SARS-CoV-2, COVID-19 and Neurodegeneration

Tönges, Lars; Klebe, Stephan

doi:10.3390/brainsci12070897

Cited by 1 publication

(1 citation statement)

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“…SARS-CoV-2 has been associated with various short-and long-term neurological manifestations, ranging from mild symptoms to severe complications [6][7][8]262,263]. Similarly to other viruses, SARS-CoV-2 can exacerbate existing neurodegenerative conditions or contribute to their development through mechanisms such as neuroinflammation, protein aggregation, ER stress and oxidative stress [42,164,240,261,[264][265][266][267][268][269][270][271]. For instance, recent studies reveal SARS-CoV-2 targeting cortical neurons, inducing MAPT/tau pathologies and neurodegeneration [164,272].…”

Section: Link Between Sars-cov-2 Er Stress and Neurodegenerationmentioning

confidence: 99%

Protein Quality Control Systems and ER Stress as Key Players in SARS-CoV-2-Induced Neurodegeneration

Gavilán,

Medina-Guzman,

Bahatyrevich-Kharitonik

et al. 2024

Cells

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The COVID-19 pandemic has brought to the forefront the intricate relationship between SARS-CoV-2 and its impact on neurological complications, including potential links to neurodegenerative processes, characterized by a dysfunction of the protein quality control systems and ER stress. This review article explores the role of protein quality control systems, such as the Unfolded Protein Response (UPR), the Endoplasmic Reticulum-Associated Degradation (ERAD), the Ubiquitin–Proteasome System (UPS), autophagy and the molecular chaperones, in SARS-CoV-2 infection. Our hypothesis suggests that SARS-CoV-2 produces ER stress and exploits the protein quality control systems, leading to a disruption in proteostasis that cannot be solved by the host cell. This disruption culminates in cell death and may represent a link between SARS-CoV-2 and neurodegeneration.

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