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Depression as a risk factor for Alzheimer's disease: A human post-mortem study
Mizuki Morisaki1, Farnoosh Rezaali1, Laurie C Lau2
1Dementia Research Group, University of Bristol, Bristol, United Kingdom.
Depression shows neuroinflammation with increased IL-6 and IL-10, unlike early Alzheimer's disease (AD). This suggests depression may increase AD risk via non-inflammatory pathways.
Area of Science:
- Neuroscience
- Psychiatry
- Immunology
Background:
- Depression is a risk factor for Alzheimer's disease (AD), potentially an early AD manifestation.
- Neuroinflammation is a common feature in both depression and AD, but mechanisms linking them are unclear.
Purpose of the Study:
- To investigate neuroinflammation in post-mortem human brain tissue from individuals with depression and early-stage AD.
- To compare inflammatory protein and endothelial marker levels between depressed individuals, AD patients, and controls.
Main Methods:
- Analysis of post-mortem dorsal prefrontal cortex tissue from 54 depressed cases, 37 controls, 16 early-stage AD cases, and 15 controls.
- Measurement of 10 inflammatory proteins (cytokines) and 2 endothelial markers using ELISA and MesoScale Multiplex Assays.
Main Results:
- Depression group showed increased Interleukin-6 (IL-6) and Interleukin-10 (IL-10), and decreased Interleukin-1β (IL-1β) compared to controls.
- Early-stage AD cases exhibited increased ICAM-1, indicating endothelial activation, but no significant changes in measured cytokines.
- Neuroinflammation was evident in depression but not in early-stage AD.
Conclusions:
- Depression is associated with neuroinflammation, while early AD shows endothelial activation without significant cytokine alterations.
- The findings suggest depression may elevate AD risk through mechanisms other than the measured inflammatory pathways.
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