ReviewEpilepsy research2009
Blood-brain barrier breakdown-inducing astrocytic transformation: novel targets for the prevention of epilepsy.
Review in Epilepsy research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 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
131 citing papers in PubMed, 261 citations in OpenAlex.
- Vagus nerve stimulation to augment recovery from severe traumatic brain injury impeding consciousness: a prospective pilot clinical trial.Neurological research · 2013Trial
- Increased oxidized low-density lipoprotein causes blood-brain barrier disruption in early-onset preeclampsia through LOX-1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Trial
- Association of carotid revascularization with epilepsy and seizures in patients with carotid stenosis.Epilepsia · 2026Article
- The Saga of Late-Onset Unexplained Epilepsy.Epilepsy currents · 2026Review
- Circular RNA PTPN4 Contributes to Blood-Brain Barrier Disruption during Early Epileptogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The spatial architecture of neuroimmune interactions in epilepsy.Frontiers in immunology · 2026Review
- Liver X Receptor Beta Regulates Glial Dynamics and Cortical Network Remodeling in a Freezing Lesion-Cortical Dysplasia Model.CNS neuroscience & therapeutics · 2025Article
- Characteristics of eclampsia not preceded by hypertensive disorders of pregnancy: a case control study.BMC pregnancy and childbirth · 2025Article
- An Exploratory Study on a Potential Biomarker for Seizures in Autoimmune Encephalitis.Journal of inflammation research · 2025Article
- Interictal blood-brain barrier dysfunction in piriform cortex of people with epilepsy.Annals of clinical and translational neurology · 2024Article
- Nanotechnology in Advancing Chimeric Antigen Receptor T Cell Therapy for Cancer Treatment.Pharmaceutics · 2024Review
- Evidence Implicating Blood-Brain Barrier Impairment in the Pathogenesis of Acquired Epilepsy following Acute Organophosphate Intoxication.The Journal of pharmacology and experimental therapeutics · 2024Review
- Unveiling the hidden connection: the blood-brain barrier's role in epilepsy.Frontiers in neurology · 2024Review
- Of potential new treatment targets and polythetic approach in meningoencephalitis of unknown origin: a review.Frontiers in veterinary science · 2024Review
- Pathophysiology, Management, and Therapeutics in Subarachnoid Hemorrhage and Delayed Cerebral Ischemia: An Overview.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023Review
- Astrocyte-neuron circuits in epilepsy.Neurobiology of disease · 2023Review
- Roles of NG2 Glia in Cerebral Small Vessel Disease.Neuroscience bulletin · 2023Review
- Astrocytes as a target for therapeutic strategies in epilepsy: current insights.Frontiers in molecular neuroscience · 2023Review
- Detection of blood-brain barrier dysfunction using advanced imaging methods to predict seizures in dogs with meningoencephalitis of unknown origin.Journal of veterinary internal medicine · 2022Article
- Molecular Mechanisms in the Genesis of Seizures and Epilepsy Associated With Viral Infection.Frontiers in molecular neuroscience · 2022Review
71 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 3 countries.
Funding
Abstract
Epileptogenesis is common following brain insults such as trauma, ischemia and infection. However, the mechanisms underlying injury-related epileptogenesis remain unknown. Recent studies demonstrated impaired integrity of the blood-brain barrier (BBB) during epileptogenesis. Here we review accumulating experimental evidence supporting the potential involvement of primary BBB lesion in epileptogenesis. Data from animal experiments demonstrate that primary breakdown of the BBB prone animals to develop focal neocortical epilepsy that is followed by neuronal loss and impaired functions. The extravasation of albumin from the circulation into the brain neuropil was found to be sufficient for the induction of epileptogenesis. Albumin binds to transforming growth factor beta receptor 2 (TGFbetaR2) in astrocytes and induces rapid transcriptional modifications, astrocytic transformation and dysfunction. We highlight a novel cascade of events which is initiated by increased BBB permeability, eventually leading to neuronal dysfunction, epilepsy and cell loss. We review potential mechanisms and existing experimental evidence for the important role of astrocytes and the TGFbeta pathway in epileptogenesis. Finally, we review evidence from human clinical data supporting the involvement of BBB lesion in epilepsy. We propose that primary vascular injury, and specifically BBB breakdown and repair, are key elements in altered interactions within the neurovascular unit and thus may serve as new therapeutic targets.
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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.