COVID-19, ferrosenescence and neurodegeneration, a mini-review
Exacerbation of cognitive, motor and nonmotor symptoms have been described in critically ill COVID-19 patients, indicating that, like prior pandemics, neurodegenerative sequelae may mark the aftermath of this viral infection. Moreover, SARS-CoV-2, the causative agent of COVID-19 disease, was associated with hyperferritinemia and unfavorable prognosis in older individuals, suggesting virus-induced ferrosenescence. We have previously defined ferrosenescence as an iron-associated disruption of both the human genome and its repair mechanisms, leading to premature cellular senescence and neurodegeneration. As viruses replicate more efficiently in iron-rich senescent cells, they may have developed the ability to induce this phenotype in host tissues, predisposing to both immune dysfunction and neurodegenerative disorders. In this mini-review, we summarize what is known about the SARS-CoV-2-induced cellular senescence and iron dysmetabolism. We also take a closer look at immunotherapy with natural killer cells, angiotensin II receptor blockers (“sartans”), iron chelators and dipeptidyl peptidase 4 inhibitors (“gliptins”) as adjunct treatments for both COVID-19 and its neurodegenerative complications.
Adonis Sfera, Carolina Osorio, Gerald Maguire, Leah Rahman, Jafri Afzaal, Michael Cummings, Jose Campo Maldonado, COVID-19, ferrosenescence and neurodegeneration, a mini-review, Progress in Neuro-Psychopharmacology and Biological Psychiatry, Volume 109, 2021, 110230, ISSN 0278-5846, https://doi.org/10.1016/j.pnpbp.2020.110230.
Progress in Neuropsychopharmacology & Biological Psychiatry