It is hypothesized that increased PGK1-mediated ATP availability in neurons allows better adaptation to the cellular challenges of aging and protein aggregation, supported by epidemiologic cohort studies of the “osins” in the treatment of Parkinson’s disease [73,74] and among patients using “osins” for benign prostatic hyperplasia (BPH) [75]. This evidence concerns the gene PGK1 and benign prostatic hyperplasia.