Xavier Ekolle Ndode-Ekane

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Angiogenesis and blood-brain-barrier (BBB) damage have been proposed to contribute to epileptogenesis and/or ictogenesis in experimental and human epilepsy. We tested a hypothesis that after brain injury angiogenesis occurs in the most damaged hippocampal areas with the highest need of tissue repair, and associates with formation of epileptogenic neuronal(More)
Reduced hippocampal GABAergic inhibition is acknowledged to be associated with epilepsy. However, there are no studies that had quantitatively compared the loss of various interneuron populations in different models of epilepsy. We tested a hypothesis that the more severe the loss of hippocampal interneurons, the more severe was the epilepsy.(More)
In a subgroup of patients, traumatic brain injury (TBI) results in the occurrence of acute epileptic seizures or even status epilepticus, which are treated with antiepileptic drugs (AEDs). Recent experimental data, however, suggest that administration of AEDs at the early post-injury phase can compromise the recovery process. The present study was designed(More)
Traumatic brain injury (TBI) can cause a myriad of sequelae depending on its type, severity, and location of injured structures. These can include mood disorders, posttraumatic stress disorder and other anxiety disorders, personality disorders, aggressive disorders, cognitive changes, chronic pain, sleep problems, motor or sensory impairments, endocrine(More)
Expression of urokinase-type plasminogen activator (uPA) is increased after brain injury, suggesting that, like in cancer tissue, uPA plays roles in brain remodeling. Here we injured brain with intrahippocampal kainic acid (KA) injection in adult Wt and uPA-/- mice. At 20 days post-injury, uPA-/- mice had more severe loss of contralateral pyramidal (p<0.05)(More)
Cerebrovascular changes following status epilepticus (SE) are not well understood, yet they may contribute to epileptogenesis. We studied hemodynamic changes in the cerebral cortex and amygdala by arterial spin labeling (ASL) and dynamic susceptibility contrast (DSC) MRI at 2 days and 14 days after pilocarpine-induced SE in rats. There were no cortical(More)
Hemodynamic and cerebrovascular factors are crucially involved in secondary damage after traumatic brain injury (TBI). With magnetic resonance imaging, this study aimed to quantify regional cerebral blood flow (CBF) by arterial spin labeling and cerebral blood volume by using an intravascular contrast agent, during 14 days after lateral fluid-percussion(More)
We tested the hypothesis that vascular remodeling in the cortex, hippocampus, and thalamus is associated with long-term functional recovery after traumatic brain injury (TBI). We induced TBI with lateral fluid-percussion (LFP) injury in adult rats. Animals were followed-up for 9 months, during which we tested motor performance using a neuroscore test,(More)
Urokinase-type plasminogen activator (uPA), a serine protease, converts plasminogen to plasmin. Activation of plasmin leads to degradation of the extracellular matrix, which is critical for tissue recovery, angiogenesis, cell migration, and axonal and synaptic plasticity. We hypothesized that uPA deficiency would cause an abnormal neurophenotype and would(More)
Mutation in Plaur gene encoding urokinase-type plasminogen activator receptor (uPAR) results in epilepsy and autistic phenotype in mice. In humans, a single nucleotide polymorphism in PLAUR gene represents a risk for autism spectrum disorders. Importantly, the expression of uPAR is elevated in the brain after various epileptogenic insults like traumatic(More)