Journal Article Review Research Support, Non-U.S. Gov't Epublish 5 citations
PubMed: 39513898 DOI: 10.3390/cells13211791
Omega-3 Fatty Acids and Neuroinflammation in Depression: Targeting Damage-Associated Molecular Patterns and Neural Biomarkers.
Cells 13(21)
Authors: Ikbal Andrian Malau, Jane Pei-Chen Chang, Yi-Wen Lin, Cheng-Chen Chang, Wei-Che Chiu, Kuan-Pin Su
Affiliations
- Mind-Body Interface Research Center (MBI-Lab), China Medical University Hospital, Taichung 404, Taiwan.
- Graduate Institute of Biomedical Sciences, College of Medicine, China Medical University, Taichung 404, Taiwan.
- Child Psychiatry Division, Department of Psychiatry, China Medical University Hospital, Taichung 404, Taiwan.
- Graduate Institute of Acupuncture Science and Chinese Medicine Research Center, College of Medicine, China Medical University, Taichung 404, Taiwan.
- Department of Psychiatry, Chung Shan Medical University Hospital, Taichung 402, Taiwan.
- School of Medicine, Chung Shan Medical University, Taichung 402, Taiwan.
- Department of Psychiatry, Cathay General Hospital, Taipei 106, Taiwan.
- School of Medicine, Fu Jen Catholic University, Taipei 242, Taiwan.
- An-Nan Hospital, China Medical University, Tainan 709, Taiwan.
Abstract
Major Depressive Disorder (MDD) is a prevalent mental health condition with a complex pathophysiology involving neuroinflammation, neurodegeneration, and disruptions in neuronal and glial cell function. Microglia, the innate immune cells of the central nervous system, release inflammatory cytokines in response to pathological changes associated with MDD. Damage-associated molecular patterns (DAMPs) act as alarms, triggering microglial activation and subsequent inflammatory cytokine release. This review examines the cellular mechanisms underlying MDD pathophysiology, focusing on the lipid-mediated modulation of neuroinflammation. We explore the intricate roles of microglia and astrocytes in propagating inflammatory cascades and discuss how these processes affect neuronal integrity at the cellular level. Central to our analysis are three key molecules: High Mobility Group Box 1 (HMGB1) and S100 Calcium Binding Protein β (S100β) as alarmins, and Neuron-Specific Enolase (NSE) as an indicator of neuronal stress. We present evidence from in vitro and ex vivo studies demonstrating how these molecules reflect and contribute to the neuroinflammatory milieu characteristic of MDD. The review then explores the potential of omega-3 polyunsaturated fatty acids (ω-3 PUFAs) as neuroinflammation modulators, examining their effects on microglial activation, cytokine production, and neuronal resilience in cellular models of depression. We critically analyze experimental data on how ω-3 PUFA supplementation influences the expression and release of HMGB1, S100β, and NSE in neuronal and glial cultures. By integrating findings from lipidomic and cellular neurobiology, this review aims to elucidate the mechanisms by which ω-3 PUFAs may exert their antidepressant effects through modulation of neuroinflammatory markers. These insights contribute to our understanding of lipid-mediated neuroprotection in MDD and may inform the development of targeted, lipid-based therapies for both depression and neurodegenerative disorders.
MeSH
Cytokines, Depression, Microglia, Cells, Neurons, Fatty Acids, Omega-3, Biomarkers, Fatty Acids
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