The Role of TDP-43 in SARS-CoV-2-Related Neurodegenerative Changes DOI Creative Commons
Dong‐Hwi Kim,

Jae‐Hyeong Kim,

Min‐Tae Jeon

и другие.

Viruses, Год журнала: 2025, Номер 17(5), С. 724 - 724

Опубликована: Май 19, 2025

The coronavirus disease 2019 (COVID-19) pandemic has been linked to long-term neurological effects with multifaceted complications of neurodegenerative diseases. Several studies have found that pathological changes in transactive response DNA-binding protein 43 kDa (TDP-43) are involved these cases. This review explores the causal interactions between severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and TDP-43 from multiple perspectives. Some viral proteins SARS-CoV-2 shown induce through its cleavage, aggregation, mislocalization. infection can cause liquid−liquid phase separation stress granule formation, which accelerate condensation TDP-43, resulting host RNA metabolism disruption. proposed interact RNA, though role replication remains be fully elucidated. interaction potentially facilitates replication, while viral-induced oxidative protease activity pathology. Evidence both clinical experimental indicates may contribute sequelae, including amyotrophic lateral sclerosis-like frontotemporal dementia-like features, as well increased phosphorylated deposition central nervous system. Biomarker further support link dysregulation COVID-19 (long COVID). In this review, we presented a novel integrative framework pathology, bridging gap mechanisms neurodegeneration. These findings underscore need for research clarify TDP-43-related neurodegeneration underlying develop therapeutic strategies aimed at mitigating patients long COVID.

Язык: Английский

The Role of TDP-43 in SARS-CoV-2-Related Neurodegenerative Changes DOI Creative Commons
Dong‐Hwi Kim,

Jae‐Hyeong Kim,

Min‐Tae Jeon

и другие.

Viruses, Год журнала: 2025, Номер 17(5), С. 724 - 724

Опубликована: Май 19, 2025

The coronavirus disease 2019 (COVID-19) pandemic has been linked to long-term neurological effects with multifaceted complications of neurodegenerative diseases. Several studies have found that pathological changes in transactive response DNA-binding protein 43 kDa (TDP-43) are involved these cases. This review explores the causal interactions between severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and TDP-43 from multiple perspectives. Some viral proteins SARS-CoV-2 shown induce through its cleavage, aggregation, mislocalization. infection can cause liquid−liquid phase separation stress granule formation, which accelerate condensation TDP-43, resulting host RNA metabolism disruption. proposed interact RNA, though role replication remains be fully elucidated. interaction potentially facilitates replication, while viral-induced oxidative protease activity pathology. Evidence both clinical experimental indicates may contribute sequelae, including amyotrophic lateral sclerosis-like frontotemporal dementia-like features, as well increased phosphorylated deposition central nervous system. Biomarker further support link dysregulation COVID-19 (long COVID). In this review, we presented a novel integrative framework pathology, bridging gap mechanisms neurodegeneration. These findings underscore need for research clarify TDP-43-related neurodegeneration underlying develop therapeutic strategies aimed at mitigating patients long COVID.

Язык: Английский

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