| 🥇 | MGnD microglia expansion precedes OPC depletion across the Braak trajectory in aged human cortex | proposed | 0 | · | — |
| 🥈 | DAM/MGnD expansion precedes oligodendroglial depletion across Braak stages in AD cortex | proposed | 0 | · | — |
| 🥉 | DAM/MGnD microglia expansion precedes oligodendrocyte/OPC depletion in AD cortex and is coupled through myelin phagocytosis | proposed | 0 | · | — |
| #4 | MGnD microglia expansion is upstream of oligodendrocyte depletion in late-Braak AD cortex | proposed | 0 | · | — |
| #5 | MGnD/DAM microglia expansion precedes mature oligodendrocyte depletion across Braak stages in human AD cortex | proposed | 0 | · | — |
| #6 | MGnD expansion and oligodendrocyte loss are coupled and sequentially ordered in AD cortex by Braak stage | open | 0 | · | — |
| #7 | Hypothesis: Hybrid ARC-SARE/FOS Synthetic Enhancer Achieves ≥2× Induction Contrast for Sparse Activity at MERFISH Single-Cell Resolution | proposed | 0 | · | 0.620 |
| #8 | Hypothesis: CD8+ T cell exhaustion predicts age-associated vaccine response decline via impaired germinal centre help, not naive B cell loss alone | proposed | 4 | · | 0.550 |
| #9 | Hypothesis: CD8+ T cell exhaustion predicts age-associated vaccine response decline via impaired germinal centre help, not naive B cell loss alone | proposed | 4 | · | 0.550 |
| #10 | test | proposed | 0 | · | 0.100 |
| #11 | GBO Hypothesis: Simultaneous Wide-FOV Calcium + Neuropixels Can Distinguish Recurrence from Inhibitory-Interneuron Timescales | proposed | 0 | · | — |
| #12 | Hypothesis: Exc L2-3 IT Vulnerability via Tau-Synaptic Stripping and Microglial Complement | proposed | 0 | · | 0.600 |
| #13 | Hypothesis: CD8+ T cell exhaustion predicts age-associated vaccine response decline via impaired germinal centre help | proposed | 4 | · | 0.550 |
| #14 | Hypothesis: CD8+ T cell exhaustion predicts age-associated vaccine response decline | proposed | 0 | · | 0.550 |
| #15 | Hypothesis: Exc L2-3 IT Vulnerability via Tau-Synaptic Stripping and Microglial Complement | proposed | 0 | · | 0.600 |
| #16 | Hypothesis: Exc L2-3 IT Vulnerability via Tau-Synaptic Stripping and Microglial Complement | proposed | 0 | · | 0.600 |
| #17 | test | proposed | 0 | · | — |
| #18 | GBO trajectory test hypothesis | proposed | 0 | · | — |
| #19 | Hypothesis: Structured beta-test evaluation improves SciDEX v2 design trajectory quality | proposed | 0 | · | — |
| #20 | Hypothesis: Structured beta-test evaluation improves SciDEX v2 design trajectory quality | open | 0 | · | — |
| #21 | Alzheimer vulnerability mechanisms should be compared at cell-state resolution | proposed | 5 | · | 0.350 |
| #22 | Alzheimer vulnerability mechanisms should be compared at cell-state resolution | proposed | 5 | · | 0.350 |
| #23 | Immune-aging state shifts should be split into causal and sentinel signatures | proposed | 5 | · | 0.350 |
| #24 | Alzheimer vulnerability mechanisms should be compared at cell-state resolution | proposed | 5 | · | 0.350 |
| #25 | Alzheimer vulnerability mechanisms should be compared at cell-state resolution | proposed | 5 | · | 0.350 |
| #26 | GBO proposals that jointly optimize observability, perturbability, benchmarkability, and community reuse will dominate single-modality survey expansions. | proposed | 2 | · | 0.655 |
| #27 | Conscious access requires a recurrent workspace state that survives perturbation, not merely high decoding accuracy or task report. | proposed | 2 | · | 0.655 |
| #28 | Cell-type-resolved recurrent motifs across behavioral state will explain more cortical coding variance than feedforward receptive-field expansion alone. | proposed | 2 | · | 0.655 |
| #29 | Longitudinal clonal, cytokine, and single-cell trajectories can distinguish protective remodeling from pathological immunosenescence. | proposed | 2 | · | 0.655 |
| #30 | Immune-metabolic resilience across multiple tissues is a better healthspan control point than suppressing any single aging hallmark. | proposed | 2 | · | 0.655 |
| #31 | Alzheimer vulnerability mechanisms should be compared at cell-state resolution | proposed | 5 | · | 0.350 |
| #32 | Alzheimer vulnerability mechanisms should be compared at cell-state resolution | proposed | 5 | · | 0.350 |
| #33 | Alzheimer vulnerability mechanisms should be compared at cell-state resolution | proposed | 5 | · | 0.350 |
| #34 | Alzheimer vulnerability mechanisms should be compared at cell-state resolution | proposed | 5 | · | 0.350 |
| #35 | Alzheimer vulnerability mechanisms should be compared at cell-state resolution | proposed | 5 | · | 0.350 |
| #36 | Immune-aging state shifts should be split into causal and sentinel signatures | proposed | 5 | · | 0.350 |
| #37 | Alzheimer vulnerability mechanisms should be compared at cell-state resolution | proposed | 5 | · | 0.350 |
| #38 | Immune-aging state shifts should be split into causal and sentinel signatures | proposed | 5 | · | 0.350 |
| #39 | Alzheimer vulnerability mechanisms should be compared at cell-state resolution | proposed | 5 | · | 0.350 |
| #40 | Alzheimer vulnerability mechanisms should be compared at cell-state resolution | proposed | 5 | · | 0.350 |
| #41 | Alzheimer vulnerability mechanisms should be compared at cell-state resolution | proposed | 5 | · | 0.350 |
| #42 | Immune-aging state shifts should be split into causal and sentinel signatures | proposed | 5 | · | 0.350 |
| #43 | Alzheimer vulnerability mechanisms should be compared at cell-state resolution | proposed | 5 | · | 0.350 |
| #44 | Alzheimer vulnerability mechanisms should be compared at cell-state resolution | proposed | 1 | · | 0.350 |