Alzheimer’s disease (AD) is characterized neuropathologically by senile plaques and neurofibrillary tangles (NFTs). Amyloid-β (Aβ) is the major component of senile plaques, while tau protein is the primary component of NFTs [1]. Recent research indicates that both Aβ and tau play crucial roles in the pathology of AD and have been highly conserved throughout evolution, suggesting they may have important physiological functions [2].
A study published in Molecular Psychiatry by Capilla-López et al. (2025) generated a transgenic mouse model exhibiting both tau and Aβ accumulation. This model allowed researchers to analyse the individual and combined effects of these proteins on brain circuits. The findings suggest that tau affects memory-related areas, while Aβ influences emotional centers [3].The study’s lead researcher,Carles Saura,noted that existing therapies targeting only one of these toxic proteins have not achieved clear clinical benefits. The research suggests that a therapeutic approach addressing multiple disease mechanisms, such as phosphorylated tau and Aβ, could be more effective. while further research is needed to confirm its applicability to humans, this study represents a significant step toward new investigative pathways for Alzheimer’s treatment [4].
References:
[1] Amyloid-β and Tau at the Crossroads of Alzheimer’s Disease
[2] The physiological roles of tau and Aβ: implications for Alzheimer’s …
[3] The two proteins involved in Alzheimer’s disease affect brain circuits …
[4] Capilla-López, M. D., et al. (2025). synaptic vulnerability to amyloid-β and tau pathologies differentially disrupts emotional and memory neural circuits. Molecular Psychiatry.
Expert Insights on Exploring New Pathways for Alzheimer’s Disease Treatment
Editor: Dr. Saura, your research underscores the limitations of current therapies targeting only one specific protein. Could you elaborate on why you think combining treatments might be more effective?
Carles Saura: therapies that focus solely on one protein, either amyloid-beta (Aβ) or phosphorylated tau, have not yielded substantial clinical benefits. This is as Alzheimer’s disease is a multifactorial condition. Treating multiple disease mechanisms simultaneously could prove more effective. For instance, addressing both tau and Aβ pathologies can mitigate their synergistic detrimental effects on neural circuits.
Editor: what motivated your latest study on the vulnerability of synapses to Aβ and tau pathologies?
Carles Saura: Our research aims to understand how these two primary proteins in Alzheimer’s disease disrupt cognitive function. Synaptic susceptibility to both Aβ and tau pathologies has a differential impact on memory and emotional circuits in the brain.By mapping these vulnerabilities, we hope to develop more targeted and effective treatment strategies.
Editor: Could you share some preliminary results from your recent study that suggests a combined approach might be beneficial?
Carles saura: Preliminary findings show that synapses are disproportionately affected by both amyloid-beta and tau pathologies. The interplay between these proteins disables key neural circuits vital for memory and emotional regulation. Our study in Molecular Psychiatry suggests that multi-mechanism therapeutic interventions addressing both proteins could offer a more holistic approach to treating Alzheimer’s.
conclusion: Dr. Carles Saura’s research maps out the complex interactions between amyloid-beta and tau proteins in Alzheimer’s disease, highlighting the importance of multi-faceted treatment approaches. as these pathways are further understood, promising new therapies may emerge, offering hope for more effective management of cognitive decline in Alzheimer’s patients..”
