Astrocytic GLUT1 & Glucose Uptake
How GLUT1 deficiency in astrocytes contributes to Alzheimer-like neurodegeneration, and whether this occurs independently of cerebrovascular alterations.
Our Science
Research
Understanding how Alzheimer's disease, astrocyte biology and brain metabolism interconnect to drive neurodegeneration.
Scientific Foundation
Brain metabolism is a multicellular enterprise
For too long, brain metabolism has been viewed through a neuron-centric lens where energy transformation and utilization are seen as primarily neuronal processes, and glia are cast in a passive, supportive role. This reductionist paradigm has constrained basic research, hindered translational progress, and created confusion in clinical research.
Over the past four decades, a mosaic of data has reshaped our understanding. Mechanistic studies have revealed that brain metabolism is, in fact, a multicellular enterprise — energetically and redox-wise — functionally integrated across cell types. From astrocytic lactate production and antioxidant export to oligodendrocytic metabolic support of neurons and axons, glial shuttles conserved from insects to mammals fuel neuronal activity and memory.
The SOLAS Lab sits at the centre of this emerging picture, connecting Alzheimer's disease, astrocyte biology and brain metabolism into one integrative research programme.
Focus Areas
What we investigate
Metabolic Reprogramming in Early AD
Astrocytes in early Alzheimer's stages may undergo hyperglycolic phases, accumulating glycogen abnormally and precipitating the metabolic cascade of the disease.
VEGF-Based Rescue Strategies
High-fat diets suppress GLUT1 in endothelial cells. VEGF compensates, and our group investigates whether this pathway can rescue cognition in AD mouse models.
Early Biomarkers of Astrocyte Dysfunction
Identifying metabolic changes in cerebrospinal fluid and blood that signal early astrocyte dysfunction — before symptom onset — as a diagnostic tool.
Multitarget Drug Discovery
Design and synthesis of multitarget compounds structurally inspired by sulfonylureas and pitolisant, combining H3R antagonism and acetylcholinesterase inhibition.
Insulin Resistance & Neurodegeneration
How brain insulin signalling failure contributes to energy dysfunction and accelerates Alzheimer's disease progression.