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Aberrant mTOR signaling and disrupted autophagy: The missing link in potential vigabatrin‐associated ocular toxicity?
Author(s) -
Vogel KR,
Ainslie GR,
Pearl PL,
Gibson KM
Publication year - 2017
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1002/cpt.581
Subject(s) - vigabatrin , epilepsy , gaba transaminase , pi3k/akt/mtor pathway , adverse effect , autophagy , medicine , toxicity , pharmacology , neuroscience , bioinformatics , anticonvulsant , biology , enzyme , signal transduction , psychiatry , biochemistry , apoptosis , glutamate decarboxylase
Vigabatrin (VGB; γ‐vinylGABA) is a unique antiepileptic directly elevating CNS GABA via inactivation of the GABA metabolic enzyme GABA‐transaminase. VGB is effective in treating infantile spasms, a rare seizure disorder associated with significant morbidity. The potential for unexplained bilateral constriction of the visual field associated with VGB intervention can severely limit its temporal utility. Removal of this potential adverse effect with adjuvant intervention(s) would represent a significant advance in epilepsy therapeutics.