Additional file 1: of Polygenic analysis of inflammatory disease variants and effects on microglia in the aging brain

Supplementary Methods, Results, and Figures. (DOCX 1972 kb

Additional file 2: Table S2. of Dissecting the role of non-coding RNAs in the accumulation of amyloid and tau neuropathologies in Alzheimer’s disease

A table to assess whether the various demographic and neuro-pathological variables may be confounding the relationship between miRNA expression and pathological AD. A linear model is used to model miRNA expression by Study, Age at death, Sex, neuronal proportion (NNLS), post-mortem interval (PMI), RNA Integrity number (RIN) and pathological AD. The effect of pathological AD on the miRNA is reported (coef.AD) as well as the probability of observing this effect or something more extreme assuming that it should be zero (pval.AD). Then for each of the covariates a model is fit without including this covariate in the model and the effect of AD on miRNA expression is calculated again; e.g. pval.AD (−Age) is from the model not including Age at death. (CSV 28 kb

Additional file 8: of Integrated biology approach reveals molecular and pathological interactions among Alzheimer’s Aβ42, Tau, TREM2, and TYROBP in Drosophila models

Table S7. Functional enrichment of DEGs identified in Tau/TREM2WT/TYROBP, Tau/TREM2R47H/TYROBP files. (XLSX 23 kb

Additional file 3: Table S4. of Dissecting the role of non-coding RNAs in the accumulation of amyloid and tau neuropathologies in Alzheimer’s disease

Reported are the p-value and beta coefficient for the association of each lincRNA with AD, NP and NFT from a series of linear models which include Study, Age at death, Sex, neuronal proportion (NNLS), post-mortem interval (PMI) and RNA Integrity number (RIN) as covariates. (CSV 69 kb

Additional file 4: of Integrated biology approach reveals molecular and pathological interactions among Alzheimer’s Aβ42, Tau, TREM2, and TYROBP in Drosophila models

Table S3. Functional enrichment of DEGs identified in Aβ42, Aβ42/TREM2WT/TYROBP, and Aβ42/TREM2R47H/TYROBP files. (XLSX 23 kb

Additional file 10: of Integrated biology approach reveals molecular and pathological interactions among Alzheimer’s Aβ42, Tau, TREM2, and TYROBP in Drosophila models

Table S9 Module membership from weighted gene co-expression network analysis for ROSMAP gene expression data. (XLSX 456 kb

Additional file 6: of Integrated biology approach reveals molecular and pathological interactions among Alzheimer’s Aβ42, Tau, TREM2, and TYROBP in Drosophila models

Table S5. Overlap between MSigDB gene ontology/pathway gene sets and fly-human conserved genes. (XLSX 299 kb

Additional file 7: of Integrated biology approach reveals molecular and pathological interactions among Alzheimer’s Aβ42, Tau, TREM2, and TYROBP in Drosophila models

Table S6. Functional enrichment of DEGs identified in TREM2WT/TYROBP, TREM2R47H/TYROBP, and Tau files. (XLSX 18 kb

Additional file 1: of Integrated biology approach reveals molecular and pathological interactions among Alzheimer’s Aβ42, Tau, TREM2, and TYROBP in Drosophila models

Figure S1. No significant alteration in either the gross morphology of brain structures or the number of neuronal and glial cells was observed in TREM2/TYROBP flies. Figure S2. Molecular pathways affected by neuronal expression of Aβ42 and glial expression of TREM2/TYROBP. Figure S3. Molecular pathways affected by tau do not overlap with those affected by glial TREM2/TYROBP. Figure S4. Gene expression signatures in tau/TREM2/TYROBP flies. Figure S5. Heatmap showing the topological overlapping matrix (TOM) from weighted gene co-expression network analysis. Table S11. Primer sequences for RT-PCR and qRT-PCR. (PDF 4937 kb

Additional file 3: of Integrated biology approach reveals molecular and pathological interactions among Alzheimer’s Aβ42, Tau, TREM2, and TYROBP in Drosophila models

Table S2. Functional enrichment of DEGs identified in TREM2WT/TYROBP, TREM2R47H/TYROBP, and Aß42 files. (XLSX 23 kb