Neuroprotection in Neurodegeneration by Omega-3-Fatty Acid

  • Unique Paper ID: 202332
  • Volume: 12
  • Issue: 12
  • PageNo: 9798-9818
  • Abstract:
  • neurodegenerative diseases, characterized by progressive neuronal loss, oxidative stress, mitochondrial dysfunction, and chronic neuroinflammation, include Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), Huntington's disease (HD), prion diseases, frontotemporal dementia (FTD), Lewy body diseases (LBD), and argyrophilic grain disease (AGD). The main omega-3-polyunsaturated fatty acids (PUFAs) are Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). They have potent antioxidant, anti-inflammatory, and neuroprotective effects. By reducing pro-inflammatory cytokines and increasing specialized pro-resolving mediators like resolvins and protectins, these essential fatty acids enhance the fluidity and integrity of neuronal membranes, regulate neurotransmission, and control inflammatory pathways. Amyloid accumulation, tau hyperphosphorylation, and synuclein aggregation are all critical aspects of AD and PD pathology that are decreased by EPA and DHA. Furthermore, by promoting mitochondrial function, neurogenesis, and the expression of brain-derived neurotrophic factor (BDNF), omega-3s aid in neuronal survival and cognitive resilience. According to clinical and experimental research, a sufficient intake of omega-3s may lower the likelihood of neurodegeneration, cognitive impairment, and mood disorders.

Copyright & License

Copyright © 2026 Authors retain the copyright of this article. This article is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

BibTeX

@article{202332,
        author = {Harshali Narayan Anap and Pawse Rutuja Sanjay and Daundkar Urmila Santosh},
        title = {Neuroprotection in Neurodegeneration by Omega-3-Fatty Acid},
        journal = {International Journal of Innovative Research in Technology},
        year = {2026},
        volume = {12},
        number = {12},
        pages = {9798-9818},
        issn = {2349-6002},
        url = {https://ijirt.org/article?manuscript=202332},
        abstract = {neurodegenerative diseases, characterized by progressive neuronal loss, oxidative stress, mitochondrial dysfunction, and chronic neuroinflammation, include Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), Huntington's disease (HD), prion diseases, frontotemporal dementia (FTD), Lewy body diseases (LBD), and argyrophilic grain disease (AGD). The main omega-3-polyunsaturated fatty acids (PUFAs) are Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).
They have potent antioxidant, anti-inflammatory, and neuroprotective effects. By reducing pro-inflammatory cytokines and increasing specialized pro-resolving mediators like resolvins and protectins, these essential fatty acids enhance the fluidity and integrity of neuronal membranes, regulate neurotransmission, and control inflammatory pathways. Amyloid accumulation, tau hyperphosphorylation, and synuclein aggregation are all critical aspects of AD and PD pathology that are decreased by EPA and DHA. Furthermore, by promoting mitochondrial function, neurogenesis, and the expression of brain-derived neurotrophic factor (BDNF), omega-3s aid in neuronal survival and cognitive resilience. According to clinical and experimental research, a sufficient intake of omega-3s may lower the likelihood of neurodegeneration, cognitive impairment, and mood disorders.},
        keywords = {Neuron, Omega-3-Fatty Acid, Neuroprotection, Neuroinflammation, Oxidative stress, neurodegenerative diseases.},
        month = {May},
        }

Cite This Article

Anap, H. N., & Sanjay, P. R., & Santosh, D. U. (2026). Neuroprotection in Neurodegeneration by Omega-3-Fatty Acid. International Journal of Innovative Research in Technology (IJIRT), 12(12), 9798–9818.

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