Mild cognitive impairment in newly diagnosed type 2 diabetes without microvascular or macrovascular complications: Prevalence, dynamics, and clinical predictors.
Mild cognitive impairment may occur early in type 2 diabetes mellitus, but data on its prevalence and longitudinal dynamics in newly diagnosed patients without overt vascular complications remain limited.
We prospectively followed 937 adults with newly diagnosed type 2 diabetes mellitus without baseline microvascular or macrovascular complications for a mean of 62.7±21.5 months. Cognitive status was assessed using the Montreal Cognitive Assessment, and mild cognitive impairment was defined as Montreal Cognitive Assessment-defined cognitive impairment. We evaluated the prevalence of mild cognitive impairment at diagnosis, the rate of mild cognitive impairment remission among patients with baseline mild cognitive impairment, and the incidence of mild cognitive impairment among cognitively normal patients. Multivariable models were used to identify clinical correlates of these outcomes.
At baseline, 286 patients (30.5%) had mild cognitive impairment. During the follow-up, 43/286 patients (15.0%) experienced remission, whereas 96/651 cognitively normal patients (14.7%) developed incident mild cognitive impairment. Higher C-peptide was strongly associated with prevalent mild cognitive impairment, and continuous C-peptide remained significantly associated with Montreal Cognitive Assessment performance in multivariable analyses. Smoking was associated with a less favorable cognitive profile, uric acid showed an inverse association with prevalent mild cognitive impairment, and participation in therapeutic patient education was independently associated with a lower risk of incident mild cognitive impairment. Incident retinopathy was also associated with incident mild cognitive impairment.
In newly diagnosed, complication-free type 2 diabetes mellitus, mild cognitive impairment defined by Montreal Cognitive Assessment is common and clinically dynamic. Our findings suggest that metabolic, behavioral, educational, and microvascular factors are associated with cognitive outcomes, but they should be interpreted as observational and hypothesis-generating rather than as evidence for immediate clinical risk stratification.
We prospectively followed 937 adults with newly diagnosed type 2 diabetes mellitus without baseline microvascular or macrovascular complications for a mean of 62.7±21.5 months. Cognitive status was assessed using the Montreal Cognitive Assessment, and mild cognitive impairment was defined as Montreal Cognitive Assessment-defined cognitive impairment. We evaluated the prevalence of mild cognitive impairment at diagnosis, the rate of mild cognitive impairment remission among patients with baseline mild cognitive impairment, and the incidence of mild cognitive impairment among cognitively normal patients. Multivariable models were used to identify clinical correlates of these outcomes.
At baseline, 286 patients (30.5%) had mild cognitive impairment. During the follow-up, 43/286 patients (15.0%) experienced remission, whereas 96/651 cognitively normal patients (14.7%) developed incident mild cognitive impairment. Higher C-peptide was strongly associated with prevalent mild cognitive impairment, and continuous C-peptide remained significantly associated with Montreal Cognitive Assessment performance in multivariable analyses. Smoking was associated with a less favorable cognitive profile, uric acid showed an inverse association with prevalent mild cognitive impairment, and participation in therapeutic patient education was independently associated with a lower risk of incident mild cognitive impairment. Incident retinopathy was also associated with incident mild cognitive impairment.
In newly diagnosed, complication-free type 2 diabetes mellitus, mild cognitive impairment defined by Montreal Cognitive Assessment is common and clinically dynamic. Our findings suggest that metabolic, behavioral, educational, and microvascular factors are associated with cognitive outcomes, but they should be interpreted as observational and hypothesis-generating rather than as evidence for immediate clinical risk stratification.
Authors
Coppola Coppola, Pujia Pujia, Castagna Castagna, Gallotti Gallotti, Falcone Falcone, Gazzaruso Gazzaruso
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