| gap-debate-20260410- | How do protein-protein interaction networks differ between PSP and CBD to produc | open | 0.75 | 0.00 | 2026-04-10 | 0 | | systems-biology |
| gap-debate-20260410- | Why have antioxidant approaches consistently failed in tauopathies despite oxida | open | 0.70 | 0.00 | 2026-04-10 | 0 | | clinical-neuroscience |
| gap-debate-20260410- | What specific cellular machinery differences between brain regions select for di | open | 0.80 | 0.00 | 2026-04-10 | 0 | | molecular-biology |
| gap-debate-20260410- | Do tau strains or regional cellular environments primarily drive PSP vs CBD path | partially_addressed | 0.90 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-debate-20260410- | Can stellate neuron-specific biomarkers predict therapeutic response in early AD | open | 0.75 | 0.00 | 2026-04-10 | 0 | | clinical-research |
| gap-debate-20260410- | How do AD pathological proteins specifically disrupt stellate neuron ion channel | open | 0.80 | 0.00 | 2026-04-10 | 0 | | molecular-biology |
| gap-debate-20260410- | What is the temporal sequence of cholinergic loss versus stellate neuron death i | open | 0.85 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-debate-20260410- | Do stellate neurons express unique α7 nicotinic receptor subtypes that could ena | partially_addressed | 0.90 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-debate-20260410- | What is the optimal timing window for gut-brain axis interventions relative to A | open | 0.71 | 0.00 | 2026-04-10 | 0 | | clinical-neurology |
| gap-debate-20260410- | How do microglial activation states beyond M1/M2 respond to gut-derived metaboli | open | 0.75 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-debate-20260410- | Which specific bacterial strains can restore tight junction integrity while surv | open | 0.78 | 0.00 | 2026-04-10 | 0 | | microbiome-therapeutics |
| gap-debate-20260410- | What are the minimum therapeutic SCFA concentrations needed in brain tissue to a | open | 0.82 | 0.00 | 2026-04-10 | 0 | | neuropharmacology |
| gap-debate-20260410- | Does restoration of cholesterol-chromatin acetylation coupling require cell-type | resolved | 0.71 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-debate-20260410- | How do astrocytes transfer chromatin-modifying metabolites to neurons and how is | open | 0.75 | 0.00 | 2026-04-10 | 0 | | neurobiology |
| gap-debate-20260410- | What are the discrete molecular components of chromatin oscillators that become | open | 0.78 | 0.00 | 2026-04-10 | 0 | | epigenetics |
| gap-debate-20260410- | Can pulsed vs continuous OSK expression achieve partial reprogramming without ne | open | 0.82 | 0.00 | 2026-04-10 | 0 | | cellular-reprogramming |
| gap-20260410-095113 | Do these mechanistic hypotheses from the SEA-AD Atlas bundle explain layer-speci | partially_addressed | 0.90 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-20260410-094512 | Do these mechanistic hypotheses explain layer-specific synaptic vulnerability in | partially_addressed | 0.90 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-20260410-093153 | Mechanistic validation of SEA-AD differential expression hypotheses: Complement | partially_addressed | 0.90 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-20260410-091509 | Investigate mechanisms of epigenetic reprogramming in aging neurons, including D | resolved | 0.90 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-20260410-091440 | Investigate mechanisms of epigenetic reprogramming in aging neurons, including D | partially_addressed | 0.90 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-20260410-091107 | Investigate mechanisms of epigenetic reprogramming in aging neurons | partially_addressed | 0.90 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-20260410-090500 | Investigate mechanisms of epigenetic reprogramming in aging neurons | resolved | 0.90 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why does IGF2BP1 exhibit dual regulatory roles in both neuronal ferroptosis and | open | 0.75 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | What are the specific molecular signals mediating IGF2BP1-dependent microglia-ne | open | 0.83 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | How does IGF2BP1 mechanistically regulate Keap1/Nrf2 signaling through m6A modif | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | Why does microglial depletion alone provide modest neuroprotection in rd10 retin | open | 0.75 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | How does IGF-I shift microglia from detrimental to protective phenotypes in neur | open | 0.82 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | What molecular mechanisms mediate IGF-I's neuroprotective effects through microg | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What determines the variable treatment response to carbamazepine and oxcarbazepi | open | 0.83 | 0.00 | 2026-04-10 | 0 | | pain-neurobiology |
| gap-pubmed-20260410- | How does focal demyelination of trigeminal afferents lead to hyperexcitable neur | open | 0.81 | 0.00 | 2026-04-10 | 0 | | pain-neurobiology |
| gap-pubmed-20260410- | What mechanisms link genetic predisposition to the specific anatomical and neuro | open | 0.79 | 0.00 | 2026-04-10 | 0 | | pain-neurobiology |
| gap-pubmed-20260410- | How can chronic pain treatment be optimized while minimizing addiction risk in l | open | 0.75 | 0.00 | 2026-04-10 | 0 | | pain-neurobiology |
| gap-pubmed-20260410- | What mechanisms underlie opioid receptor plasticity and how do they contribute t | open | 0.80 | 0.00 | 2026-04-10 | 0 | | synaptic-biology |
| gap-pubmed-20260410- | What determines the region-specific patterns of microglial synaptic engulfment i | open | 0.75 | 0.00 | 2026-04-10 | 0 | | synaptic-biology |
| gap-pubmed-20260410- | Why does reduced microglial amyloid engulfment not worsen amyloid pathology in t | open | 0.82 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does microglial C1q induce astrocytic C3 protein without affecting C3 mRNA l | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | Do elevated LPS-containing bEVs in AD plasma represent cause or consequence of n | open | 0.74 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What is the molecular mechanism linking microglial Piezo1 activation to C1q-C3 c | open | 0.76 | 0.00 | 2026-04-10 | 0 | | synaptic-biology |
| gap-pubmed-20260410- | How does LPS specifically enable bacterial extracellular vesicles to penetrate t | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | How does complement activation contribute to cognitive deficits across different | open | 0.78 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What mechanisms determine when complement-mediated synaptic pruning switches fro | open | 0.85 | 0.00 | 2026-04-10 | 0 | | synaptic-biology |
| gap-pubmed-20260410- | What drives the coordinated epigenomic-transcriptomic dysregulation patterns in | open | 0.79 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How do epigenomic stability dynamics causally contribute to cognitive resilience | open | 0.82 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What molecular mechanisms drive the widespread epigenome relaxation observed dur | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why do different diagnostic methods across studies still yield consistent geneti | open | 0.70 | 0.00 | 2026-04-10 | 0 | | psychiatric-genetics |
| gap-pubmed-20260410- | What are the functional roles of FBXL4 and RSRC1 upregulation in MDD pathogenesi | open | 0.76 | 0.00 | 2026-04-10 | 0 | | psychiatric-neurobiology |
| gap-pubmed-20260410- | How do genetic variants at 6q16.2, 12q24.31, and 16p13.3 mechanistically regulat | open | 0.80 | 0.00 | 2026-04-10 | 0 | | psychiatric-genetics |
| gap-debate-20260410- | How do small molecules partition into and modulate the composition of pathologic | open | 0.75 | 0.00 | 2026-04-10 | 0 | | drug-discovery |
| gap-debate-20260410- | What biomarkers can detect condensate dysfunction in living patients with neurod | resolved | 0.80 | 0.00 | 2026-04-10 | 0 | | clinical-neuroscience |