Diogo Trigo, PhD, is a dedicated neuroscientist whose work has significantly advanced the field of neurology. He earned his PhD in Neurology from the prestigious University College London, where he laid the foundation for his future research endeavors. Currently, Dr. Trigo serves as an Assistant Researcher at the Universidade de Aveiro in Portugal, specifically within the Neuroscience and Signalling Group at the Institute of Biomedicine (iBiMED) in the Medical Sciences Department.

His research is at the forefront of promoting neuroregeneration, particularly in the context of injury and aging-associated diseases. Dr. Trigo's work explores the critical role of mitochondria homeostasis and retinoid signaling in neural health. Additionally, he is pioneering the use of therapeutic nanomaterials to develop innovative treatments for neurodegenerative conditions. Through his commitment to understanding and improving neural function, Dr. Trigo continues to make a lasting impact on the field of neuroscience.

Title : Metabolism, energy, and oxidative stress: mitochondria in Alzheimer's disease.

Alzheimer’s Disease (AD) is a neurodegenerative disorder characterized by amyloid deposits and mitochondrial dysfunction. Understanding the molecular mechanisms underlying these processes is crucial for developing effective therapies. Retinoid signalling is a potential therapeutic avenue for AD, targeting amyloid precursor protein (APP) towards non-amyloidogenic processing and the restoring of impaired mitochondrial function. Pharmacological modulation of Retinoic Acid Receptor (RAR) mediates APP β-cleavage, via alterations in secretase protein levels and phosphorylation-mediated modifications of protein activity.

In parallel, retinoid signalling reverses Aβ and oxidative stress-induced mitochondrial dysfunction, highlighting a multifaceted impact on cellular processes implicated in AD pathology, suggesting a promising therapeutic strategy. However, further research is warranted to fully elucidate the therapeutic potential of retinoid signalling in AD. This work was supported by multiple funding sources, including FCT EXPL/BTM-SAL/0902/2021, 2020.02006.CEECIND, 2022.12945.BD, and La Caixa Foundation CI21-00276.