(Chen et al. 2018) Excessive buildup of  Tau, a protein that binds to microtubules in the brain, has been found in patients with Alzheimer’s Disease, and specifically, in a mouse model of Alzheimer’s with epilepsy. As such, finding ways to reduce the buildup of Tau has been the subject of research in epilepsy for the past several years. Mapt, the gene that codes for the production of Tau in mice, can be deleted and this deletion has been shown to reduce hyperexcitability as well as disease symptoms in mouse models of epilepsy including Scn1a and Kcna1.

This study looked at two additional mouse models (Scn1b and Scn8a) and how deletion of Mapt affects disease course. Unfortunately, the authors found deletion of Mapt did not prolong the survival of mice in either model, suggesting it is a gene-specific phenomenon and not generalizable across multiple epilepsy syndromes.

Chen C, Holth JK, Bunton-Stasyshyn R, Anumonwo CK, Meisler MH, Noebels JL, Isom LL. Mapt deletion fails to rescue premature lethality in two models of sodium channel epilepsy. Ann Clin Transl Neurol. 2018 Jul 5;5(8):982-987. doi: 10.1002/acn3.599. eCollection 2018 Aug. PubMed PMID: 30128323; PubMed Central PMCID: PMC6093838.