Prior studies have also reported significant depletion of sulfatides in Alzheimer’s disease (AD), without descriptions of the link to chain length, number of double bonds, or hydroxylation stage37,38; moreover, there is strong evidence that these changes in sulfatides in the AD brain are associated with apolipoprotein E (APOE)-related mechanisms within amyloid plaques21,39. This evidence concerns the gene APOE and early-onset autosomal dominant Alzheimer disease.