TABLE 8.

Summary of discussion.

Candidate biomarker	Significant target genes	Description
hsa-miR-199a-5p	GLUT4, PIN1	Upregulated in DM and AD, causes the downregulation of target genes, resulted in hyperphosphorylation of Tau and cell death.
hsa-miR-199b-5p	PIN1	Upregulated in DM and AD, causes downregulation of PIN1, resulted in hyperphosphorylation of Tau.
hsa-miR-124-3p	BACE1, APOC1	Downregulated in DM and AD, causes upregulation of target genes, resulted in hyperphosphorylation of Tau and changing in lipid metabolism.
hsa-miR-1908-5p, hsa-miR-491-5p	APOE	Upregulated in DM and AD, causes downregulation of APOE, resulted in failing the clearance of Aβ plaques.
hsa-miR-423-5p	NECTIN2, TOMM40, HLA-C, HLA-DQA1	Dysregulated in AD causes changing in the regulation of target genes.
hsa-miR-744-5p	APOE, PIN1	Upregulated in AD, causes downregulation of target genes, resulted in failing the clearance of Aβ plaques and hyperphosphorylation of Tau.
hsa-miR-665	APOE	Downregulated in DM and AD, causes upregulation of APOE, resulted in changing in lipid metabolism.
hsa-miR-506-3p, hsa-miR-663a, hsa-miR-873- 5p, hsa-miR-1321	APOE, APOC1, TOMM40, NECTIN2, HLA-C, HLA-DQA1, HLA-DRB1	Dysregulated in AD. Introduced in this study as novel miRNAs for further analysis.
hsa-miR-4731-5p, hsa-miR-1286, hsa-miR-3184-5p	APOC1, TOMM40, NECTIN2, HLA-C, HLA-DQA1, HLA-DRB1	Introduced in this study as novel miRNAs for further analysis.
NEAT1, XIST	has-miR-124-3p, BACE1	Upregulated in AD and DM, causes downregulation of hsa-miR-124-3p, resulted in upregulation of BACE1 and hyperphosphorylation of Tau.
KCNQ1OT1	hsa-miR-199a-5p, hsa-miR-199b-5p, hsa-miR-124-3p	Dysregulated of this lncRNAs could lead to oxidative stress.
LINC00963	has-miR-665	Causes oxidative stress by target Foxo signaling pathway.
AC011481.2		Increased risk of developing T2DM and AD simultaneously by mutation in a specific loci (rs6857).
KRTAP5-AS1, STAG3LSP, SLC9A3-AS1, AC092127.1, AC010327.5, AC069281.2	hsa-miR-199a-5p, hsa-miR-199b-5p, hsa-423-5p	Introduced in this study as novel lncRNAs in the cross-talk between DM and AD.