ReviewJournal of neural transmission (Vienna, Austria : 1996)2011
Traumatic brain injury and recovery mechanisms: peptide modulation of periventricular neurogenic regions by the choroid plexus-CSF nexus.
Review in Journal of neural transmission (Vienna, Austria : 1996), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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
55 citing papers in PubMed, 114 citations in OpenAlex.
- Primary Blast-Induced Traumatic Brain Injury as a Risk Factor for (Cerebro)vascular Disorder: Clinical Manifestations, Blast Physics, Biomechanics, Pathobiology, and Critical Gaps.International journal of molecular sciences · 2026Review
- Perceiving traumatic brain injury from glymphatic system.Molecular psychiatry · 2025Review
- Divergent neurodegeneration associations with choroid plexus volume and degree of calcification in cognitively normal APOE ε4 carriers and non-carriers.Scientific reports · 2025Article
- Ependymal cells: roles in central nervous system infections and therapeutic application.Journal of neuroinflammation · 2024Review
- Ginsenoside Rg3 attenuates neuroinflammation and hippocampal neuronal damage after traumatic brain injury in mice by inactivating the NF-kB pathway via SIRT1 activation.Cell cycle (Georgetown, Tex.) · 2024Article
- Brain Fluid Clearance After Traumatic Brain Injury Measured Using Dynamic Positron Emission Tomography.Neurotrauma reports · 2024Article
- Altered endocannabinoid metabolism compromises the brain-CSF barrier and exacerbates chronic deficits after traumatic brain injury in mice.Experimental neurology · 2023Article
- Nanowired Delivery of Cerebrolysin with Mesenchymal Stem Cells Attenuates Heat Stress-Induced Exacerbation of Neuropathology Following Brain Blast Injury.Advances in neurobiology · 2023Article
- Nanowired Delivery of Cerebrolysin Together with Antibodies to Amyloid Beta Peptide, Phosphorylated Tau, and Tumor Necrosis Factor Alpha Induces Superior Neuroprotection in Alzheimer's Disease Brain Pathology Exacerbated by Sleep Deprivation.Advances in neurobiology · 2023Review
- The pathological potential of ependymal cells in mild traumatic brain injury.Frontiers in cellular neuroscience · 2023Review
- The endogenous progenitor response following traumatic brain injury: a target for cell therapy paradigms.Neural regeneration research · 2022Review
- Systems spatiotemporal dynamics of traumatic brain injury at single-cell resolution reveals humanin as a therapeutic target.Cellular and molecular life sciences : CMLS · 2022Article
- Choroid plexus function in neurological homeostasis and disorders: The awakening of the circadian clocks and orexins.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Review
- Targeting choroid plexus epithelium as a novel therapeutic strategy for hydrocephalus.Journal of neuroinflammation · 2022Review
- Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Article
- Functional brain activity constrained by structural connectivity reveals cohort-specific features for serum neurofilament light chain.Communications medicine · 2022Article
- The Roles of Neurotrophins in Traumatic Brain Injury.Life (Basel, Switzerland) · 2021Review
- Overexpression of RAPGEF3 enhances the therapeutic effect of dezocine in treatment of neuropathic pain.Genetics and molecular biology · 2021Article
- Inflammatory Regulation of CNS Barriers After Traumatic Brain Injury: A Tale Directed by Interleukin-1.Frontiers in immunology · 2021Review
- Editorial: Targeting Neuroinflammation in Central Nervous System Disorders: Uncovering Mechanisms, Pharmacological Targets, and Neuropharmaceutical Developments.Frontiers in pharmacology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
In traumatic brain injury (TBI), severe disruptions occur in the choroid plexus (CP)-cerebrospinal fluid (CSF) nexus that destabilize the nearby hippocampal and subventricular neurogenic regions. Following invasive and non-invasive injuries to cortex, several adverse sequelae harm the brain interior: (i) structural damage to CP epithelium that opens the blood-CSF barrier (BCSFB) to protein, (ii) altered CSF dynamics and intracranial pressure (ICP), (iii) augmentation of leukocyte traffic across CP into the CSF-brain, (iv) reduction in CSF sink action and clearance of debris from ventricles, and (v) less efficient provision of micronutritional and hormonal support for the CNS. However, gradual post-TBI restitution of the injured CP epithelium and ependyma, and CSF homeostatic mechanisms, help to restore subventricular/subgranular neurogenesis and the cognitive abilities diminished by CNS damage. Recovery from TBI is facilitated by upregulated choroidal/ependymal growth factors and neurotrophins, and their secretion into ventricular CSF. There, by an endocrine-like mechanism, CSF bulk flow convects the neuropeptides to target cells in injured cortex for aiding repair processes; and to neurogenic niches for enhancing conversion of stem cells to new neurons. In the recovery from TBI and associated ischemia, the modulating neuropeptides include FGF2, EGF, VEGF, NGF, IGF, GDNF, BDNF, and PACAP. Homeostatic correction of TBI-induced neuropathology can be accelerated or amplified by exogenously boosting the CSF concentration of these growth factors and neurotrophins. Such intraventricular supplementation via the CSF route promotes neural restoration through enhanced neurogenesis, angiogenesis, and neuroprotective effects. CSF translational research presents opportunities that involve CP and ependymal manipulations to expedite recovery from TBI.
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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.