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Background  Growing evidence shows that epigenetic modifications play a role in Alzheimer’s disease (AD). We performed an epigenome-wide association study (EWAS) to evaluate the DNA methylation differences using postmortem superior temporal gyrus (STG) and inferior frontal gyrus (IFG) samples.    Results  Samples from 72 AD patients and 62 age-matched cognitively normal controls were assayed using Illumina ©  Infinium MethylationEPIC BeadChip. Five and 14 differentially methylated positions (DMPs) associated with pathology (i.e., Braak stage) with p value less than Bonferroni correction threshold of 6.79 × 10 –8  in the STG and IFG were identified, respectively. These cytosine–phosphate–guanine (CpG) sites included promoter associated cg26263477 annotated to  ABCA7  in the STG ( p  = 1.21 × 10 –11 ), and cg14058329 annotated to the  HOXA5/HOXA3/HOXA-AS3  gene cluster ( p  = 1.62 × 10 –9 ) and cg09448088 ( p  = 3.95 × 10 –9 ) annotated to  MCF2L  in the IFG. These genes were previously reported to harbor DMPs and/or differentially methylated regions (DMRs). Previously reported DMPs annotated to  RMGA ,  GNG7 ,  HOXA3 ,  GPR56 ,  SPG7 ,  PCNT ,  RP11-961A15.1, MCF2L ,  RHBDF2 ,  ANK1 ,  PCNT ,  TPRG1 , and  RASGEF1C  were replicated ( p  < 0.0001). One hundred twenty-one and 173 DMRs associated with pathology in the STG and IFG, respectively, were additionally identified. Of these, DMRs annotated to 30 unique genes were also identified as significant DMRs in the same brain region in a recent meta-analysis, while additional DMRs annotated to 12 genes were reported as DMRs in a different brain region or in a cross-cortex meta-analysis. The significant DMRs were enriched in promoters, CpG islands, and exons in the genome. Gene set enrichment analysis of DMPs and DMRs showed that gene sets involved in neuroinflammation (e.g., microglia differentiation), neurogenesis, and cognition were enriched (false discovery rate (FDR) < 0.05).    Conclusions  Twenty-two DMPs and 30 DMRs associated with pathology were replicated, and novel DMPs and DMRs were discovered.

Epigenome-wide association study of Alzheimer’s disease replicates 22 differentially methylated positions and 30 differentially methylated regions