ArticleHuman molecular genetics2018
Traumatic injury induces stress granule formation and enhances motor dysfunctions in ALS/FTD models.
Article in Human molecular genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 2 of them syntheses that pooled it.
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Who cites it
69 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Environmental risk factors, protective factors, and biomarkers for amyotrophic lateral sclerosis: an umbrella review.Frontiers in aging neuroscience · 2025Pooled it
- The utilization of small non-mammals in traumatic brain injury research: A systematic review.CNS neuroscience & therapeutics · 2021Pooled it
- MicroRNAs in the pathogenesis of neurodegenerative disorders: Potential as therapeutic targets.Neural regeneration research · 2026Article
- A human Staufen1 BAC transgenic mouse exhibits abnormal autophagy and neurodegeneration across the central nervous system.Cell death & disease · 2026Article
- De novo variants in KDM2A cause a syndromic neurodevelopmental disorder.American journal of human genetics · 2026Article
- Exploring the versatility ofFly · 2025Review
- Small-molecule dissolution of stress granules by redox modulation benefits ALS models.Nature chemical biology · 2025Article
- A human Staufen1 BAC transgenic mouse exhibits abnormal autophagy and neurodegeneration across the central nervous system.Research square · 2025Article
- Biogenesis of stress granules and their role in the regulation of stress-induced male reproduction disorders.Cell communication and signaling : CCS · 2025Review
- Repetitive Mild but Not Single Moderate Brain Trauma Is Associated with TAR DNA-Binding Protein 43 Mislocalization and Glial Activation in the Mouse Spinal Cord.Biomedicines · 2025Article
- HuD impairs neuromuscular junctions and induces apoptosis in human iPSC and Drosophila ALS models.Nature communications · 2024Article
- Regulation of DNA damage response by RNA/DNA-binding proteins: Implications for neurological disorders and aging.Ageing research reviews · 2024Review
- Lifestyle and medical conditions in relation to ALS risk and progression-an introduction to the Swedish ALSrisc Study.Journal of neurology · 2024Article
- RNA-binding properties orchestrate TDP-43 homeostasis through condensate formation in vivo.Nucleic acids research · 2024Article
- Traumatic injury causes selective degeneration and TDP-43 mislocalization in human iPSC-derivedbioRxiv : the preprint server for biology · 2024Article
- Ferroptosis regulation through Nrf2 and implications for neurodegenerative diseases.Archives of toxicology · 2024Review
- Mild traumatic brain injury in Drosophila melanogaster alters reactive oxygen and nitrogen species in a sex-dependent manner.Experimental neurology · 2024Article
- Exploring the Research Focus of RNA-Binding Proteins in Trauma and Burns.Analytical cellular pathology (Amsterdam) · 2024Review
- Repeated mild traumatic brain injury triggers pathology in asymptomatic C9ORF72 transgenic mice.Brain : a journal of neurology · 2023Article
- Drosha-dependent microRNAs modulate FUS-mediated neurodegeneration in vivo.Nucleic acids research · 2023Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Traumatic brain injury (TBI) has been predicted to be a predisposing factor for amyotrophic lateral sclerosis (ALS) and other neurological disorders. Despite the importance of TBI in ALS progression, the underlying cellular and molecular mechanisms are still an enigma. Here, we examined the contribution of TBI as an extrinsic factor and investigated whether TBI influences the susceptibility of developing neurodegenerative symptoms. To evaluate the effects of TBI in vivo, we applied mild to severe trauma to Drosophila and found that TBI leads to the induction of stress granules (SGs) in the brain. The degree of SGs induction directly correlates with the level of trauma. Furthermore, we observed that the level of mortality is directly proportional to the number of traumatic hits. Interestingly, trauma-induced SGs are ubiquitin, p62 and TDP-43 positive, and persistently remain over time suggesting that SGs might be aggregates and exert toxicity in our fly models. Intriguingly, TBI on animals expressing ALS-linked genes increased mortality and locomotion dysfunction suggesting that mild trauma might aggravate neurodegenerative symptoms associated with ALS. Furthermore, we found elevated levels of high molecular weight ubiquitinated proteins and p62 in animals expressing ALS-causing genes with TBI, suggesting that TBI may lead to the defects in protein degradation pathways. Finally, we observed that genetic and pharmacological induction of autophagy enhanced the clearance of SGs and promoted survival of flies in vivo. Together, our study demonstrates that trauma can induce SG formation in vivo and might enhance neurodegenerative phenotypes in the fly models of ALS.
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