Does SARS-CoV-2 affect neurodegenerative disorders? TLR2, a potential receptor for SARS-CoV-2 in the CNS

Experimental & Molecular Medicine, Journal Year: 2022, Volume and Issue: 54(4), P. 447 - 454

Published: April 8, 2022

Abstract The coronavirus (COVID-19) pandemic, caused by severe acute respiratory system 2 (SARS-CoV-2), has created significant challenges for scientists seeking to understand the pathogenic mechanisms of SARS-CoV-2 infection and identify best therapies infected patients. Although ACE2 is a known receptor virus been shown mediate viral entry into lungs, accumulating reports highlight presence neurological symptoms resulting from infection. As expression low in central nervous (CNS), these are unlikely be ACE2-virus binding. In this review, we will discuss proposed interaction between Toll-like (TLR2) CNS. TLR2 an innate immune that recognizes exogenous microbial components but also interact with multiple components, including envelope (E) protein SARS-CoV-2. addition, plays important role pathogenesis neurodegenerative diseases such as Alzheimer’s disease (AD) Parkinson’s (PD). Based on observations, hypothesize may play critical response infiltration CNS, thereby induction or acceleration AD PD pathologies

Language: Английский

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Serum neurofilament light chain levels in Covid-19 patients without major neurological manifestations

Journal of Neurology, Journal Year: 2022, Volume and Issue: 269(11), P. 5691 - 5701

Published: July 4, 2022

Language: Английский

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COVID-19 as a Risk Factor for Alzheimer’s Disease

Journal of Alzheimer s Disease, Journal Year: 2022, Volume and Issue: 91(1), P. 1 - 23

Published: Oct. 29, 2022

Severe acute respiratory disease coronavirus 2 (SARS-CoV-2) is responsible for the 2019 (COVID-19) pandemic. Although a primarily disease, recent reports indicate that it also affects central nervous system (CNS). Over 25% of COVID-19 patients report neurological symptoms such as memory loss, anosmia, hyposmia, confusion, and headaches. The outcomes may be result viral entry into CNS and/or resulting neuroinflammation, both which underlie an elevated risk Alzheimer’s (AD). Herein, we ask: Is factor AD? To answer, identify literature review mechanisms by COVID-19-mediated neuroinflammation can contribute to development AD, evaluate effects versus chronic phases infection, lastly, discuss potential therapeutics address rising rates sequelae.

Language: Английский

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Alzheimer’s disease and COVID-19: Interactions, intrinsic linkages, and the role of immunoinflammatory responses in this process

Frontiers in Immunology, Journal Year: 2023, Volume and Issue: 14

Published: Feb. 9, 2023

Alzheimer’s disease (AD) and COVID-19 share many common risk factors, such as advanced age, complications, APOE genotype, etc. Epidemiological studies have also confirmed the internal relationship between two diseases. For example, found that AD patients are more likely to suffer from COVID-19, after infection with has a much higher of death than other chronic diseases, what’s interesting is developing in future significantly COVID-19. Therefore, this review gives detailed introduction perspectives epidemiology, susceptibility mortality. At same time, we focused on important role inflammation immune responses promoting onset

Language: Английский

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Generation and characterization of a humanized ACE2 mouse model to study long‐term impacts of SARS‐CoV‐2 infection

Journal of Medical Virology, Journal Year: 2024, Volume and Issue: 96(1)

Published: Jan. 1, 2024

Abstract Although the COVID‐19 pandemic has officially ended, persistent challenge of long‐COVID or post‐acute COVID sequelae (PASC) continues to impact societies globally, highlighting urgent need for ongoing research into its mechanisms and therapeutic approaches. Our team recently developed a novel humanized ACE2 mouse model (hACE2ki) designed explicitly long‐COVID/PASC research. This exhibits human expression in tissue cell‐specific patterns akin Ace2. When we exposed young adult hACE2ki mice (6 weeks old) various SARS‐CoV‐2 lineages, including WA, Delta, Omicron, at dose 5 × 10 PFU/mouse via nasal instillation, demonstrated distinctive phenotypes characterized by differences viral load lung, trachea, turbinate, weight loss, changes pro‐inflammatory cytokines immune cell profiles bronchoalveolar lavage fluid. Notably, no mortality was observed this age group. Further, assess model's relevance studies, investigated tau protein pathologies, which are linked Alzheimer's disease, brains these post infection. findings revealed accumulation longitudinal propagation tau, confirming potential our preclinical studies long‐COVID.

Language: Английский

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