In contrast to the rather large (299 amino acid encompassing) KCC2-CTD with its well-established protein structural role in synapse formation,4, 5 ectopic expression of the relatively compact, 100 amino acid spanning, KCC2-NTD (Supplementary Figure 1A) is a novel suitable but non-exclusive strategy to prevent neurodegeneration in TLE and other neurodegenerative diseases as it would work independently of the KCC2-CTD (involved in regulation of synapse formation) or full-length KCC2-dependent regulation of chloride transport. Here, SLC12A5 is linked to neurodegenerative disease.