AI Article Synopsis
- Neurodegenerative diseases like Alzheimer's, Parkinson's, Huntington's, and ALS are increasingly associated with issues in mitochondria and inflammation of the nervous system.
- Mitochondrial damage causes the release of molecules (mtDAMPs) such as mitochondrial DNA and reactive oxygen species, which trigger inflammatory responses that worsen these diseases.
- The review highlights how understanding mtDAMPs can lead to new treatments aimed at reducing neuroinflammation and slowing down disease progression, potentially leading to better outcomes for patients.
Article Abstract
Neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS) are increasingly linked to mitochondrial dysfunction and neuroinflammation. Central to this link are mitochondrial damage-associated molecular patterns (mtDAMPs), including mitochondrial DNA, ATP, and reactive oxygen species, released during mitochondrial stress or damage. These mtDAMPs activate inflammatory pathways, such as the NLRP3 inflammasome and cGAS-STING, contributing to the progression of neurodegenerative diseases. This review delves into the mechanisms by which mtDAMPs drive neuroinflammation and discusses potential therapeutic strategies targeting these pathways to mitigate neurodegeneration. Additionally, it explores the cross-talk between mitochondria and the immune system, highlighting the complex interplay that exacerbates neuronal damage. Understanding the role of mtDAMPs could pave the way for novel treatments aimed at modulating neuroinflammation and slowing disease progression, ultimately improving patient outcome.
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| http://dx.doi.org/10.1016/j.neuropharm.2024.110217 | DOI Listing |
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