๐๐๐ก๐๐ฉ๐ค๐ฃ๐๐ฃ: ๐ ๐๐๐ง๐ง๐ค๐ฅ๐ฉ๐ค๐จ๐๐จ ๐๐ฃ๐๐๐๐๐ฉ๐ค๐ง ๐ฌ๐๐ฉ๐ ๐ฅ๐ค๐ฉ๐๐ฃ๐ฉ๐๐๐ก ๐ฉ๐๐๐ง๐๐ฅ๐๐ช๐ฉ๐๐ ๐๐๐๐๐๐๐๐ฎ ๐๐ค๐ง ๐๐๐๐๐ก๐๐ง๐๐ฉ๐๐ ๐๐ง๐๐๐ฃ ๐๐๐๐ฃ๐ ๐๐ฃ๐ ๐ฃ๐๐ช๐ง๐ค๐๐๐๐๐ฃ๐๐ง๐๐ฉ๐๐ค๐ฃ.
#LongCovid
โฆarneurodegeneration.biomedcentral.com/articles/10.11โฆ
2) Ferroptosis, an iron-dependent form of regulated cell death, has been proposed as a potential driver of organ damage in COVID-19 and the post-COVID trajectory of aging and neurodegeneration.
3) COVID-19 infection promotes several events that can lead to ferroptosis, including neuroinflammation, iron dysregulation, oxidative stress, ACE2 receptor disruption, and clock gene alteration.
4) Melatonin has properties that allow it to address all of these ferroptosis-promoting factors. It is an antioxidant, anti-inflammatory, iron chelator, and modulator of the renin-angiotensin system and clock genes
5) Melatonin has shown effectiveness against viral infections, aging, and neurodegenerative diseases like Alzheimer's and Parkinson's in both experimental and clinical research.
This review proposes ferroptosis...
6) ... as a key mechanism behind post-COVID aging/neurodegeneration and presents melatonin as a potential treatment due to its unique ability to inhibit ferroptosis through multiple mechanisms. More research is needed to validate this hypothesis.
7) In summary, the paper puts forth the novel proposition that ferroptosis contributes to long-term issues seen after COVID-19, and identifies melatonin as a promising intervention given its multi-targeted effects against ferroptosis.
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