ArticleMolecular neurobiology2026
Traumatic Brain Injury and Endocytosis: Reduced Rodent Hippocampal Endocytosis Proteins and Human Clathrin Light Chain Polymorphisms Are Associated with Impaired Neurological Outcomes After TBI.
Article in Molecular neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Traumatic brain injury (TBI) can result in enduring cognitive, emotional, and somatic impairments, which may be mediated in part by impaired synaptic function. Prior studies in experimental models of TBI have implicated molecular disturbances within the synaptic vesicular pool as a mediator of altered neurotransmission. Endocytosis maintains the pre-synaptic pool through recycling and replenishment of neurotransmitter-containing vesicles, and dysregulation of this mechanism is a plausible candidate for TBI-induced synaptic dysfunction. We sought to determine if TBI had a detrimental effect on clathrin-mediated endocytosis (CME)-associated proteins, a response underexplored. We hypothesized that the abundance of CME in the brain decreases in rats subjected to a controlled cortical impact (CCI) injury. Assessments of hippocampal CME proteins revealed similar responses to CCI in female and male rats with decreased hippocampal abundance of clathrin light chain, AP180, dynamin, and Rab5 at 14 days post-injury. While we did not directly test the role of CME modulation in this study, reductions in protein abundances were temporally aligned with neurobehavioral impairments in motor, spatial learning, and spatial memory performance, independent of sex. Sex-dependent differences were observed in the open-field testing. We also sought to examine if the presence of single nucleotide polymorphisms (SNPs) in clathrin genes were associated with outcomes in severe TBI patients. Human SNP analysis for clathrin light chain A (CLTA) revealed a minor allele (rs4879960) was associated with improved outcomes on the Glasgow Outcome Scale and Disability Rating Scale in severe TBI patients. These data provide insight into synaptic changes in CME proteins that show associational changes with cognitive impairments post-injury preclinically. This study identifies clinically relevant SNPs that are correlated with long-term outcomes post-TBI.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.