The interaction of SNRPD2 with nuclear retention elements significantly inhibits the export of long non-coding RNAs (lncRNAs) and mRNAs from the nucleus to the cytoplasm and knockdown of SNRPD2 leads to an increase in the cytoplasmic distribution of endogenous lncRNAs (56), which might correlate with the pathogenesis from MCI to AD; however, further study is needed. The gene discussed is SNRPD2; the disease is Alzheimer disease.