Pathophysiological regulation of the production, aggregation and toxicity of the amyloid beta-peptide in Alzheimer's disease
Society increase in live expectancy will cause a rise in Alzheimer’s Disease (AD) diagnosis, thus, there is a need to further understand how it works. One of the main culprits of this disease amyloid-β peptide (Aβ), this protein has a physiological function as monomers. But, once starts to aggregate...
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| Tipo de recurso: | tesis doctoral |
| Estado: | Versión publicada |
| Fecha de publicación: | 2022 |
| País: | España |
| Institución: | CBUC, CESCA |
| Repositorio: | TDR. Tesis Doctorales en Red |
| OAI Identifier: | oai:www.tdx.cat:10803/675512 |
| Acceso en línea: | http://hdl.handle.net/10803/675512 |
| Access Level: | acceso abierto |
| Palabra clave: | Alzheimer’s Disease Amyloid-beta peptide Calcium Oxidative stress Malaltia d’Alzheimer Proteïna beta amiloide Calci Estrès oxidatiu 616.8 |
| Sumario: | Society increase in live expectancy will cause a rise in Alzheimer’s Disease (AD) diagnosis, thus, there is a need to further understand how it works. One of the main culprits of this disease amyloid-β peptide (Aβ), this protein has a physiological function as monomers. But, once starts to aggregate, Aβ becomes neurotoxic. In this thesis, I have demonstrated a novel physiological function of monomeric Aβ as inductor of insulin receptor signalling, while its oligomers block the same signalling. I have described a neurotoxic feedback loop between oligomeric Aβ and an increase in BACE1 presence. I have studied novel calcium regulators in the development of the disease. I showed a novel pathway that links Aβ as a blocker of LTP. Finally, I have characterised the region of interaction of albumin c-terminus with Aβ and its neuroprotective effect. |
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