| gap-pubmed-20260411- | What molecular mechanisms drive age-associated epigenetic drift and its relation | open | 0.78 | 0.00 | 2026-04-11 | 0 | | aging-neurobiology |
| gap-pubmed-20260411- | How can KEAP1-NRF2 system be therapeutically modulated without disrupting normal | open | 0.76 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What determines the balance between NRF2's cytoprotective versus proliferative f | open | 0.74 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does KEAP1-NRF2 system dysfunction contribute to specific neurodegenerative | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What mechanisms underlie the 'delayed start' effect preventing catch-up in lecan | open | 0.76 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why do ApoE ε4 homozygotes show different lecanemab efficacy/safety compared to | resolved | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How do impaired extracellular matrix signaling pathways contribute to early axon | open | 0.78 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What molecular mechanisms link somatodendritic ECM/WNT changes to axonal PLK1/in | open | 0.79 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does PLK1 upregulation promote mutant motor neuron survival without triggeri | resolved | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why do PD and AD show distinct neuronal vulnerability patterns despite shared gl | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What mechanisms drive the selective abatement of neuron-astrocyte interactions i | open | 0.82 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | What molecular mechanisms cause the inverse correlation between α-synuclein path | open | 0.85 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does circadian BBB regulation influence the progression of specific neurodeg | open | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What are the specific molecular mechanisms by which circadian clocks regulate BB | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurovascular-biology |
| gap-pubmed-20260411- | Which specific genes should be prioritized for CRISPR targeting in early-onset v | resolved | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What are the optimal delivery methods for CRISPR/Cas9 to cross the blood-brain b | resolved | 0.85 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does apoE specifically promote vascular versus parenchymal amyloid depositio | open | 0.76 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why does the Aβ40:42 ratio differ dramatically between CAA-positive and apoE-def | open | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What molecular mechanisms explain how apoE promotes cerebral amyloid angiopathy | partially_addressed | 0.89 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does AMPK activation specifically restore mitochondrial superoxide to physio | open | 0.79 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What molecular mechanisms link reduced mitochondrial function to non-mitochondri | open | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why do antioxidant therapies fail despite evidence of oxidative stress in diabet | open | 0.85 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What mechanisms link iron chelation to increased frontal brain volume loss in Al | resolved | 0.78 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why does iron chelation accelerate cognitive decline despite successfully reduci | open | 0.85 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does phospho-MAPT/tau initially trigger mitochondrial stress that activates | resolved | 0.81 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What determines the selectivity of PRKN for RHOT1 degradation versus other mitoc | open | 0.82 | 0.00 | 2026-04-11 | 0 | | synaptic-biology |
| gap-pubmed-20260411- | Why does PRKN-mediated mitophagy, typically protective, cause harmful mitochondr | partially_addressed | 0.89 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why does plasma p-tau217 show higher accuracy for amyloid-PET (AUC=0.95) than AD | resolved | 0.81 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What mechanisms drive the disease-specific enrichment of VEGF signaling in AD ve | open | 0.76 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why do AD and DLB show the highest proteomic similarity despite distinct patholo | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What methodological barriers prevent clinical translation of epigenetic-stem cel | open | 0.72 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How can stem cell therapy and epigenetic modulation be optimally integrated for | open | 0.76 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What are the specific mechanisms by which epigenetic modifications causally link | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why do cholinergic neurons show cell loss in pathological but not normal aging? | open | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Do β-amyloid plaques and neurofibrillary tangles cause or result from cholinergi | partially_addressed | 0.88 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What mechanisms cause cholinergic dysfunction in early AD/MCI without neuronal l | open | 0.85 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Does p38MAPK inhibition affect neuromelanin formation and dopaminergic neuron su | open | 0.77 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does TLR4 signaling crosstalk with MC1R pathways to regulate melanogenesis i | open | 0.79 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does anterograde transport of damaged mitochondria contribute to distal axon | open | 0.79 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why do tubulovesicular structures form in both mitochondrial and presynaptic mem | open | 0.74 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What molecular mechanisms cause iPLA2β deficiency to specifically damage mitocho | partially_addressed | 0.89 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What are the 'additional context-dependent constraints' limiting HSP70-CHIP regu | open | 0.81 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why does G132N CHIP restore binding in isolated domains but only partially in fu | resolved | 0.84 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What downstream effectors mediate NFκB-dependent tumor growth following PROS1-AX | open | 0.78 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does nivolumab treatment paradoxically increase AXL activation while blockin | open | 0.85 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | Why does AXL knockdown selectively induce apoptosis in mesenchymal but not prone | open | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How do changes in VEGFA-VEGFR2 pathway activity causally link to vascular dysfun | open | 0.76 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What molecular mechanisms cause decreased intercellular communication between en | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why does TRPA1 emerge as a therapeutic target when the study focuses on TRPV1 me | open | 0.74 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | How does NOD2 mechanistically link to TRPV1-MAPK/NF-κB signaling in alcohol-indu | open | 0.77 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |