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Inflammatory hypothesis as a link between Alzheimer's disease and diabetes mellitus
Melda Bozluolcay1, Gülnur Andican2, Sinem Fırtına3
1Department of Neurology, Istanbul University Cerrahpasa Medical Faculty, Istanbul, Turkey.
Aims:
The aim of the present study was to evaluate whether there was an inflammation-mediated link between Alzheimer's disease (AD) and type 2 diabetes mellitus (DM) status.
Methods:
An age-matched control group and patient groups designated as AD without treatment (AD); AD under cholinesterase inhibitors (AD-CEI); DM without treatment (DM); DM under oral antidiabetic agents (DM-OAD); AD under treatment, who had newly diagnosed DM (AD-CEI+DM); and DM under treatment, who had newly diagnosed probable AD (DM-OAD+AD) were studied. Serum inflammation status was evaluated by the determination of serum C-reactive protein (CRP), tumor necrosis factor-alpha, interleukin (IL)-1β and IL-6 levels. CRP levels were determined by an immunonephelometric method. The others were assayed by enzyme-linked immunosorbent assay methods.
Results:
IL-1β levels were found to be significantly lower in the DM group than in the control group (P < 0.01). The AD group had significantly higher serum IL-1β levels than the DM group (P < 0.01). IL-6 levels were significantly higher in the AD and DM groups than in controls (P < 0.01 and P < 0.01). Serum tumor necrosis factor-alpha and CRP levels in the AD (P < 0.05 and P < 0.001, respectively) and DM groups (P < 0.05 and P < 0.001, respectively) were significantly higher when compared with the controls. The presence of AD or DM or therapies of the diseases did not significantly change in serum tumor necrosis factor-alpha levels. The AD-CEI + DM and DM-OAD+AD groups had significantly higher CRP levels than the AD-CEI group (P < 0.05) and DM-OAD groups (P < 0.001), respectively. Serum CRP levels showed a positive correlation with Mini-Mental State Examination scores (r = 0.339, P < 0.01).
Conclusion:
Our findings support the presence of a low-grade systemic inflammation link between AD and DM. Geriatr Gerontol Int 2016; 16: 1161-1166.
Insights
This study reveals a low-grade systemic inflammation link between Alzheimer's disease (AD) and type 2 diabetes mellitus (DM). Elevated inflammatory markers like IL-6 and CRP were observed in both AD and DM patients, suggesting a shared inflammatory pathway.
Area of Science:
- Biomedical Science
- Neuroscience
- Endocrinology
Background:
- Alzheimer's disease (AD) and type 2 diabetes mellitus (DM) are prevalent chronic conditions.
- Both AD and DM have been independently associated with inflammatory processes.
- A potential shared inflammatory pathway between AD and DM requires further investigation.
Purpose of the Study:
- To investigate the potential inflammation-mediated link between Alzheimer's disease (AD) and type 2 diabetes mellitus (DM).
- To compare serum inflammatory marker levels in patients with AD, DM, and comorbid conditions against a control group.
Main Methods:
- Serum levels of C-reactive protein (CRP), tumor necrosis factor-alpha, interleukin (IL)-1β, and IL-6 were measured.
- Participants included an age-matched control group and various patient cohorts: AD (treated and untreated), DM (treated and untreated), and combined AD-DM groups.
- Inflammatory markers were quantified using immunonephelometric and enzyme-linked immunosorbent assay (ELISA) methods.
Main Results:
- Interleukin-6 (IL-6) levels were significantly elevated in both AD and DM groups compared to controls.
- Serum C-reactive protein (CRP) and tumor necrosis factor-alpha levels were also significantly higher in AD and DM groups versus controls.
- A positive correlation was observed between serum CRP levels and Mini-Mental State Examination (MMSE) scores in AD patients.
Conclusions:
- The study findings support a low-grade systemic inflammation link between Alzheimer's disease and type 2 diabetes mellitus.
- Shared inflammatory pathways may contribute to the pathophysiology of both AD and DM.
- Further research into these inflammatory mechanisms could offer novel therapeutic targets.
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