The specific neuroprotective role of GD1a was further evidenced in the study by Bernardo et al. (2009) where increased brain levels of GD1a, through inhibition of GD3S and synthesis of gangliosides from the b-series, was shown to mitigate Aβ-associated neurotoxicity and rescue spatial-memory impairment in the double-transgenic (APP/PSEN1) mouse model of Alzheimer’s disease. The gene discussed is APP; the disease is early-onset autosomal dominant Alzheimer disease.