Female mice showed enhanced long-term memory formation when exposed to acetate, driven by specific histone H2A.Z acetylation patterns and gene expression changes in the dorsal hippocampus. The metabolic compound triggered upregulation of learning-associated genes, but only during active memory consolidation and recall phases, not during passive exposure. This sex-specific finding adds crucial nuance to our understanding of how metabolic intermediates influence cognitive function through epigenetic mechanisms. The research bridges metabolic biochemistry with neuroscience, suggesting that simple organic compounds can directly modulate memory through chromatin remodeling rather than just serving as energy substrates. For women seeking cognitive enhancement, this points toward acetate supplementation as a potential memory aid, though the precise timing and context appear critical for effectiveness. The sex specificity raises important questions about whether current memory enhancement strategies adequately account for biological differences. While promising, the single-study nature and animal model limitations require human validation before clinical applications. This represents a potentially significant advance in precision approaches to cognitive enhancement.