Results: 3

1.
Figure 2

Figure 2. From: Molecular signatures in post-mortem brain tissue of younger individuals at high risk for Alzheimer's disease as based on APOE genotype.

Heat map showing regional up- and downregulations on a case-by-case basis for the 70 transcripts identified as significant. A hierarchical clustering algorithm was applied to the expression data. The 70 transcripts identified as significant in the univariate analysis (all P-values < 0.001) are on the y axis and cases, grouped according to their similarity to their neighbors, are on the x axis. Log intensities of temporal/primary somatosensory cortex ratios are represented in colored cells. Red cells indicate relatively strong upregulation in BA 21 (temporal cortex) and downregulation in BA 1/2/3 (primary somatosensory cortex), whereas green cells indicate the converse. An APOE4 homozygote was the right-most case.

C Conejero-Goldberg, et al. Mol Psychiatry. ;16(8):836-847.
2.
Figure 3

Figure 3. From: Molecular signatures in post-mortem brain tissue of younger individuals at high risk for Alzheimer's disease as based on APOE genotype.

Gene network illustration demonstrating multiple interrelationships among eight key transcripts that were validated in RT-qPCR experiments and were found to be network eligible by IPA. Transcripts shown in red were upregulated in BA 21 (temporal cortex) in the APOE4 group and were considered susceptibility related; transcripts shown in green were upregulated in BA 1/2/3 (primary somatosensory cortex) and were considered neuroprotective in the APOE4 group. Edges indicate multiple direct and indirect relationships among the transcripts and their character. Other relevant genes added by IPA algorithm to connect smaller networks into larger networks are also shown. Most strikingly, connections between the key transcripts and APP, misprocessing of which results in amyloid aggregation, and MAPT, related to tau fibrillization, were also identified. Two of the transcripts were also identified as hub molecules: CTNNB1 and EGFR. These may have especially important roles in AD pathogenesis. A network legend is provided in the Supplementary Materials.

C Conejero-Goldberg, et al. Mol Psychiatry. ;16(8):836-847.
3.
Figure 1

Figure 1. From: Molecular signatures in post-mortem brain tissue of younger individuals at high risk for Alzheimer's disease as based on APOE genotype.

Cluster analysis of transcript patterns. (a–d) An unsupervised cluster analysis of transcript profiles yielded four patterns. Use of z-scores controlled for effects of absolute levels of signal. (a) Cluster 1 was modal and involved upregulation of the transcript in APOE4 BA 21 temporal cortex and downregulation in APOE4 BA 1/2/3 primary somatosensory cortex; expression levels in these two regions were not strikingly different in the APOE3 group. (b–c) The next most frequent pattern involved upregulation of expression in primary somatosensory cortex of the APOE4 group, with downregulation in the temporal cortex; differences between these regions in the E3 group were relatively smaller. (d) This pattern was least frequent. (e) CASP6, an example of a transcript included in cluster1. CASP6 is involved in programmed cell death. It is strongly upregulated in the temporal cortex of the APOE4 group, while modestly downregulated in the primary somatosensory cortex of the APOE4 group. This may represent a response in the APOE4 group that confers susceptibility to AD pathology. (f) FKBPL, an example of a transcript from cluster 2. FKBPL is an immunophilin that has neuroprotective properties. It was strongly upregulated in BA 1/2/3 (primary somatosensory cortex) of the APOE4 group and modestly downregulated in BA 21 (temporal cortex) of the APOE3 group, reflecting a possible neuroprotective response in BA 1/2/3. Units on the y axis represent expression in signal intensity units. Along the x axis are temporal and parietal variables, as a function of APOE group.

C Conejero-Goldberg, et al. Mol Psychiatry. ;16(8):836-847.

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