ArticleJournal of visualized experiments : JoVE2017
A Novel Method to Model Chronic Traumatic Encephalopathy in Drosophila.
Article in Journal of visualized experiments : JoVE, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- The utilization of small non-mammals in traumatic brain injury research: A systematic review.CNS neuroscience & therapeutics · 2021Pooled it
- Adverse impact of female reproductive signaling on age-dependent neurodegeneration after mild head trauma ineLife · 2024Article
- Recent insights from non-mammalian models of brain injuries: an emerging literature.Frontiers in neurology · 2024Review
- Article
- Review
- Dietary restriction ameliorates TBI-induced phenotypes in Drosophila melanogaster.Scientific reports · 2022Article
- Glial immune-related pathways mediate effects of closed head traumatic brain injury on behavior and lethality in Drosophila.PLoS biology · 2022Article
- Drosophila as a model to explore secondary injury cascades after traumatic brain injury.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Review
- Dynamic neural and glial responses of a head-specific model for traumatic brain injury inProceedings of the National Academy of Sciences of the United States of America · 2020Article
- What triggers tauopathy in chronic traumatic encephalopathy?Neural regeneration research · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic Traumatic Encephalopathy (CTE) is an established neurodegenerative disease that is closely associated with exposure to repetitive mild Traumatic Brain Injury (mTBI). The mechanisms responsible for its complex pathological changes remain largely elusive, despite a recent consensus to define the neuropathological criteria. Here, we describe a novel method to develop a model of CTE in Drosophila melanogaster (Drosophila ) in an attempt to identify the key genes and pathways that lead to the characteristic hyperphosphorylated tau accumulation and neuronal death in the brain. Adjustable-strength impacts to inflict mild closed injury are delivered directly to the fly head, subjecting the head to rapid acceleration and deceleration. Our method eliminates the potential problems inherent with other Drosophila mTBI models (e.g.,animal death might be induced by damage to other parts of the body or to internal organs). The less labor- and cost-intensive animal care, short life span, and extensive genetic tools make the fruit fly ideal to study CTE pathogenesis and make it possible to perform large-scale, genome-wide forward genetic and pharmacological screens. We anticipate that the ongoing characterization of the model will generate important mechanistic insights on disease prevention and therapeutic approaches.
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Registered trials
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