Furthermore, competing theories suggested that overexpression and aggregation of GAPDH serve as the pro-apoptotic regulator in neurodegenerative diseases, which possibly interacts with a voltage-dependent anion channel and mediating permeability transition of the mitochondria, a mechanism recognized as the non-glycolytic function of GAPDH (Ishitani and Chuang, 1996; Kish et al., 1998; Tarze et al., 2007; Nakajima et al., 2009; Itakura et al., 2015; Lazarev et al., 2020). Here, GAPDH is linked to neurodegenerative disease.