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COVID ‐19 and neurodegeneration: The mitochondrial connection
Author(s) -
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.
Publication year - 2022
Publication title -
aging cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.103
H-Index - 140
eISSN - 1474-9726
pISSN - 1474-9718
DOI - 10.1111/acel.13727
Subject(s) - neurodegeneration , biology , disease , neuroscience , central nervous system , mechanism (biology) , mitochondrion , neuroinflammation , covid-19 , immunology , inflammation , medicine , pathology , infectious disease (medical specialty) , genetics , philosophy , epistemology
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.

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