The redox status in TPI deficiency is proposed to be altered by abnormal flux through the pentose-phosphate pathway as well as potential accumulation of advanced glycation end-products (AGEs) [16,20,33,59–61], and the accumulation of redox damage in the nervous system is strongly linked with several neurodegenerative diseases [62–64]. The gene discussed is TPI1; the disease is neurodegenerative disease.