Some lncRNA polymorphisms are associated with AD pathogenesis. For example, rs7990916 (T > C) located in the lincRNA TCONS_00021856/linc-SLITRK5-11 gene showed significant differences between AD patients and a normal control group.29 Rad18 is involved in proliferating cell nuclear antigen (PCNA) ubiquitination and plays an important role in DNA repair following nerve injury. After Aβ-induced apoptosis, the Rad18 gene antisense transcription product lncRNA NAT-Rad18, which exerts post-transcriptional control over Rad18, is upregulated, suggesting that it may enhance susceptibility to neuronal apoptosis; excess cell loss may contribute to AD.30 lncRNA 51A is an antisense transcript of intron 1 of the sorting protein-related receptor 1 (SORL1) gene, resulting in Aβ42 accumulation by altering the spliced form of SORL1 mRNA.31 Zhou et al.32 have found 24 upregulated and 84 downregulated lncRNAs in AD patients compared with controls, most being intergenic. Gene set enrichment analysis identified a downregulated lncRNA, n341006, in association with the protein ubiquitination pathway, and a significantly upregulated lncRNA, n336934, linked to cholesterol homeostasis. The lncRNA GDNFOS is a transcriptional product transcribed from the opposite strand of glial-cell-line-derived neurotrophic factor (GDNF) that may negatively regulate the expression of GDNF to promote the course of AD.33 Neuroblastoma differentiation marker 29 (NDM29), which is an RNA polymerase (pol) III-transcribed ncRNA, can be promoted by inflammatory stimuli and induces APP synthesis, leading to the increase of Aβ secretion and the process may occur in AD (Figure 1).34Figure 1Role of lncRNAs in ADBACE1-AS can bind to BACE1 mRNA, increase the stability of the latter, and promote the synthesis of BACE1 protein, further increasing the production of cell Aβ. miRNA miR-485-5p has an inhibitory effect on BACE1 expression, whereas miRNA miR-485-5p and BACE1-AS have the same binding sites on BACE1 mRNA, so their regulation of BACE1 mRNA expression is antagonistic. BC1 induces APP mRNA translation via association with FMRP. Under inflammatory stimulation, lncRNA-17A can direct GPR51 splicing to produce GABAB receptor isoform variant B, thus causing the synthesis of a non-functional GABAB receptor. In addition, overexpression of 17A causes overproduction of Aβ.