Long COVID as a Tauopathy: Of “Brain Fog” and “Fusogen Storms” DOI Open Access
Adonis Sfera,

Leah Rahman,

Carlos Manuel Zapata-Martín del Campo

et al.

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(16), P. 12648 - 12648

Published: Aug. 10, 2023

Long COVID, also called post-acute sequelae of SARS-CoV-2, is characterized by a multitude lingering symptoms, including impaired cognition, that can last for many months. This symptom, often "brain fog", affects the life quality numerous individuals, increasing medical complications as well healthcare expenditures. The etiopathogenesis SARS-CoV-2-induced cognitive deficit unclear, but most likely cause chronic inflammation maintained viral remnant thriving in select body reservoirs. These sanctuaries are comprised fused, senescent cells, microglia and astrocytes, pathogen convert into neurotoxic phenotypes. Moreover, enteric nervous system contains neurons glia, virus lingers gastrointestinal tract well, accounting intestinal symptoms long COVID. Fusogens proteins overcome repulsive forces between cell membranes, allowing to coalesce with host cells enter cytoplasm. In intracellular compartment, hijacks actin cytoskeleton, fusing each other engendering pathological syncytia. Cell-cell fusion enables infect healthy neighboring cells. We surmise syncytia formation drives impairment facilitating "seeding" hyperphosphorylated Tau, documented COVID-19. our previous work, we hypothesized SARS-CoV-2 induces premature endothelial senescence, permeability blood-brain barrier. migration microbes and/or their components circulation, eventually reaching brain where they may induce dysfunction. For example, translocated lipopolysaccharides or microbial DNA Tau hyperphosphorylation, memory problems. this perspective article, examine pathogenetic mechanisms potential biomarkers cell-free DNA, interleukin 22, phosphorylated beneficial effect transcutaneous vagal nerve stimulation.

Language: Английский

Antioxidant Genetic Profile Modifies Probability of Developing Neurological Sequelae in Long-COVID DOI Creative Commons
Marko Ercegovac, Milika Ašanin, Ana Savić-Radojevic

et al.

Antioxidants, Journal Year: 2022, Volume and Issue: 11(5), P. 954 - 954

Published: May 12, 2022

Understanding the sequelae of COVID-19 is utmost importance. Neuroinflammation and disturbed redox homeostasis are suggested as prevailing underlying mechanisms in neurological propagation long-COVID. We aimed to investigate whether variations antioxidant genetic profile might be associated with Neurological examination (SOD2, GPXs GSTs) determination, well as, genotype analysis Nrf2 ACE2, were conducted on 167 patients. Polymorphisms determined by appropriate PCR methods. Only polymorphisms GSTP1AB GSTO1 independently long-COVID manifestations. Indeed, individuals carrying GSTP1 Val or Asp allele exhibited lower odds myalgia development, both combination. Furthermore, combined presence Ile Ala alleles cumulative risk regarding carriers GPX1 LeuLeu/GPX3 CC genotype. Moreover, GSTM1-null/GPX1LeuLeu more prone developing "brain fog", while this probability further enlarged if A was also present. The fact that certain variants enzymes, combination, affect manifestations, emphasizes involvement susceptibility when SARS-CoV-2 infection initiated host cells, months after.

Language: Английский

Citations

25

Mechanisms, Effects, and Management of Neurological Complications of Post-Acute Sequelae of COVID-19 (NC-PASC) DOI Creative Commons
Ian Ong, Dennis L. Kolson, Matthew K. Schindler

et al.

Biomedicines, Journal Year: 2023, Volume and Issue: 11(2), P. 377 - 377

Published: Jan. 27, 2023

With a growing number of patients entering the recovery phase following infection with SARS-CoV-2, understanding long-term neurological consequences disease is important to their care. The complications post-acute sequelae SARS-CoV-2 (NC-PASC) represent myriad symptoms including headaches, brain fog, numbness/tingling, and other that many people report long after acute has resolved. Emerging reports are being published concerning COVID-19 its chronic effects, yet limited knowledge mechanisms challenged therapeutic efforts. To address these issues, we review broadly literature spanning 2020-2022 proposed underlying NC-PASC, outline associated COVID-19, discuss potential clinical interventions.

Language: Английский

Citations

16

Oxidative Biomarkers Associated with the Pulmonary Manifestation of Post-COVID-19 Complications DOI Open Access
Kamil Siekacz,

Anna Kumor‐Kisielewska,

Joanna Miłkowska-Dymanowska

et al.

Journal of Clinical Medicine, Journal Year: 2023, Volume and Issue: 12(13), P. 4253 - 4253

Published: June 25, 2023

The role of mitochondria in post coronavirus disease 2019 (post-COVID-19) complications is unclear, especially the long-term pulmonary complications. This study aims to investigate association between post-COVID-19 and mitochondrial regulatory proteins context oxidative stress.Patients who had recovered from COVID-19 were enrolled. According evidence persistent interstitial lung lesions on computed tomography (CT), patients divided into a group (P(+)) control without (P(-)). We randomly selected 80 for investigation (40 subjects each group). Biomarkers levels determined by enzyme-linked immunosorbent assay (ELISA).The serum concentrations significantly higher P(+) group, including PTEN-induced kinase 1 (PINK1): 1.62 [1.02-2.29] ng/mL vs. 1.34 [0.94-1.74] (p = 0.046); Dynamin-1-like protein (DNM1L): 1.6 [0.9-2.4] IQR 0.9 [0.5-1.6] 0.004); Mitofusin-2 (MFN2): 0.3 [0.2-0.5] 0.2 [0.1-0.3] 0.001). Patients also chemokine ligand 18 (PARC, CCL18), IL-6, tumour necrosis factor-alpha (TNF-α) cytokines than P(-) group. concentration interferon alpha (IFN-α) was decreased Furthermore, we observed statistically significant correlations advanced glycation end product (sRAGE) TNF-α (Pearson's factor R 0.637; p < 0.001) DNM1L IFN-α 0.501; 0.002) patients.Elevated biomarkers with indicate their possible pathobiology sequelae. Oxidative stress associated immune response inflammation after COVID-19. could be promising biomarker predicting may potential target therapeutic intervention

Language: Английский

Citations

15

Neurological Consequences, Mental Health, Physical Care, and Appropriate Nutrition in Long-COVID-19 DOI Creative Commons
Pasquale Picone,

Tiziana Sanfilippo,

Rossella Guggino

et al.

Cellular and Molecular Neurobiology, Journal Year: 2022, Volume and Issue: 43(5), P. 1685 - 1695

Published: Sept. 14, 2022

SARS-CoV-2 pandemic has caused a collapse of the world health systems. Now, vaccines and more effective therapies have reversed this crisis but scenario is further aggravated by appearance new pathology, occurring as infection consequence: long-COVID-19. This term commonly used to describe signs symptoms that continue or develop after acute COVID-19 up several months. In review, consequences disease on mental neurological implications due long-COVID are described. Furthermore, appropriate nutritional approach some recommendations relieve pathology presented. Data collected indicated in next future will affect an increasing number individuals interdisciplinary action needed counteract it.

Language: Английский

Citations

20

Long COVID as a Tauopathy: Of “Brain Fog” and “Fusogen Storms” DOI Open Access
Adonis Sfera,

Leah Rahman,

Carlos Manuel Zapata-Martín del Campo

et al.

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(16), P. 12648 - 12648

Published: Aug. 10, 2023

Long COVID, also called post-acute sequelae of SARS-CoV-2, is characterized by a multitude lingering symptoms, including impaired cognition, that can last for many months. This symptom, often "brain fog", affects the life quality numerous individuals, increasing medical complications as well healthcare expenditures. The etiopathogenesis SARS-CoV-2-induced cognitive deficit unclear, but most likely cause chronic inflammation maintained viral remnant thriving in select body reservoirs. These sanctuaries are comprised fused, senescent cells, microglia and astrocytes, pathogen convert into neurotoxic phenotypes. Moreover, enteric nervous system contains neurons glia, virus lingers gastrointestinal tract well, accounting intestinal symptoms long COVID. Fusogens proteins overcome repulsive forces between cell membranes, allowing to coalesce with host cells enter cytoplasm. In intracellular compartment, hijacks actin cytoskeleton, fusing each other engendering pathological syncytia. Cell-cell fusion enables infect healthy neighboring cells. We surmise syncytia formation drives impairment facilitating "seeding" hyperphosphorylated Tau, documented COVID-19. our previous work, we hypothesized SARS-CoV-2 induces premature endothelial senescence, permeability blood-brain barrier. migration microbes and/or their components circulation, eventually reaching brain where they may induce dysfunction. For example, translocated lipopolysaccharides or microbial DNA Tau hyperphosphorylation, memory problems. this perspective article, examine pathogenetic mechanisms potential biomarkers cell-free DNA, interleukin 22, phosphorylated beneficial effect transcutaneous vagal nerve stimulation.

Language: Английский

Citations

12