Overview

• The high-fat, Western-style feeding made hippocampal CCK interneurons hyperactive within four days, impairing short-term memory.
• The effect preceded measurable weight gain or diabetes, indicating a rapid, obesity‑independent impact on brain function.
• Restoring brain glucose or applying intermittent fasting normalized the neurons and reversed the memory deficits in the mice.
• Researchers identified PKM2 as a key metabolic mediator of the interneuron overactivity under low-glucose conditions.
• The mouse findings, published in Neuron, prompt plans to test translation to humans and to probe links to dementia risk.