The neurovasculature as a target in temporal lobe epilepsy.
Yvonne ReissSebastian BauerBastian DavidKavi DevrajElif FidanElke HattingenStefan LiebnerNico MelzerSven G MeuthFelix RosenowTheodor RüberLaurent M WillemsKarl H PlatePublished in: Brain pathology (Zurich, Switzerland) (2023)
The blood-brain barrier (BBB) is a physiological barrier maintaining a specialized brain micromilieu that is necessary for proper neuronal function. Endothelial tight junctions and specific transcellular/efflux transport systems provide a protective barrier against toxins, pathogens, and immune cells. The barrier function is critically supported by other cell types of the neurovascular unit, including pericytes, astrocytes, microglia, and interneurons. The dysfunctionality of the BBB is a hallmark of neurological diseases, such as ischemia, brain tumors, neurodegenerative diseases, infections, and autoimmune neuroinflammatory disorders. Moreover, BBB dysfunction is critically involved in epilepsy, a brain disorder characterized by spontaneously occurring seizures because of abnormally synchronized neuronal activity. While resistance to antiseizure drugs that aim to reduce neuronal hyperexcitability remains a clinical challenge, drugs targeting the neurovasculature in epilepsy patients have not been explored. The use of novel imaging techniques permits early detection of BBB leakage in epilepsy; however, the detailed mechanistic understanding of causes and consequences of BBB compromise remains unknown. Here, we discuss the current knowledge of BBB involvement in temporal lobe epilepsy with the emphasis on the neurovasculature as a therapeutic target.
Keyphrases
- blood brain barrier
- temporal lobe epilepsy
- cerebral ischemia
- end stage renal disease
- healthcare
- newly diagnosed
- chronic kidney disease
- resting state
- white matter
- inflammatory response
- multiple sclerosis
- palliative care
- prognostic factors
- single cell
- functional connectivity
- subarachnoid hemorrhage
- endothelial cells
- brain injury
- single molecule
- spinal cord
- drug induced
- patient reported