Background And Aim: There have been few studies from South Asia which have shown increased prevalence of cognitive impairment (CI) in diabetes. CI may further hamper self-care and independent living. The present study was designed to evaluate the impairment in cognition and self-care among patients with type 2 diabetes.
Materials And Methods: We assessed cognitive function in 54 type 2 diabetes participants and compared them with 54 healthy controls, using Addenbrooke's Cognitive Examination-III (ACE-III) test. Assessment of self-care was done by using Katz index of independence in activities of daily living and revised Summary of Diabetes Self-Care Activities (SDSCA) measures.
Results: The mean age and HbA1c of cases was 64.5 ± 5.3 years and 8.8 ± 2.5%, respectively. Cognitive impairment was more prevalent among type 2 diabetes participants (Odds ratio 31.3, CI: 10-100, P < 0.0001) with mean Addenbrooke's score of 74.9 ± 11.2 compared to 86.9 ± 5.3 in controls (t-statistic = 7.09, 95% CI: 8.6 to 15.3, P < 0.0001). The adjusted Odds ratio for CI was 9.46 after adjustment for hypertension. All the sub-domains of cognition were affected. The burden of CI was more among females and in those with poor glycemic control (HbA1C > 7.5%) when compared to controls. The diabetic participants with CI had poor SDSCA scores compared to those with no CI.
Conclusion: Diabetes may cause CI and is related to poor self-care. Considering a high prevalence of CI in diabetes, cognitive assessment should be a part of overall evaluation. ACE-III is a sensitive and convenient tool for this purpose.
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http://dx.doi.org/10.1016/j.dsx.2021.05.020 | DOI Listing |
Geroscience
January 2025
Dept. of Bioinformatics, Semmelweis University, 1094, Budapest, Hungary.
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Pharmacy Department, Baotou Central Hospital, Baotou, 014040, Inner Mongolia, China.
Microglial polarization and ferroptosis are important pathological features in Alzheimer's disease (AD). Ghrelin, a brain-gut hormone, has potential neuroprotective effects in AD. This study aimed to explore the potential mechanisms by which ghrelin regulates the progression of AD, as well as the crosstalk between microglial polarization and ferroptosis.
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