Multisensory impairment is increasingly recognized as a contributor to cognitive decline in type T2DM. A study published in Diabetes, Obesity and Metabolism examined how sensory dysfunction across visual, somatosensory, and olfactory systems relates to cognitive performance, with emphasis on the specific role of olfactory impairment.

Resting-state functional magnetic resonance imaging (fMRI) was conducted in 152 adults with T2DM and 50 non-diabetic controls. Seed-based functional connectivity analyses from primary sensory cortices were used to quantify neural alterations. A Multisensory Dysfunction Index (MSDI) captured integrated sensory impairment. Cognitive function was assessed using the Montreal Cognitive Assessment (MoCA), and moderated mediation analyses evaluated the indirect contribution of olfactory dysfunction, stratified by DPN status.

Higher MSDI scores were associated with greater sensory complication burden and lower global cognition (MoCA mean 21.8 ± 3.9 in high MSDI vs 26.4 ± 2.8 in low MSDI; p < 0.001). Mediation analysis showed that olfactory dysfunction significantly mediated the MSDI–MoCA relationship in individuals without DPN (indirect effect β = –0.38; 95% CI –0.65 to –0.15; p = 0.002), but not in those with DPN (β = –0.12; 95% CI –0.39 to 0.14; p = 0.35). Direct effects of olfactory impairment on cognition were also observed in DPN-negative participants (β = –0.41; 95% CI –0.69 to –0.14; p = 0.001).

These findings indicate that olfactory dysfunction is a key pathway linking multisensory impairment to cognitive decline in T2DM, particularly in individuals without diabetic peripheral neuropathy. Preservation of sensory network integrity may hold relevance for cognitive health and personalized management strategies in T2DM.