Therapeutic targeting of obesity-induced neuroinflammation and neurodegeneration
Obesity is a major modifiable risk factor leading to neuroinflammation and neurodegeneration. Excessive fat storage in obesity promotes the progressive infiltration of immune cells into adipose tissue, resulting in the release of pro-inflammatory factors such as cytokines and adipokines. These infla...
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Frontiers Media S.A.
2025-01-01
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| Series: | Frontiers in Endocrinology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fendo.2024.1456948/full |
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| author | Jialiu Zeng Jialiu Zeng Lenny Yi Tong Cheong Chih Hung Lo Chih Hung Lo |
| author_facet | Jialiu Zeng Jialiu Zeng Lenny Yi Tong Cheong Chih Hung Lo Chih Hung Lo |
| author_sort | Jialiu Zeng |
| collection | DOAJ |
| description | Obesity is a major modifiable risk factor leading to neuroinflammation and neurodegeneration. Excessive fat storage in obesity promotes the progressive infiltration of immune cells into adipose tissue, resulting in the release of pro-inflammatory factors such as cytokines and adipokines. These inflammatory mediators circulate through the bloodstream, propagating inflammation both in the periphery and in the central nervous system. Gut dysbiosis, which results in a leaky intestinal barrier, exacerbates inflammation and plays a significant role in linking obesity to the pathogenesis of neuroinflammation and neurodegeneration through the gut-brain/gut-brain-liver axis. Inflammatory states within the brain can lead to insulin resistance, mitochondrial dysfunction, autolysosomal dysfunction, and increased oxidative stress. These disruptions impair normal neuronal function and subsequently lead to cognitive decline and motor deficits, similar to the pathologies observed in major neurodegenerative diseases, including Alzheimer’s disease, multiple sclerosis, and Parkinson’s disease. Understanding the underlying disease mechanisms is crucial for developing therapeutic strategies to address defects in these inflammatory and metabolic pathways. In this review, we summarize and provide insights into different therapeutic strategies, including methods to alter gut dysbiosis, lifestyle changes, dietary supplementation, as well as pharmacological agents derived from natural sources, that target obesity-induced neuroinflammation and neurodegeneration. |
| format | Article |
| id | doaj-art-7a635c8db48145e9a0c019076bab3fd5 |
| institution | Kabale University |
| issn | 1664-2392 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Endocrinology |
| spelling | doaj-art-7a635c8db48145e9a0c019076bab3fd52025-01-17T05:10:05ZengFrontiers Media S.A.Frontiers in Endocrinology1664-23922025-01-011510.3389/fendo.2024.14569481456948Therapeutic targeting of obesity-induced neuroinflammation and neurodegenerationJialiu Zeng0Jialiu Zeng1Lenny Yi Tong Cheong2Chih Hung Lo3Chih Hung Lo4Department of Biomedical and Chemical Engineering, Syracuse University, Syracuse, NY, United StatesInterdisciplinary Neuroscience Program, Syracuse University, Syracuse, NY, United StatesLee Kong Chian School of Medicine, Nanyang Technological University, Singapore, SingaporeInterdisciplinary Neuroscience Program, Syracuse University, Syracuse, NY, United StatesDepartment of Biology, Syracuse University, Syracuse, NY, United StatesObesity is a major modifiable risk factor leading to neuroinflammation and neurodegeneration. Excessive fat storage in obesity promotes the progressive infiltration of immune cells into adipose tissue, resulting in the release of pro-inflammatory factors such as cytokines and adipokines. These inflammatory mediators circulate through the bloodstream, propagating inflammation both in the periphery and in the central nervous system. Gut dysbiosis, which results in a leaky intestinal barrier, exacerbates inflammation and plays a significant role in linking obesity to the pathogenesis of neuroinflammation and neurodegeneration through the gut-brain/gut-brain-liver axis. Inflammatory states within the brain can lead to insulin resistance, mitochondrial dysfunction, autolysosomal dysfunction, and increased oxidative stress. These disruptions impair normal neuronal function and subsequently lead to cognitive decline and motor deficits, similar to the pathologies observed in major neurodegenerative diseases, including Alzheimer’s disease, multiple sclerosis, and Parkinson’s disease. Understanding the underlying disease mechanisms is crucial for developing therapeutic strategies to address defects in these inflammatory and metabolic pathways. In this review, we summarize and provide insights into different therapeutic strategies, including methods to alter gut dysbiosis, lifestyle changes, dietary supplementation, as well as pharmacological agents derived from natural sources, that target obesity-induced neuroinflammation and neurodegeneration.https://www.frontiersin.org/articles/10.3389/fendo.2024.1456948/fullobesitymetabolic dysfunctionneuroinflammationneurodegenerationbody-brain interactionstherapeutic targeting |
| spellingShingle | Jialiu Zeng Jialiu Zeng Lenny Yi Tong Cheong Chih Hung Lo Chih Hung Lo Therapeutic targeting of obesity-induced neuroinflammation and neurodegeneration Frontiers in Endocrinology obesity metabolic dysfunction neuroinflammation neurodegeneration body-brain interactions therapeutic targeting |
| title | Therapeutic targeting of obesity-induced neuroinflammation and neurodegeneration |
| title_full | Therapeutic targeting of obesity-induced neuroinflammation and neurodegeneration |
| title_fullStr | Therapeutic targeting of obesity-induced neuroinflammation and neurodegeneration |
| title_full_unstemmed | Therapeutic targeting of obesity-induced neuroinflammation and neurodegeneration |
| title_short | Therapeutic targeting of obesity-induced neuroinflammation and neurodegeneration |
| title_sort | therapeutic targeting of obesity induced neuroinflammation and neurodegeneration |
| topic | obesity metabolic dysfunction neuroinflammation neurodegeneration body-brain interactions therapeutic targeting |
| url | https://www.frontiersin.org/articles/10.3389/fendo.2024.1456948/full |
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