Professor Maite Solas, a researcher at the Faculty of Pharmacy of the University of Navarra, has been awarded an ERC Consolidator Grant, one of Europe’s most prestigious research grants, to develop the HyperAstroMet project. The initiative aims to investigate whether an early failure in the brain’s use of glucose — specifically in cells known as astrocytes — could be one of the initial triggers of Alzheimer’s disease.
Beyond Amyloid and Tau Proteins
For decades, Alzheimer’s research has been dominated by the study of two proteins: beta-amyloid and tau, whose abnormal accumulation in the brain is associated with neurodegeneration. However, therapeutic advances based on this approach have been limited, prompting the scientific community to explore new hypotheses.
HyperAstroMet does not reject the role of these proteins, but instead proposes that before their effects become detectable, there may already be a silent and difficult-to-identify problem: an energy imbalance in the brain. “What we propose is that, in the earliest stages of the disease, glucose use begins to fail,” explains Solas. This malfunction could occur even before neurons start to deteriorate.
An Early Failure Before Symptoms Appear
One of the most significant aspects of this research is that it places the origin of Alzheimer’s in a preclinical phase, when there are still no visible symptoms or obvious cognitive decline. “All of this could be happening even before neurons begin to die,” says Solas. Detecting these early alterations could pave the way for earlier diagnoses and preventive strategies capable of acting before the damage becomes irreversible.
The project also suggests that the excessive accumulation of proteins such as beta-amyloid and tau may send abnormal signals to astrocytes, increasing their energy demands and creating a vicious cycle that accelerates the disease.
New Therapeutic Pathways
This metabolic approach could have important clinical implications. Instead of focusing exclusively on eliminating protein deposits, future treatments could combine therapies aimed at improving brain energy metabolism with existing strategies. “Perhaps future treatments should be synergistic,” the researcher notes, combining vaccines or drugs targeting proteins with interventions designed to stabilize astrocyte metabolism and reduce brain inflammation.
If confirmed, this hypothesis could redefine Alzheimer’s not only as a disease of protein accumulation, but also as a disorder of the brain’s energy balance.
A Major Boost for Spanish Science
The ERC Consolidator Grant marks a turning point both for the project and for Solas’s scientific career. The grant, aimed at researchers with 7 to 12 years of postdoctoral experience, provides long-term funding and helps establish high-level research teams.
Thanks to this funding, the project will have financial support for five years, enabling the recruitment of additional researchers and allowing the team to work without the constant pressure of short-term funding — one of the major challenges facing science in Spain. “Long-term funding provides stability and allows researchers to truly focus on science,” says Solas.
The project strengthens the role of Spanish research in the search for new answers to Alzheimer’s disease — a complex condition that continues to pose enormous medical, social, and economic challenges worldwide, and for which every new advance represents a genuine source of hope.