MIND Pattern Nutritional Intervention Modulates Mediterranean Diet Adherence and Gut Microbiota in Alzheimer’s Disease: An Observational Case–Control Study

Abstract

Background: Evidence on non-restrictive MIND pattern interventions in Alzheimer’s (ALZ) disease remains limited. Methods: In an observational case–control study, 60 participants (ALZ, n = 30; cognitively healthy controls, n = 30) completed baseline (T0) and follow-up (T1) after structured MIND counseling. Adherence was assessed via the MEDAS questionnaire. Stool samples (16S rRNA profiling) were taken and anthropometry and cognitive/functional measures were recorded at T0/T1. Results: In the ALZ group, MEDAS improved as adherence to the Mediterranean diet increased (increasing the use of vegetables ≥ 2/day, p < 0.01; and lowering butter adoption ≤ 1/day, p = 0.02), with a shift from low to moderate/high adherence; in controls, baseline Mediterranean diet adherence was already high, and changes in MEDAS categories were modest (low adherence from 13.8% to 3.6%, high adherence from 37.9% to 50.0%), with no statistically significant overall change (p = 0.39). Regarding gut microbiota (GM), in the ALZ group, alpha diversity increased significantly and Bray–Curtis PCoA separated T0 from T1. Species-level analysis showed increases in SCFA-linked taxa (e.g., Anaerobutyricum hallii, Blautia luti, Eubacterium coprostanoligenes) and reductions in dysbiosis/mucin-degrading taxa (e.g., Mediterraneibacter torques, M. gnavus, Agathobacter rectalis). Between-group Δ(T1 − T0) comparisons at the genus level indicated larger positive shifts in ALZ for Anaerobutyricum, Oscillibacter, Faecalicatena, Romboutsia, Mediterraneibacter, and Blautia, and more negative Δ for Gemmiger, Subdoligranulum, Bifidobacterium, Clostridium, and Collinsella. sPLS-DA showed partial separation (first two components ≈ 9% variance). Conclusions: A structured, non-restrictive MIND intervention was feasible, improved dietary adherence, and accompanied higher diversity and compositional remodeling of the GM in ALZ’s disease. Larger randomized mechanistic studies are warranted.