Published on: Feb 03, 2026
Researchers have identified both key drivers of neuronal aging and molecules that help preserve nervous system health in later life using the nematode Caenorhabditis elegans as a model. Although its nervous system consists of only 302 neurons—far fewer than the roughly 90 billion in the human brain C. elegans neurons perform comparable functions, making it an ideal system to study brain aging. Because all neural connections are mapped, scientists can track the aging of individual neurons across the organism’s entire lifespan.
Professor Dr. Björn Schumacher of the CECAD Cluster of Excellence for Aging Research and bioinformatician Dr. David Meyer developed a precise aging clock that determines the biological age of each neuron based on gene expression changes. Their study, “Aging clocks delineate neuron types vulnerable or resilient to neurodegeneration and identify neuroprotective interventions,” published in Nature Aging, revealed striking differences in neuronal aging even in young animals. Some neurons appeared biologically older than the organism itself.
Further work by neuroscientist Dr. Christian Gallrein showed that these prematurely aged neurons rapidly underwent degeneration, with nerve processes breaking down in a short time. The team identified heightened protein production as a major molecular driver of neuronal aging: neurons with especially active protein biosynthesis aged faster. Importantly, pharmacological inhibition of this process helped preserve these vulnerable neurons.
Because neuronal aging in C. elegans mirrors key aspects of human brain aging, the researchers applied an AI-driven, machine-learning approach to classify compounds based on their effects on neuronal aging. This strategy identified neuroprotective molecules, including syringic acid a natural compound found in blueberries and blue grapes and the dopamine reuptake inhibitor vanoxerin. In contrast, substances such as the serotonin 5-HT1A receptor antagonist WAY-100635 and resveratrol were found to accelerate neuronal aging and promote neurodegeneration.
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