Background:

D-Galactose is a natural aldohexose and C-4 epimer of glucose.

Galactose is important for the survival and virulence of bacteria. In Escherichia coli galactose is utilized by the Leloir pathway. Two anomers of d-galactose are used for different purposes, α-d-galactose as a carbon source and β-d-galactose for induction of UDP-galactose synthesis for biosynthetic glycosylation[1].

Chronic D-galactose exposure induces neurodegeneration by enhancing caspase-mediated apoptosis and inhibiting neurogenesis and neuron migration in mice, as well as increasing oxidative damage. In addition, D-galactose-induced toxicity in mice is a useful model for studying the mechanisms of neurodegeneration and neuroprotective drugs and agents[2]. D-galactose given by oral route causes cognitive impairments in rats which are accompanied by oxidative damage. Cognitive impairments is observed in the open-field test in the 4th and 6th weeks after d-gal administration, as well as an impairment in spatial memory in the radial maze test after the 6th week of d-gal administration[3].

[1]. Csiszovszki Z, et al. Structure and function of the D-galactose network in enterobacteria. MBio. 2011 Jun 28;2(4):e00053-11. [2]. Cui X, et al. Chronic systemic D-galactose exposure induces memory loss, neurodegeneration, and oxidativedamage in mice: protective effects of R-alpha-lipoic acid. J Neurosci Res. 2006 Aug 15;84(3):647-54. [3]. Budni J, et al. Oral administration of d-galactose induces cognitive impairments and oxidative damage in rats. Behav Brain Res. 2016 Apr 1;302:35-43.