Mouse study reveals molecular link between high-fat diets and impaired brain function
The molecular mechanisms linking a high-calorie diet to cognitive impairment remain unclear. Researchers at the Institute of Science Tokyo, Japan, investigated this association in mice, finding that the diet reduced expression of the nuclear protein PQBP1, disrupting the alternative splicing of genes involved in synaptic function. This was associated with synaptic abnormalities and cognitive…
A recent study published in Molecular Psychiatry provides insight into the molecular connection between a high-fat diet and impaired brain function. Researchers at the Institute of Science Tokyo fed mice a calorie-rich diet and observed reduced levels of the protein PQBP1 in the cerebral cortex, a brain region essential for cognitive functions.
This decrease in PQBP1 was linked to changes in alternative RNA splicing, a process that generates different RNA transcripts from a single gene, potentially leading to variations in protein isoforms. By analyzing gene expression changes, the team found that lower PQBP1 levels disrupted the splicing of genes involved in synaptic function, ultimately resulting in synaptic abnormalities and cognitive impairment in the mice.
Treatment with pioglitazone, a diabetes medication that activates the PPARγ pathway, and gene therapy to restore PQBP1 levels, partially reversed the detrimental effects of the high-fat diet on synaptic and cognitive functions. The study highlights PQBP1-dependent alternative RNA splicing as a potential therapeutic target for countering diet-associated cognitive impairment, offering a promising avenue for developing new interventions.
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