| gap-debate-20260410- | What experimental frameworks can systematically identify and validate tau epitop | open | 0.75 | 0.00 | 2026-04-10 | 0 | | drug-discovery |
| gap-debate-20260410- | How can therapeutic selectivity be achieved to avoid disrupting essential physio | open | 0.80 | 0.00 | 2026-04-10 | 0 | | pharmacology |
| gap-debate-20260410- | What structural features make pathological tau epitopes druggable compared to ph | open | 0.85 | 0.00 | 2026-04-10 | 0 | | structural-biology |
| gap-debate-20260410- | Which specific post-translational modifications distinguish pathological from ph | partially_addressed | 0.90 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-debate-20260410- | Are altered glycosylation patterns causative in tau pathology or downstream cons | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-debate-20260410- | Can glycosyltransferase modulation selectively affect tau vesicles without disru | open | 0.75 | 0.00 | 2026-04-10 | 0 | | biochemistry |
| gap-debate-20260410- | What are the mechanisms of tau vesicle trafficking and surface accessibility for | open | 0.85 | 0.00 | 2026-04-10 | 0 | | cell-biology |
| gap-debate-20260410- | Do tau-containing vesicles exhibit distinct surface glycosylation patterns compa | partially_addressed | 0.90 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-debate-20260410- | What is the relationship between HSP90 client sensitivity and partial chaperone | open | 0.75 | 0.00 | 2026-04-10 | 0 | | molecular-biology |
| gap-debate-20260410- | Can competitive displacement of tau-stabilizing immunophilins achieve therapeuti | open | 0.85 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-debate-20260410- | What are the minimal structural features required for PROTAC-mediated tau degrad | open | 0.80 | 0.00 | 2026-04-10 | 0 | | chemical-biology |
| gap-debate-20260410- | Do tau-specific HSP90 conformational states exist that differ from other client | partially_addressed | 0.90 | 0.00 | 2026-04-10 | 0 | | structural-biology |
| gap-debate-20260410- | How do metabolite concentrations quantitatively control epigenetic enzyme activi | open | 0.75 | 0.00 | 2026-04-10 | 0 | | metabolic-biochemistry |
| gap-debate-20260410- | What is the temporal stability and reversibility of epigenetic memory states est | open | 0.78 | 0.00 | 2026-04-10 | 0 | | epigenetics |
| gap-debate-20260410- | How does tissue-specific chromatin context influence therapeutic targeting of me | open | 0.82 | 0.00 | 2026-04-10 | 0 | | pharmacogenomics |
| gap-debate-20260410- | Do different priming stimuli create distinct chromatin landscapes or converge on | partially_addressed | 0.90 | 0.00 | 2026-04-10 | 0 | | epigenetics |
| gap-debate-20260410- | What are the long-term safety implications of chronic circadian rhythm manipulat | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurotoxicology |
| gap-debate-20260410- | How do REV-ERB agonists balance anti-inflammatory effects against disruption of | open | 0.75 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-debate-20260410- | Do adult therapeutic circadian interventions produce different outcomes than dev | open | 0.85 | 0.00 | 2026-04-10 | 0 | | chronobiology |
| gap-debate-20260410- | Can circadian interventions selectively target microglia without affecting other | partially_addressed | 0.90 | 0.00 | 2026-04-10 | 0 | | neuropharmacology |
| gap-debate-20260410- | How do astrocytic SQSTM1 levels affect intercellular protein aggregate propagati | open | 0.73 | 0.00 | 2026-04-10 | 0 | | protein-aggregation |
| gap-debate-20260410- | What is the therapeutic window for mitophagy enhancement before mitochondrial to | open | 0.85 | 0.00 | 2026-04-10 | 0 | | mitochondrial-biology |
| gap-debate-20260410- | Do different microglial activation states require distinct autophagy enhancement | open | 0.78 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-debate-20260410- | Can cell-type-specific autophagy modulation be achieved without cross-cellular c | open | 0.82 | 0.00 | 2026-04-10 | 0 | | drug-delivery |
| gap-pubmed-20260410- | What accounts for the selective shortening and partial stabilization of labile d | resolved | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How do tau and MAP6 actively create rather than simply bind to pre-existing stab | open | 0.79 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What molecular mechanisms determine whether tau and MAP6 segregate to different | open | 0.77 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What defines the expanded criteria for classifying proteins as microtubule-assoc | open | 0.72 | 0.00 | 2026-04-10 | 0 | | cellular-neuroscience |
| gap-pubmed-20260410- | How do MAP6's diverse molecular functions integrate to produce its effects on br | open | 0.76 | 0.00 | 2026-04-10 | 0 | | synaptic-biology |
| gap-pubmed-20260410- | What molecular pathways link specific gut bacteria changes to upregulation of Aβ | open | 0.76 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does PH-PS cross the blood-brain barrier to directly modulate brain glial po | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | What molecular mechanisms link C1q-mediated synaptosome phagocytosis to proteaso | open | 0.85 | 0.00 | 2026-04-10 | 0 | | synaptic-biology |
| gap-pubmed-20260410- | How does Alectinib, a kinase inhibitor, achieve high-affinity binding to complem | partially_addressed | 0.87 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | What is the molecular trajectory linking acute SARS-CoV-2 infection to persisten | open | 0.78 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How do peripheral immune cell infiltration patterns through the disrupted BBB de | open | 0.76 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | What molecular mechanisms drive the shared transcriptomic signatures between Lon | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What are the specific mechanisms by which SGLT2 inhibitors reduce beta-amyloid a | open | 0.76 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How do GLP-1 agonists achieve cardioprotection despite increasing sympathetic ac | open | 0.79 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why do DPP-4 inhibitors show neuroprotective effects but increase heart failure | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What temporal relationship exists between systemic inflammatory triggers and AD | open | 0.81 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How can therapeutic targeting distinguish between protective and pathological im | resolved | 0.82 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | What specific mechanisms link peripheral inflammaging to central neuroinflammati | open | 0.85 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | How does loss of PIP3 binding capacity causally link to proteostasis, apoptosis, | open | 0.76 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What molecular mechanisms cause the remarkable overlap in PIP3-binding protein a | resolved | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How do FOXO functions differ between healthy, aged, and diseased brain states? | open | 0.82 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What are the specific molecular mechanisms by which FOXO/DAF-16 regulates neuron | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-debate-20260410- | What is the therapeutic window between effective TDP-43 modulation and disruptio | open | 0.75 | 0.00 | 2026-04-10 | 0 | | translational-medicine |
| gap-debate-20260410- | How do post-translational modifications quantitatively alter TDP-43 phase separa | resolved | 0.80 | 0.00 | 2026-04-10 | 0 | | molecular-biophysics |
| gap-debate-20260410- | Which TDP-43 biomarkers can reliably distinguish between reversible phase separa | resolved | 0.85 | 0.00 | 2026-04-10 | 0 | | clinical-neuroscience |
| gap-debate-20260410- | What are the specific design principles for small molecules that can selectively | partially_addressed | 0.90 | 0.00 | 2026-04-10 | 0 | | medicinal-chemistry |