Table 2.
List of differential regulated genes (DRGs) and corresponding p-value<0.05 of differential co-expression enrichment (DCe) in temporal cortex, frontal cortex and hippocampus datasets
| Gene name | DCe p-value | Description | |
|---|---|---|---|
| Temporal cortex | ARID1A | 0.00069 | ARID1A was among down-regulated genes in AD model mice (17) |
| Cdc42 | 0.01224 | Cdc42 activity was increased in hippocampus neurons treated with fibrillary β-amyloid (18) | |
| LPPR4 | 0.01395 | LPPR4 was up-regulated in incipient AD patients (19) | |
| PITHD1 | 0.01863 | // | |
| SGIP1 | 0.02064 | // | |
| SZT2 | 0.01936 | // | |
| ZMPSTE24 | 0.01936 | // | |
| Frontal cortex | CHD5 | 5.19E-14 | The depletion of CHD5 was shown to be linked with AD associated gene sets (20) |
| EFHD2 | 3.00E-07 | EFhd2 has been found to be associated with aggregated tau in the brain in AD and in a mouse model of frontotemporal dementia (21,22) | |
| Prxs | 7.82E-07 | Peroxiredoxins (Prxs) may be associated with AD by reducing ROS elicited by amyloid β (Aβ) accumulation that could be a causative factor in the pathogenesis of AD (23) | |
| MAGIE3 | 1.68E-06 | // | |
| EXTL1 | 4.14E-06 | // | |
| HPCAL4 | 2.09E-05 | HPCAL4 could be used as a prognostic marker for cognitive decline in AD (24) | |
| LPHN2 | 2.59E-05 | LPHN2 is likely to be participated in AD as an altered protein in Lipid Raft (25) | |
| NIPAL3 | 8.35E-05 | NIPAL3 was shown as a biomarker in Late-Onset Major Depressive Disorder (26) | |
| CACNA1E | 0.00017 | CACNA1E was down-regulated in cerebral Cockayne syndrome (27) | |
| IFI16 | 0.00033 | IFI16 was participated in delaying onset of AD (28) | |
| HHLA3 | 0.00122 | // | |
| KCNK1 | 0.00202 | KCNK1 exhibited alternative splicing in patients with mesial temporal lobe epilepsy (29) | |
| rnpc3 | 0.00384 | // | |
| DCAF6 | 0.00542 | // | |
| IPO13 | 0.00581 | IPO13 mutants involved in chronic inflammatory diseases (30) | |
| RPL11 | 0.00585 | RPL11 revealed significant altered expression profiles in the neuron model of AD treated with rhTFAM (31) | |
| S100A1 | 0.00716 | S100A1 modulates inflammation in AD (32) | |
| CNTN2 | 0.02606 | CNTN2 associated with AD via BACE1 activity (33) | |
| GRIK3 | 0.03774 | GRIK3 was highly expressed in major depression (34) | |
| Hippocampus | KCNK1 | 1.55E-09 | // |
| CHRNB2 | 2.37E-09 | CHRNB2 was found to interfere with the immune system in neurologic disorders (35) | |
| HAPLN2 | 3.43E-05 | Hapln2 has been recently shown to be accumulated in the neurofibrillary tangle of Alzheimer’s brain (36) | |
| Slc2a1 | 0.00207 | Slc2a1 down-regulation exacerbated AD (37) | |
| FABP3 | 0.00298 | serum levels of brain-type FABP are elevated in a significant proportion of patients with various neurodegenerative diseases including AD (38) | |
| DEGS1 | 0.00327 | DEGS1 is likely to be involved in AD as an altered protein in Lipid Raft (25) | |
| NKAIN1 | 0.00435 | // | |
| S100A1 | 0.00434 | S100A1 modulates inflammation in AD (32) | |
| CNTN2 | 0.00511 | CNTN2 associated with AD via b-Secretase (BACE1) activity (33) | |
| SFPQ | 0.00816 | SFPQ was shown as a transcription factor with an altered nucleo-cytoplasmic distribution under neurodegenerative conditions (39) | |
| GPSM2 | 0.01073 | // | |
| GSTM1 | 0.01591 | GSTM1 null genotype was found as risk factor for late-onset Alzheimer’s disease in Italian patients (40) | |
| CACHD1 | 0.02830 | CACHD1 is a substrate of BACE1 responsible for generating the amyloid-b protein (41) | |
//
showing DRGs with ambiguous role in neurologic disorders.