Serum seladin-1 levels in diabetes mellitus and Alzheimer's disease patients
| Autor: | Kürşad Öneç, Merve Alpay, Yildiz Degirmenci, Attila Önmez, I. Ethem Şahin, Serkan Torun |
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| Přispěvatelé: | [Belirlenecek] |
| Rok vydání: | 2020 |
| Předmět: |
Risk
System Male medicine.medical_specialty Oxidoreductases Acting on CH-CH Group Donors Neurology medicine.medical_treatment DHCR24 Expression Nerve Tissue Proteins Disease Gene Gastroenterology Pathogenesis Diabetes Complications 03 medical and health sciences 0302 clinical medicine Downregulation and upregulation Alzheimer Disease Internal medicine Diabetes mellitus medicine Diabetes Mellitus Insulin Humans 030212 general & internal medicine Aged Aged 80 and over business.industry Significant difference General Medicine Alzheimer's disease medicine.disease Seladin-1 Postprandial Cholesterol synthesis Dementia Female Neurology (clinical) business 030217 neurology & neurosurgery Biomarkers |
| Zdroj: | Acta neurologica Belgica. 120(6) |
| ISSN: | 2240-2993 |
| Popis: | Background Diabetes mellitus (DM) has been shown to increase the risk of Alzheimer's disease (AD). Downregulation of selective Alzheimer's disease indicator-1 (seladin-1) occurs in the cerebral regions affected by AD. However, inconsistent results have been reported for the relationship between seladin-1 levels and AD. The effect of DM on serum seladin-1 levels in AD is unknown. The present study is aimed to investigate serum seladin-1 levels in diabetic and non-diabetic patients with AD. Methods Forty-six patients with AD and 25 healthy volunteers over 65 years of age were included in this study. The patients were divided into three groups-those with AD only, those with DM and AD, and control groups. Demographic characteristics and serum seladin-1 levels were compared among the groups. Results There was no statistically significant difference in seladin-1 levels in the AD only group compared to the control group (p = 0.376). However, seladin-1 levels were significantly lower in the DM and AD group compared to the AD only and control groups (p = 0.002, p = 0.001; respectively). Negative correlations were present between seladin-1 and fasting glucose, postprandial glucose, HbA1c, and insulin (p < 0.05; all). Conclusion Decreased serum seladin-1 values in the presence of DM and inverse correlations with diabetic parameters in patients with AD, together with a non-significant difference from the control group, suggests that seladin-1 may be altered only in the presence of DM in patients with AD. Lower serum seladin-1 levels may also play a role in the pathogenesis of AD in patients with DM. WOS:000538345300002 2-s2.0-85085994149 PubMed: 32506354 |
| Databáze: | OpenAIRE |
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