In both retinoic acid‐differentiated SH‐SY5Y cells and primary rat mesencephalic neurons challenged with α‐synuclein plus rotenone to mimic PD, BCH‐dependent GDH activation significantly ameliorated cell viability, improved mitochondrial ATP synthesis and lessened to control levels the cellular redox burden. The gene discussed is GLUD1; the disease is Parkinson disease.