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Analysis of Brain Mitochondria Using Serial Block-Face Scanning Electron Microscopy
Published on: July 9, 2016
Putative role of mitochondria in SARS-CoV-2 mediated brain dysfunctions: a prospect
Shashank K Maurya1, Meghraj S Baghel2, Gaurav3
1Department of Zoology, University of Delhi, Delhi, India.
Abstract:
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of the COVID-19 pandemic. Though the virus primarily damages the respiratory and cardiovascular systems after binding to the host angiotensin-converting enzyme 2 (ACE2) receptors, it has the potential to affect all major organ systems, including the human nervous system. There are multiple clinical reports of anosmia, dizziness, headache, nausea, ageusia, encephalitis, demyelination, neuropathy, memory loss, and neurological complications in SARS-CoV-2 infected individuals. Though the molecular mechanism of these brain dysfunctions during SARS-CoV-2 infection is elusive, the mitochondria seem to be an integral part of this pathogenesis. Emerging research findings suggest that the dysfunctional mitochondria and associated altered bioenergetics in the infected host cells lead to altered energy metabolism in the brain of Covid-19 patients. The interactome between viral proteins and mitochondrial proteins during Covid-19 pathogenesis also provides evidence for the involvement of mitochondria in SARS-CoV-2-induced brain dysfunctions. The present review discusses the possible role of mitochondria in disturbing the SARS-CoV-2 mediated brain functions, with the potential to use this information to prevent and treat these impairments.
Insights
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) impacts the nervous system, causing brain dysfunction. Mitochondria play a key role in these COVID-19 neurological impairments, offering potential therapeutic targets.
Area of Science:
- Neuroscience
- Virology
- Cell Biology
Background:
- Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19 and affects multiple organ systems, including the brain.
- Neurological symptoms like anosmia, dizziness, and memory loss are reported in infected individuals.
- The precise mechanisms behind SARS-CoV-2-induced brain dysfunction remain unclear.
Purpose of the Study:
- To review the role of mitochondria in SARS-CoV-2-related neurological complications.
- To explore how mitochondrial dysfunction contributes to altered brain energy metabolism during COVID-19.
- To identify potential therapeutic strategies targeting mitochondria for neurological impairments.
Main Methods:
- Literature review of existing research on SARS-CoV-2, neuroscience, and mitochondrial function.
- Analysis of studies investigating viral protein interactions with mitochondrial components.
- Synthesis of findings on bioenergetic alterations in infected host cells.
Main Results:
- Mitochondrial dysfunction and altered bioenergetics are implicated in SARS-CoV-2-induced brain impairments.
- Evidence suggests an interaction between viral and mitochondrial proteins contributes to pathogenesis.
- Altered energy metabolism in brain cells is a consequence of mitochondrial involvement.
Conclusions:
- Mitochondria are central to the pathogenesis of neurological complications associated with SARS-CoV-2 infection.
- Understanding mitochondrial roles may lead to novel prevention and treatment strategies for COVID-19-related brain dysfunction.
- Targeting mitochondrial pathways presents a promising avenue for therapeutic intervention.
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