Short-term high-fat diet consumption impairs synaptic plasticity in the aged hippocampus via IL-1 signaling

More Americans are consuming diets higher in saturated fats and refined sugars than ever before. These trends could have serious consequences for the older population because high-fat diet (HFD) consumption, known to induce neuroinflammation, has been shown to accelerate and aggravate memory declines. We have previously demonstrated that short-term HFD consumption, which does not evoke obesity-related comorbidities, produced profound impairments to hippocampal-dependent memory in aged rats. These impairments were precipitated by increases in proinflammatory cytokines, primarily interleukin-1 beta (IL-1 & beta;). Here, we explored the extent to which short-term HFD consumption disrupts hippocampal synaptic plasticity, as measured by long-term potentiation (LTP), in young adult and aged rats. We demonstrated that (1) HFD disrupted late-phase LTP in the hippocampus of aged, but not young adult rats, (2) HFD did not disrupt early-phase LTP, and (3) blockade of the IL-1 receptor rescued L-LTP in aged HFD-fed rats. These findings suggest that hippocampal memory impairments in aged rats following HFD consumption occur through the deterioration of synaptic plasticity and that IL-1 & beta; is a critical driver of that deterioration.

Automated summary

More Americans are consuming high-fat diets, which can accelerate and aggravate memory decline, particularly in the elderly. In a study with rats, it was found that short-term high-fat diet consumption disrupted hippocampal synaptic plasticity in aged rats, leading to memory impairments. The increase in proinflammatory cytokines, specifically interleukin-1 beta, was identified as a critical factor in the deterioration of synaptic plasticity.