Patients with type 2 diabetes and low amyloid-β ratios faced a higher risk of progressing to mild cognitive impairment, according to a recent study.
In the cohort study, published in JAMA Network Open, investigators identified notable risk factors associated with accelerated brain atrophy and progression from normal cognition to mild cognitive impairment (MCI) over a 20-year mean follow-up. The longitudinal analysis followed 185 patients with normal cognition, examining baseline structural magnetic resonance imaging (MRI) and cerebrospinal fluid (CSF) biomarker data associated with Alzheimer's disease pathology.
The investigators demonstrated that type 2 diabetes (T2D) and low amyloid-β (Aβ42:Aβ40) ratios in CSF were independently associated with increased rates of brain atrophy and a heightened risk of progression to MCI. Specifically, patients with type 2 diabetes (T2D) had a 41% increased risk of MCI (hazard ratio [HR] = 1.41, 95% confidence interval [CI] = 1.06–1.76, P = .04), while a low Aβ42:Aβ40 ratio yielded an HR of 1.48 (95% CI = 1.09–1.88, P = .04). The patients with both T2D and low Aβ42:Aβ40 ratios exhibited a combined HR of 1.55 (95% CI = 1.13–1.98, P = .03), suggesting a synergistic association between these factors.
Accelerated atrophy in white matter and ventricular enlargement were also associated with MCI progression, with HRs of 1.86 (95% CI = 1.24–2.49, P = .001) for white matter atrophy and 1.71 (95% CI = 1.19–2.24, P = .009) for ventricular expansion. These structural changes were associated with T2D and amyloid pathology in neurodegeneration, suggesting their potential as biomarkers for identifying patients at higher risk for MCI.
This investigators emphasized that managing modifiable factors, such as diabetes, could be relevant in reducing cognitive decline risk. The findings suggested that early identification of patients with accelerated brain atrophy and combined T2D and amyloid pathology could inform preventive strategies against MCI.
Full disclosures can be found in the published study.
