INTRODUCTIONCognitive trajectories may clarify how type 2 diabetes (T2D) and impaired fasting glucose (IFG) relate to dementia risk, but longitudinal associations remain unclear, particularly in the c

The gap

Consensus across the literature

Supporting evidence — 3 representative gaps

• Threshold effects of insulin resistance on cognitive function in coronary heart disease: the non-linear diagnostic value of the triglyceride-glucose index (2026) · doi

  investigation A primary strength of this is the detailed assessment of the dose-response relationship between insulin resistance and cognitive status. By utilizing restricted cubic splines rather than treating cognitive impairment as a binary outcome, we identified a distinctive threshold-dependent association for severe impairment. Additionally, the application of hierarchical clustering allowed us to visualize a specific “metabolic-inflammatory” phenotype, offering mechanistic insight into how the TyG index captures residual risk beyond traditional hemodynamic factors. However, several methodological the cross-sectional design limitations warrant consideration: First, inherently precludes causal inference. While our findings suggest that metabolic dysregulation accelerates neurodegeneration, we cannot rule out reverse causality, where cognitive decline leads to poorer self-care and subsequent metabolic deterioration.

  Keywords: cognitive metabolic impairment investigation primary strength detailed assessment dose response relationship insulin resistance status utilizing
• Diabetes, impaired fasting glucose, and cognitive trajectories: a multi-cohort study (2026) · doi

  INTRODUCTIONCognitive trajectories may clarify how type 2 diabetes (T2D) and impaired fasting glucose (IFG) relate to dementia risk, but longitudinal associations remain unclear, particularly in the context of stroke.

  Keywords: introductioncognitive trajectories clarify type diabetes impaired fasting glucose relate dementia risk longitudinal associations remain unclear
• Astrocytic SCAP deletion ameliorates diabetes-associated cognitive impairment by suppressing microglial neuroinflammation and lipid droplet accumulation via the LCN2–24p3R–mTOR axis (2026) · doi

  Abstract Diabetes-associated cognitive impairment (DACI) is a prevalent and debilitating complication of type 2 diabetes, yet the mechanisms linking metabolic dysregulation to neuroinflammation and cognitive decline remain incompletely understood.

  Keywords: diabetes cognitive abstract associated impairment daci prevalent debilitating complication type mechanisms linking metabolic dysregulation neuroinflammation