We further find that the bioenergetic deficits at nerve terminals resulting from loss of SLC13A5 can be reversed by approaches that activate glycolysis, including the use of Terazosin, an FDA-approved treatment for benign prostate hyperplasia that has also been shown to activate phosphoglycerate kinase-1, the first ATP producing enzyme in glycosis16,22,23. Here, PGK1 is linked to benign prostatic hyperplasia.