At the molecular level and consistent with numerous reports on placing mitochondrial dysfunction at the center of initiation and propagation of cognitive and behavioral abnormalities in neurological/neurodegenerative diseases20, our research group was the first to report mitochondrial dysfunction (reflected as a shift from mitochondrial bioenergetics to glycolysis, a.k.a. the Warburg effect) in carriers of the premutation even before developing overt FXTAS symptoms21–24, results expanded by our team and others in a variety of biospecimens21–23,25–29 and mouse Fmr1 premutation models26,30,31. Here, FMR1 is linked to fragile X-associated tremor/ataxia syndrome.