3 Minutes
Background: Diet, brain circuits and memory
New laboratory research shows that a short exposure to a high-fat, junk-food–style diet can rapidly change neural activity in the hippocampus, the brain region responsible for forming and retrieving memories. In this study, mice were given a diet designed to mimic the saturated-fat content and palatability of processed junk food, then tested on behavioral and memory tasks. The experiments focused on a population of inhibitory neurons known as CCK (cholecystokinin-expressing) interneurons, which help regulate hippocampal network rhythms that underlie memory encoding.
Experiment details and key discoveries
Remarkably, researchers detected abnormal CCK interneuron activity after only four days on the high-fat regimen—well before any measurable weight gain or metabolic disease such as diabetes. This rapid change implies that dietary fats can alter brain function almost immediately. The altered firing of these glucose-sensitive interneurons disrupted hippocampal rhythms linked to memory performance, and the mice showed corresponding deficits on memory tasks.
Interventions restore brain function
The study also tested whether changing brain energy availability could reverse these effects. Restoring brain glucose levels reduced the excessive activity of CCK interneurons and rescued memory impairments in the mice. Comparable improvements followed nonpharmacological measures: intermittent fasting periods after the high-fat exposure were sufficient to normalize interneuron activity and improve behavioral performance. Researchers propose that targeted dietary changes or pharmacological interventions that stabilize brain glucose may help preserve hippocampal function in contexts of obesity-related neurodegeneration.
As lead author Song noted, "This work highlights how what we eat can rapidly affect brain health and how early interventions, whether through fasting or medicine, could protect memory and lower the risk of long-term cognitive problems linked to obesity and metabolic disorders."
Implications and future directions
The findings underscore the sensitivity of memory circuits to nutritional status and raise concerns that diets high in saturated fat could increase long-term risk for neurodegenerative diseases such as dementia and Alzheimer’s disease. Ongoing work aims to map exactly how glucose-sensitive interneurons alter hippocampal network rhythms and to test whether the interventions identified in mice can be translated safely to humans. Researchers will also evaluate lifestyle strategies—dietary patterns that reduce saturated fat intake or stabilize cerebral glucose—as potential population-level measures to protect cognitive health.
Conclusion
Short-term consumption of high-fat, junk-food–style diets can quickly dysregulate CCK interneurons in the hippocampus and impair memory in mice. Restoring brain glucose or using intermittent fasting can normalize neuronal activity and recover memory function, suggesting practical avenues for preventing obesity-related cognitive decline. Further translational research is needed to determine whether these mechanisms contribute to human Alzheimer’s risk and which interventions are most effective.
Source: scitechdaily
Comments