PMC:6891841 / 24100-24848 JSONTXT

{"project":"testtesttest","denotations":[{"id":"T229","span":{"begin":96,"end":98},"obj":"Body_part"},{"id":"T230","span":{"begin":576,"end":578},"obj":"Body_part"}],"attributes":[{"id":"A229","pred":"uberon_id","subj":"T229","obj":"http://purl.obolibrary.org/obo/UBERON_0001885"},{"id":"A230","pred":"uberon_id","subj":"T230","obj":"http://purl.obolibrary.org/obo/UBERON_0001885"}],"text":"Highlights\nThe concepts underlying TLE have changed, especially with respect to the role of the DG.\nMesial temporal sclerosis and selective vulnerability of hilar cells are still discussed but we know that there is more to TLE than MTS. Concepts like MF sprouting are still important but the role of glia, inflammation, and diverse aspects of genetics are increasingly appreciated.\nThe advent of animal models with spontaneous seizures has been a boost to epilepsy research, but also creates debate about what is the best model.\nMore evidence has been gathered to support the DG “gate” hypothesis but much more needs to be done. Fortunately, improved methods have provided exciting new opportunities for both empirical and computational approaches."}