Sex-conditioned effects as derived from the pathway analyses
| Sex-association | Functionality | FDR |
|---|---|---|
| Male (Younger Group) | Conservation of energy | 6.5 × 10–8 |
| Activation of AMPK by NMDAR | 3.6 × 10–3 | |
| BDNF and NGF signaling | 1.6 × 10–3 | |
| Pluripotency | 1.6 × 10–3 | |
| p38 alpha-beta signaling | 1.4 × 10–5 | |
| Dyrk1a in cell proliferation | 1.4 × 10–5 | |
| Female (Younger Group) | Post-synaptic events associated to NMDAR activation | 1.7 × 10–8 |
| Trafficking of GluR2-containing AMPAR | 5.8 × 10–6 | |
| NOS1 activity | 1.6 × 10–3 | |
| RAS activation by NMDAR | 1.0 × 10–4 | |
| PKC-gamma and Ca2+ ion signaling | 1.0 × 10–4 | |
| CREB1P-NMDAR activation | 1.0 × 10–4 | |
| BDNF signaling | 1.0 × 10–3 | |
| LTP | 4.0 × 10–5 | |
| Female (MCI Group) | p75NTR signaling | 1.6 × 10–5 |
| Cell death (mediated by NRAGE, NRIF, NADE) | 1.4 × 10–2 | |
| NTRK2/TrkB through adapters FRS2 and FRS3 | 4.8 × 10–4 |
FDR: false discovery rate; NMDAR: N-methyl-D-aspartate receptors; NTRK: neurotrophic tropomyosin-receptor kinases; BDNF: brain-derived neurotrophic factor; NGF: nerve growth factor; AMPAR: α-methyl-D-aspartate-3-hydroxy-5-methyl-4isoxazolepropionic acid receptors; LTP: long-term synaptic potentiation; MCI: mild cognitive impairment