AI Article Synopsis
- Microglial activation has been linked to neurodegenerative diseases like Alzheimer's and Parkinson's, but its role in metabolic disorders, particularly insulin resistance and type 2 diabetes, is gaining attention.
- The text examines the biochemical pathways involved in this connection, including IKKβ/NF-κβ and IRS-1/PI3K/Akt, as well as the impact of non-coding RNAs on insulin resistance.
- Finally, potential therapeutic strategies, both pharmaceutical and lifestyle-based, are discussed to reduce microglial activation and mitigate its effects on metabolism.
Article Abstract
Historically, microglial activation has been associated with diseases of a neurodegenerative and neuroinflammatory nature. Some, like Alzheimer's disease, Parkinson's disease, and multiple system atrophy, have been explored extensively, while others pertaining to metabolism not so much. However, emerging evidence points to hypothalamic inflammation mediated by microglia as a driver of metabolic dysregulations, particularly insulin resistance and type 2 diabetes mellitus. Here, we explore this connection further and examine pathways that underlie this relationship, including the IKKβ/NF-κβ, IRS-1/PI3K/Akt, mTOR-S6 Kinase, JAK/STAT, and PPAR-γ signaling pathways. We also investigate the role of non-coding RNAs, namely microRNAs and long non-coding RNAs, in insulin resistance related to neuroinflammation and their diagnostic and therapeutic potential. Finally, we explore therapeutics further, searching for both pharmacological and non-pharmacological interventions that can help mitigate microglial activation.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11642714 | PMC |
| http://dx.doi.org/10.3390/ijms252313169 | DOI Listing |
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