The expression of both MAP2 and TUBB4 were decreased in postmortem posterior hypothalamus from Prader–Willi syndrome.92 Our findings on decreased SNORD116-13 expression in AD LCLs compared with controls, and increased expression in LCLs exhibiting higher Aβ sensitivity, suggest that some genes regulated by SNORD116 may be implicated in neurodegeneration, possibly by modifying cellular responses to chronic Aβ exposure. This evidence concerns the gene SNORD116 and Alzheimer disease.