New Alzheimer’s Treatment Looks to Sugary Solution
A groundbreaking study at the Buck Institute for Research on Aging has revealed that sugar stored in brain cells may play a pivotal role in protecting against Alzheimer’s disease and other forms of cognitive decline.
The researchers from Novato, California, recently changed long-standing assumptions about glycogen – the stored form of glucose – in neurons. Traditionally thought to be insignificant in the brain, neuronal glycogen is now shown to affect tau protein accumulation, a key marker of Alzheimer’s.
The team discovered that when glycogen isn’t properly broken down, it binds with tau, disrupting sugar metabolism and weakening the brain’s ability to manage oxidative stress, a major driver of neurodegeneration.
By boosting the activity of glycogen phosphorylase (GlyP) – the enzyme responsible for breaking down glycogen – the team were able to reduce the toxic build-up in the brains of dementia patients. Notably, this process helps re-route sugar and enhance cellular defences.
The findings also shed light on why GLP-1 drugs, which are widely used for weight loss, may offer protection against dementia: the medication appears to mimic the benefits of dietary restriction, which naturally elevates GlyP activity.
“By discovering how neurons manage sugar, we may have unearthed a novel therapeutic strategy: one that targets the cell’s inner chemistry to fight age-related decline,” said senior author, Professor Pankaj Kapahi.
The study underscores the potential of metabolic interventions in slowing or even reversing the progression of Alzheimer’s, offering renewed hope for millions affected by neurodegenerative diseases.
