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Alzheimer’s disease, a neurodegenerative condition considered one of the most common causes of dementia in older adults, is theorized to be the result of an accumulation of amyloid-beta (Aβ) protein in the brain. In a new study, a team of researchers unveiled new evidence pointing to another theory: metabolic dysfunction.
According to a report, published in the journal eLife, researchers at Yale-NUS college in Singapore suggest that metabolic defects, occurring before any increase in amyloid-beta protein, could be a primary cause of Alzheimer’s disease.
In the study, researchers utilized Caenorhabditis elegans due to its resemblance to human cells at the molecular level. Upon administering metformin, a common treatment for type 2 diabetes, they found that the anti-diabetes drug significantly improved metabolic defects and strengthened the Caenorhabditis elegans’ lifespan.
“Treatment with an anti-diabetes drug, metformin, reversed Aβ-induced metabolic defects, reduced protein aggregation and normalized lifespan,” the findings indicated. “Our results point to metabolic dysfunction as an early and causative event in Aβ-induced pathology and a promising target for intervention.”
Jan Gruber, the study’s lead researcher, added: “Based on the emerging strong links between mitochondrial dysfunction and Alzheimer’s pathology, it might be better to adopt a preventative strategy by targeting metabolic defects, especially mitochondrial defects, directly and early, well before protein aggregates are even present.”
“Current trials of Alzheimer’s drugs targeting proteins have failed despite billions of dollars being invested.”