disease: AKAP150-NFAT signalling as a molecular target
Alzheimer's disease (AD) is the most common form of dementia worldwide and to this day no effective cure has been found. Various studies suggest that synaptic dysfunction is one of the earliest pathological events in this disease, preceding even clinical symptoms. In this regard, soluble amyloi...
| Autores: | , |
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| Tipo de documento: | dissertação |
| Data de publicação: | 2025 |
| País: | España |
| Recursos: | Universitat Autònoma de Barcelona |
| Repositório: | Dipòsit Digital de Documents de la UAB |
| Idioma: | inglês |
| OAI Identifier: | oai:ddd.uab.cat:320136 |
| Acesso em linha: | https://ddd.uab.cat/record/320136 |
| Access Level: | Acceso aberto |
| Palavra-chave: | Malaltia d'Alzheimer Oligòmers de beta-amiloide AKAP79/150 NFATc3 Calcineurina Canals de calci tipus L Disfunció sinàptica Enfermedad de Alzheimer Oligómeros de beta-amiloide Canales de calcio tipo Disfunción sináptica Alzheimer's disease Amyloid-beta oligomers Calcineurin L-type calcium channels Synaptic dysfunction |
| Resumo: | Alzheimer's disease (AD) is the most common form of dementia worldwide and to this day no effective cure has been found. Various studies suggest that synaptic dysfunction is one of the earliest pathological events in this disease, preceding even clinical symptoms. In this regard, soluble amyloid-beta oligomers (Aβo) have been identified as neurotoxic compounds that can alter synaptic function. The aim of this study is to investigate the molecular effects of Aβo on some key components of the postsynaptic signalling complex in hippocampal neuronal cultures, focusing on the AKAP-CaN-NFAT |
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