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Neurological Research
A Journal of Progress in Neurosurgery, Neurology and Neurosciences
Volume 39, 2017 - Issue 7
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Original Research Paper

Linking senile dementia to type 2 diabetes: role of oxidative stress markers, C-reactive protein and tumor necrosis factor-α

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Pages 587-595 | Received 21 Sep 2016, Accepted 23 Mar 2017, Published online: 09 Apr 2017
 

Abstract

Diabetes is considered an independent risk factor for cognitive impairments.

Objectives: The aim of this study was to evaluate the cognitive disorder of elderly outpatients with and without type 2 diabetes (T2DM) in releationto oxidative stress markers and some inflammatory markers

Methodology: Two hundred and twelve participants were classified into four groups according to their fasting blood glucose level, glycosylated hemoglobin (HbA1c) and mini-mental state examination (MMSE) score. Control subjects were 118 subjects, diabetic group without dementia was 54 subjects, diabetic group with dementia was 26 subjects and 14 subjects of dementia without diabetes. Body mass index and waist/hip ratio were measured. Blood glucose, HbA1c, plasma malondialdehyde (MDA), total antioxidant activity (TAC), and some inflammatory markers: C-reactive protein (CRP) and tumor necrosis factor-α (TNF-α) were measured.

Results: Diabetic patients have significant increases in FBG, HbA1c, MDA with a significant decrease in TAC compared to control group. In all groups of patients, the levels of CRP, and TNF-α were significantly higher as compared to control group. The highest level of inflammatory markers was detected in diabetic group with dementia. MMSE score was negatively correlated with HbA1c levels and TNF-α and HbA1c levels were positively correlated with all inflammatory markers. In multivariate logistic regression analysis, MDA,CRP, Hb1c, TNF-a, and FBG were the most predictive risk factors for dementia

Conclusions: These results suggest that a decrease in anti-oxidant levels and an increase in anti-inflammatory and oxidative stress markers might be involved in the pathophysiology of cognitive disorder associated with T2DM.

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