A research team from Universitat Autònoma de Barcelona (Inc-UAB) has discovered that the two basic pathological characteristics of Alzheimer’s-Tau’s proteins and the Beta-Hmmine-Amyloid Proteins are in distinct and homogeneous ways, particularly there. They are associated with memory and emotions. The study was conducted in collaboration with Centro de Investigación Biomédica en Red Enfermedades Neurodegenerativas (Ciberned) and Universidad Pablo De Olavide (UPO).
Published Molecular psychiatry (Nature Group), findings reveal that the accumulation of TAU in the hippocampus leads to memory deficits, while the accumulation of β-amyloid in the almonds causes emotional disorders such as anxiety and fear-as early symptoms of the disease. In addition, the combination of these two pathologies intensifies inflammation and brain dysfunction, enhancing their overall effect.
For decades, research on Alzheimer’s disease has been shaped by two theories: one that suggests that the disease comes from tau accumulation in the neurons and another that indicates beta-amyloid accumulation as a capital trigger. These perspectives have largely dictated the current therapeutic approaches, with treatments aimed at preventing the accumulation of either Tau or beta-amyloid in the hope of slowing down the progression of the disease. However, the research team led by researchers Carles Saura and Arnaldo Parra-Damas, from the Department of Biochemistry and Molecular Biology and Molecular Biology and Inc-UAB, argues that a double targeted therapeutic strategy for effective fight against of that disease.
This discovery was made possible by the development of a new model of transgenic mouse that reproduces both TAU and beta-amyloid pathologies.
Although both proteins accumulate in the brains of Alzheimer’s patients, most animal models used to study the disease usually focus on only one of these factors. “
Maria Dolores Capilla, researcher, chief author of the study
“In our research we have created a transgenic mouse model that presents both TAU accumulation and beta-amyloid, allowing us to analyze their individual and combined results,” adds the Inc-UAB researcher.
These findings could reform current treatment strategies, which often target only one of these toxic proteins. “Existing treatments have not achieved clear clinical benefits.
While further research is needed to confirm its possibility of being implemented in humans, this study represents an important step towards the new exploratory pathways to treat Alzheimer’s, the research team concludes.
Source:
Magazine report:
Capilla-López, MD, et al. (2025). Synaptic vulnerability to amyloid-B and Tau pathologies differentiates the emotional and nerve circuits. Molecular psychiatry. Doi.org/10.1038/S41380-025-02901-9.
