A new study published in the journal Neuron reveals that high-fat, junk food diets can disrupt brain function in just a matter of days. The research shows that fatty diets impair memory by rewiring a specific group of brain cells in the hippocampus, the brain's memory hub.
In the study, mice were fed a high-fat diet that mimics typical Western-style junk food, including items rich in saturated fats like cheeseburgers and fries. Just four days into the diet, the researchers observed a marked disruption in the normal function of CCK interneurons.
"We knew that diet and metabolism could affect brain health, but we didn't expect to find such a specific and vulnerable group of brain cells, CCK interneurons in the hippocampus, that were directly disrupted by short-term high-fat diet exposure," said UNC School of Medicine's Juan Song, PhD, principal investigator, professor of pharmacology, who is a member of the UNC Neuroscience Center. "What surprised us most was how quickly these cells changed their activity in response to reduced glucose availability, and how this shift alone was enough to impair memory."
Importantly, the study also demonstrated that restoring glucose levels in the brain could reverse the damage. Interventions such as intermittent fasting or pharmacological treatment helped normalize neuron activity and improve memory in mice. This suggests that even after dietary damage, brain function may be recoverable with timely intervention.
With ongoing research now exploring connections to Alzheimer’s and other neurodegenerative conditions, this study emphasizes the critical role of diet in brain health and the potential of early lifestyle changes to reduce cognitive decline.
Reference: Taylor Landry, Laura Perrault, David Melville, Zhe Chen, Ya-Dong Li, Ping Dong, W. Todd Farmer, Brent Asrican, Hannah Lee, Libo Zhang, Ryan N. Sheehy, Corina Damian, Thomas Collins, Nehemiah Stewart, E.S. Anton, Juan Song. Targeting glucose-inhibited hippocampal CCK interneurons prevents cognitive impairment in diet-induced obesity. Neuron, 2025; DOI: 10.1016/j.neuron.2025.08.016
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