COVID‐19 and neurodegeneration: The mitochondrial connection. Issue 11 (11th October 2022)

• Record Type: Journal Article
• Authors: Denaro, Christopher A.; Haloush, Yara I.; Hsiao, Samuel Y.; Orgera, John J.; Osorio, Teresa; Riggs, Lindsey M.; Sassaman, Joshua W.; Williams, Sarah A.; Monte Carlo, Anthony R.; Da Costa, Renata T.; Grigoriev, Andrey; Solesio, Maria E.
• Is Part Of: Aging cell. Volume 21:Issue 11(2022)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2022-10-11
• Subjects: Alzheimer's disease -- bioenergetics -- COVID‐19 -- inflammation -- mitochondria -- neurodegeneration -- Parkinson's disease -- SARS‐CoV‐2; Cells -- Aging -- Periodicals; 571.8783605
• DOI: 10.1111/acel.13727
• Languages: English
• ISSNs: 1474-9718

Abstract

Abstract: There is still a significant lack of knowledge regarding many aspects of the etiopathology and consequences of the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection in humans. For example, the variety of molecular mechanisms mediating this infection, and the long‐term consequences of the disease remain poorly understood. It first seemed like the SARS‐CoV‐2 infection primarily caused a serious respiratory syndrome. However, over the last years, an increasing number of studies also pointed towards the damaging effects of this infection has on the central nervous system (CNS). In fact, evidence suggests a possible disruption of the blood–brain barrier and deleterious effects on the CNS, especially in patients who already suffer from other pathologies, such as neurodegenerative disorders. The molecular mechanisms behind these effects on the CNS could involve the dysregulation of mitochondrial physiology, a well‐known early marker of neurodegeneration and a hallmark of aging. Moreover, mitochondria are involved in the activation of the inflammatory response, which has also been broadly described in the CNS in COVID‐19. Here, we critically review the current bibliography regarding the presence of neurodegenerative symptoms in COVID‐19 patients, with a special emphasis on the mitochondrial mechanisms of these disorders.