Diabetes mellitus (DM) is one of the most devastating diseases that currently affects the aging population. Recent evidence indicates that DM is a risk factor for many brain disorders, due to its direct effects on cognition. New findings have shown that the microtubule‐associated protein tau is pathologically processed in DM; however, it remains unknown whether pathological tau modifications play a central role in the cognitive deficits associated with DM. To address this question, we used a gain‐of‐function and loss‐of‐function approach to modulate tau levels in type 1 diabetes (T1DM) and type 2 diabetes (T2DM) mouse models. Our study demonstrates that tau differentially contributes to cognitive and synaptic deficits induced by DM. On one hand, overexpressing wild‐type human tau further exacerbates cognitive and synaptic impairments induced by T1DM, as human tau mice treated under T1DM conditions show robust deficits in learning and memory processes. On the other hand, neither a reduction nor increase in tau levels affects cognition in T2DM mice. Together, these results shine new light onto the different molecular mechanisms that underlie the cognitive and synaptic impairments associated with T1DM and T2DM.

BackgroundPoor air quality increases the risk of developing chronic rhinosinusitis (CRS) and other airway diseases. However, there are limited data on air pollutants and CRS‐specific disease severity. We assessed the impact of air pollutants on sinonasal‐specific and general quality‐of‐life (QOL) measures in a multi‐institutional cohort of patients with CRS.MethodsParticipants with CRS were prospectively enrolled in a cross‐sectional study and self‐selected continued appropriate medical therapy or endoscopic sinus surgery (ESS). The 22‐item SinoNasal Outcome Test (SNOT‐22) and Medical Outcomes Study Questionnaire Short‐Form 6‐D (SF‐6D) health utility value scores were recorded. Patient exposure to air pollutants was determined using residence zip codes. Unadjusted group differences were compared and correlation coefficients were evaluated to identify the magnitude of bivariate association.Results486 patients were enrolled and followed for a mean of 6.9 [SD±2.3] months. Pollutant exposure did not significantly correlate with baseline SNOT‐22 or SF‐6D scores. Revision ESS was associated with higher median fine particulate matter (PM2.5; Δ = 0.12, (95% CI: 0.003, 0.234); p = 0.006) compared to primary surgery. PM2.5, PM10 and nitrogen dioxide concentrations (ug/m3) did not correlate with change in total SNOT‐22 or SF‐6D scores after treatment. Nevertheless, sulfur dioxide (SNOT‐22: ρ = ‐0.121 (95% CI: ‐0.210, ‐0.030); p = 0.007; SF‐6D: ρ = 0.095 (95% CI: 0.002, 0.186); p = 0.04) and carbon monoxide (SNOT‐22: ρ = ‐0.141 (95% CI: ‐0.230, 0.050); p = 0.002) exposure did correlate with these outcome measures.ConclusionAir pollutants may contribute, at least in part, to disease severity in CRS; future investigation is needed to further elucidate the nature of this relationship.This article is protected by copyright. All rights reserved