There is a direct role for BBB dysfunction in epileptogenesis and progression of brain diseases. Under conditions of compromised BBB, efflux of serum proteins (specifically albumin) result through the TGF-b pathway with astrocytic activation and disturbed homeostasis of extracellular potassium and glutamate. These changes, in turn, are associated with neuronal hyperexcitability and altered network connectivity.
Lasting blood-brain barrier disruption induces epileptic focus in the rat somatosensory cortex.
TGF-beta receptor-mediated albumin uptake into astrocytes is involved in neocortical epileptogenesis.
Astrocytic dysfunction in epileptogenesis: consequence of altered potassium and glutamate homeostasis?
Albumin induces excitatory synaptogenesis through astrocytic TGF-β/ALK5 signalling in a model of acquired epilepsy following blood-brain barrier dysfunction.
Epileptiform activity and spreading depolarization in the blood-brain barrier-disrupted peri-infarct hippocampus are associated with impaired GABAergic inhibition and synaptic plasticity.
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