Targeting aging and alzheimer's disease: from gm1 ganglioside to amyloid-beta peptide
- Autores: Victoria Valls Comamala
- Directores de la Tesis: Francisco José Muñoz López (dir. tes.)
- Lectura: En la Universitat Pompeu Fabra ( España ) en 2018
- Idioma: español
- Tribunal Calificador de la Tesis: Andrés Ozaita Mintegui (presid.), Xavier Altafaj (secret.), Aurelio Vázquez de la Torre Cervera (voc.)
- Programa de doctorado: Programa de Doctorado en Biomedicina por la Universidad Pompeu Fabra
- Materias:
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- Resumen
Aging is the main challenge that humanity will face on the near future. Brain aging is associated with cognitive deficiencies and is the main risk factor for Alzheimer’s Disease (AD). AD is the most common neurodegenerative disease leading to dementia caused by the aggregation of amyloid-β peptide (Aβ). In this thesis, we have shown that neuronal aging leads to alteration in the ganglioside membrane content. Specifically, increased levels of GM1 ganglioside in membrane leads to a decrease in the calcium entry through NMDA receptors and a reduction of dendritic spines. Overall, pointing a role in the alterations in learning and memory associated to aging. On the other hand, we have showed the inhibitory effect of the human gamma immunoglobulins (IgG) in Aβ aggregation through the antigen-binding fragment (Fab), which binds to Aβ blocking fibrillation progression.
