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Melatonin: a ferroptosis inhibitor with potential therapeutic efficacy for the post-COVID-19 trajectory of accelerated brain aging and neurodegeneration

Yehia et al., Molecular Neurodegeneration, doi:10.1186/s13024-024-00728-6
Apr 2024  
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Melatonin for COVID-19
10th treatment shown to reduce risk in December 2020
 
*, now known with p = 0.0000002 from 18 studies.
Lower risk for mortality, ventilation, and recovery.
No treatment is 100% effective. Protocols combine complementary and synergistic treatments. * >10% efficacy in meta analysis with ≥3 clinical studies.
4,100+ studies for 60+ treatments. c19early.org
Review of melatonin as a potential ferroptosis inhibitor for the post-COVID-19 trajectory of accelerated brain aging and neurodegeneration. Authors propose that ferroptosis, an iron-dependent cell death triggered by lipid peroxidation, may underlie post-COVID cognitive impairment and neurodegeneration. SARS-CoV-2 infection induces neuroinflammation, iron dysregulation, oxidative stress, antioxidant system repression, renin-angiotensin system disruption, and clock gene alteration, which can all promote ferroptosis. Melatonin is suggested as a potential treatment due to its anti-inflammatory, antioxidant, iron chelating, and clock gene regulating properties that could inhibit the events leading to ferroptosis. Authors outline the detailed mechanisms by which melatonin may counter ferroptosis in the post-COVID-19 context.
Yehia et al., 19 Apr 2024, peer-reviewed, 2 authors. Contact: abulseoud.osama@mayo.edu.
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Melatonin: a ferroptosis inhibitor with potential therapeutic efficacy for the post-COVID-19 trajectory of accelerated brain aging and neurodegeneration
Asmaa Yehia, Osama A Abulseoud
Molecular Neurodegeneration, doi:10.1186/s13024-024-00728-6
The unprecedented pandemic of COVID-19 swept millions of lives in a short period, yet its menace continues among its survivors in the form of post-COVID syndrome. An exponentially growing number of COVID-19 survivors suffer from cognitive impairment, with compelling evidence of a trajectory of accelerated aging and neurodegeneration. The novel and enigmatic nature of this yet-to-unfold pathology demands extensive research seeking answers for both the molecular underpinnings and potential therapeutic targets. Ferroptosis, an iron-dependent cell death, is a strongly proposed underlying mechanism in post-COVID-19 aging and neurodegeneration discourse. COVID-19 incites neuroinflammation, iron dysregulation, reactive oxygen species (ROS) accumulation, antioxidant system repression, renin-angiotensin system (RAS) disruption, and clock gene alteration. These events pave the way for ferroptosis, which shows its signature in COVID-19, premature aging, and neurodegenerative disorders. In the search for a treatment, melatonin shines as a promising ferroptosis inhibitor with its repeatedly reported safety and tolerability. According to various studies, melatonin has proven efficacy in attenuating the severity of certain COVID-19 manifestations, validating its reputation as an anti-viral compound. Melatonin has well-documented anti-aging properties and combating neurodegenerative-related pathologies. Melatonin can block the leading events of ferroptosis since it is an efficient anti-inflammatory, iron chelator, antioxidant, angiotensin II antagonist, and clock gene regulator. Therefore, we propose ferroptosis as the culprit behind the post-COVID-19 trajectory of aging and neurodegeneration and melatonin, a well-fitting ferroptosis inhibitor, as a potential treatment.
Yehia and Abulseoud Molecular Neurodegeneration (2024) 19:36 against the ferroptosis-induced post-COVID-19 aging and neurodegeneration. Authors' contributions AY wrote the first draft under the supervision of OAA. Both authors read and approved the final manuscript. Declarations Consent for publication This manuscript does not contain data from any individual person so the consent for publication is not applicable. Ethics approval and consent to participate Not applicable. Ethics approval and consent are not indicated due to the review nature of this paper. Competing interests The authors declare that they have no competing interests. Publisher's Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
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{ 'DOI': '10.1186/s13024-024-00728-6', 'ISSN': ['1750-1326'], 'URL': 'http://dx.doi.org/10.1186/s13024-024-00728-6', 'abstract': '<jats:title>Abstract</jats:title><jats:p>The unprecedented pandemic of COVID-19 swept ' 'millions of lives in a short period, yet its menace continues among its survivors in the form ' 'of post-COVID syndrome. An exponentially growing number of COVID-19 survivors suffer from ' 'cognitive impairment, with compelling evidence of a trajectory of accelerated aging and ' 'neurodegeneration. The novel and enigmatic nature of this yet-to-unfold pathology demands ' 'extensive research seeking answers for both the molecular underpinnings and potential ' 'therapeutic targets. Ferroptosis, an iron-dependent cell death, is a strongly proposed ' 'underlying mechanism in post-COVID-19 aging and neurodegeneration discourse. COVID-19 incites ' 'neuroinflammation, iron dysregulation, reactive oxygen species (ROS) accumulation, ' 'antioxidant system repression, renin-angiotensin system (RAS) disruption, and clock gene ' 'alteration. These events pave the way for ferroptosis, which shows its signature in COVID-19, ' 'premature aging, and neurodegenerative disorders. In the search for a treatment, melatonin ' 'shines as a promising ferroptosis inhibitor with its repeatedly reported safety and ' 'tolerability. According to various studies, melatonin has proven efficacy in attenuating the ' 'severity of certain COVID-19 manifestations, validating its reputation as an anti-viral ' 'compound. Melatonin has well-documented anti-aging properties and combating ' 'neurodegenerative-related pathologies. Melatonin can block the leading events of ferroptosis ' 'since it is an efficient anti-inflammatory, iron chelator, antioxidant, angiotensin II ' 'antagonist, and clock gene regulator. Therefore, we propose ferroptosis as the culprit behind ' 'the post-COVID-19 trajectory of aging and neurodegeneration and melatonin, a well-fitting ' 'ferroptosis inhibitor, as a potential treatment.</jats:p>', 'alternative-id': ['728'], 'article-number': '36', 'assertion': [ { 'group': {'label': 'Article History', 'name': 'ArticleHistory'}, 'label': 'Received', 'name': 'received', 'order': 1, 'value': '7 February 2024'}, { 'group': {'label': 'Article History', 'name': 'ArticleHistory'}, 'label': 'Accepted', 'name': 'accepted', 'order': 2, 'value': '15 April 2024'}, { 'group': {'label': 'Article History', 'name': 'ArticleHistory'}, 'label': 'First Online', 'name': 'first_online', 'order': 3, 'value': '19 April 2024'}, {'group': {'label': 'Declarations', 'name': 'EthicsHeading'}, 'name': 'Ethics', 'order': 1}, { 'group': {'label': 'Consent for publication', 'name': 'EthicsHeading'}, 'name': 'Ethics', 'order': 2, 'value': 'This manuscript does not contain data from any individual person so the consent ' 'for publication is not applicable.'}, { 'group': {'label': 'Ethics approval and consent to participate', 'name': 'EthicsHeading'}, 'name': 'Ethics', 'order': 3, 'value': 'Not applicable. 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