Cerebral glucose hypometabolism — the brain's progressive inability to efficiently metabolize its primary fuel — precedes clinical Alzheimer's symptoms by decades. Across 32 human trials (2014–2024) involving adults ≥60 with normal cognition through early AD, several nutritional strategies demonstrated measurable cognitive effects: omega-3 supplementation (≥1g/day DHA, ≥6 months) benefited MCI populations; MCT/ketogenic diets improved cognition proportional to plasma ketone elevation in MCI and early AD; anserine/carnosine dipeptides enhanced verbal memory and executive function, especially in APOE4 carriers over 70; and L-arginine improved global cognition in frail hypertensive older adults.
The framing here is genuinely important. Rather than treating nutrition as broadly neuroprotective, this review positions specific nutrients as metabolic bypass agents — supplying ketones, supporting mitochondrial efficiency, or modulating neurotransmitter precursors when glucose transport falters. The APOE4-carnosine signal is particularly worth watching; genotype-stratified responses suggest precision nutrition may outperform one-size-fits-all approaches.
That said, this is a scoping review — not a meta-analysis — meaning effect sizes are not pooled, and the underlying trials are small, short, and heterogeneous. The consistent pattern of benefits appearing only in early disease stages underscores a critical window that the field must urgently define. For healthy aging adults, the evidence remains suggestive rather than prescriptive, but the mechanistic rationale is sound enough to justify prioritizing longer, biomarker-anchored trials. Incremental, but strategically directional.
