RT Conference Proceedings
T1 Late-life depression accelerates cognitive impairment and tau-associated pathology in an Alzheimer´s disease model.
A1 Vegas-Gómez, Laura
A1 Gutiérrez-Sastre, Cristina
A1 Arredondo-Alcalá, María Ángeles
A1 Gutiérrez-Pérez, Antonia
A1 Moreno-González, Inés
K1 Alzheimer, Enfermedad de
K1 Depresión en ancianos
AB Clinical studies suggest that depression could be considered an important risk factor for the future development of cognitive impairment and Alzheimer's disease (AD). In fact, there is a strong association between late-life depression and AD. The age of AD onset has been shown to be accelerated in patients with mild cognitive impairment (MCI) with a history of depression, and women appear to be particularly more vulnerable to this condition. In addition, individuals with MCI who present depressive symptoms have an elevated burden of amyloid-beta (Aβ), the main toxic protein associated with Alzheimer's pathology, and a higher risk of developing AD compared to non-depressed MCI patients. Although it has been described that some transgenic models of AD can develop signs similar to depression in advanced stages, the induction of Alzheimer's pathology due to a depressive process has not been studied under experimental conditions to emulate late-life depression as a risk factor for AD. In this study, we induced chronic unpredictable mild stress (CUMS) in P301S tau transgenic mice to determine whether depression is a cause, rather than a consequence, of the development of AD pathology. Our results suggest that transgenic tau mice subjected to CUMS seem to develop a depressive state. This animals display enhanced cognitive impairment compared to controls. In addition, histological studies show increased tau deposition, suggesting that late-life depression could worse AD progression by accelerating tau aggregation and worsening clinical signs. The findings generated in this project could provide evidence of depression as a risk factor for AD, providing new insights on molecular mechanisms involved in AD onset and progression.
YR 2023
FD 2023
LK https://hdl.handle.net/10630/27801
UL https://hdl.handle.net/10630/27801
LA eng
NO Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech.
DS RIUMA. Repositorio Institucional de la Universidad de Málaga
RD 30 ene 2026