A study from the University of California, Davis, highlights that a ketogenic diet significantly delays the onset of Alzheimer’ s-related memory loss in mice. This early stage of memory decline parallels the mild cognitive impairment seen in humans, which often leads to full-blown Alzheimer’s disease. These findings have been published in Communications Biology, a journal of the Nature Group.
The ketogenic diet, characterized by low carbohydrate, high fat, and moderate protein intake, shifts the body’s metabolism from glucose to fat-burning and ketone production for energy. Prior research by UC Davis revealed that mice on this diet lived 13% longer, indicating potential longevity benefits linked to dietary changes.
Building on earlier work, this study identified that the molecule beta-hydroxybutyrate (BHB) plays a crucial role in preventing early memory decline, with its levels increasing almost seven-fold on a ketogenic diet. Gino Cortopassi, a biochemist and pharmacologist at UC Davis School of Veterinary Medicine, noted, “The data support the idea that the ketogenic diet in general, and BHB specifically, delays mild cognitive impairment and it may delay full blown Alzheimer’s disease, though it clearly doesn’t eliminate the disease entirely.”
In their experiments, scientists administered BHB to mice in amounts equivalent to those experienced after seven months on a ketogenic diet. This led to significant improvements in the function of synapses—the vital structures that connect nerve cells in the brain. Better synaptic connections enhance memory function, which can alleviate the issues related to mild cognitive impairment, as pointed out by Izumi Maezawa, professor of pathology at the UC Davis School of Medicine.
Cortopassi also mentioned that BHB is available as a supplement, potentially supporting memory in mice, although its effects on human memory have yet to be demonstrated. The study also noted significant increases in biochemical pathways related to memory formation in mice following the ketogenic diet, with females showing higher BHB levels than males.
These observations suggest that if such results were to translate to humans, they could be especially significant for women, particularly those with the ApoE4 gene variant, who are at a higher risk for Alzheimer’s. This aspect of the research highlights the potential for gender-specific therapeutic strategies in combating cognitive decline.
More information: Jacopo Di Lucente et al, Ketogenic diet and BHB rescue the fall of long-term potentiation in an Alzheimer’s mouse model and stimulates synaptic plasticity pathway enzymes, Communications Biology. DOI: 10.1038/s42003-024-05860-z
Journal information: Communications Biology Provided by University of California, Davis
