- In Alzheimer’s disease, the brain gradually loses its ability to turn glucose into energy.
- Florey researchers have identified a protein structure that may be contributing to a blockage that is potentially causing an energy failure in the brain.
- Dr Francesca Alves has received a CASS Foundation grant to study how this protein structure may affect brain function and its role in Alzheimer’s disease.
One of the earliest and most consistent changes in people with Alzheimer’s disease is evidence of brain regions that are slowly being starved of glucose, the brain’s main source of fuel.
What causes this energy failure in Alzheimer’s disease, the most common form of dementia, and what part it plays in the progression of the disease remains unclear.
Dementia researcher Dr Francesca Alves is leading research at The Florey Institute of Neuroscience and Mental Health in this emerging field of study.
She has been awarded the 2026 CASS Foundation’s Daniel Rechtman Research Award to continuing building on her team’s novel preliminary findings.
“This grant will help my team to explore a new idea: that Alzheimer’s disease involves a blockage in how brain cells turn glucose into energy,” Dr Alves said.
“A simple way to think about this is to imagine a broken traffic light stuck on red at a major fuel-delivery intersection. As the fuel trucks build up, fewer trucks get through to deliver fuel where it is needed.
“We are seeing evidence of a similar traffic jam emerging in our preliminary Alzheimer’s disease data that is showing glucose-related molecules building up before a key control point, resulting in the molecules needed for energy production not getting through as efficiently.”
The CASS Foundation funding will allow the team to analyse brain tissue from Alzheimer’s disease and healthy patients to determine where in the brain this change occurs and which cell types are affected.
“Most current Alzheimer’s disease treatments focus on removing amyloid, one of the abnormal proteins that builds up in the brain, but do not directly target the brain’s energy issues,” Dr Alves said. “These treatments are an important advance, but their benefits are modest.”
“Understanding what’s causing the glucose-related energy deficit could pave the way for new treatments for Alzheimer’s disease, one of the greatest health challenges facing our ageing population.
“If successful, the results will provide the foundation for larger national funding applications to investigate whether restoring glucose flow and protecting brain energy production can slow neurodegeneration in Alzheimer’s disease.”
