| gap-pubmed-20260410- | How do mitochondrial ROS responses modulate TRP ion channel activity and thermos | resolved | 0.77 | 0.00 | 2026-04-10 | 0 | | thermosensory-neuroscience |
| gap-pubmed-20260410- | What molecular mechanisms mediate translational control of Period2 by physiologi | open | 0.79 | 0.00 | 2026-04-10 | 0 | | circadian-neurobiology |
| gap-pubmed-20260410- | How does TDP-43 proteinopathy mechanistically promote cell death following mecha | resolved | 0.82 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why are deep-layer cortical neurons selectively vulnerable to mechanical injury | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What molecular mechanisms explain how KCNJ2 inhibition mitigates TBI-induced neu | partially_addressed | 0.89 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What is the optimal timing and combination strategy for Aβ and tau co-targeting | open | 0.78 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why do tau-targeting therapies fail clinically despite tau's stronger correlatio | open | 0.85 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why do Alzheimer's disease genes confer risk across α-synucleinopathies despite | open | 0.83 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What molecular mechanisms link RhoA/actin cytoskeleton dysfunction to α-synuclei | open | 0.84 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does PSEN2 mechanistically regulate α-synuclein expression and pathology in | partially_addressed | 0.89 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Do the PFOA-induced transcriptomic changes directly cause AD pathology or repres | open | 0.76 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does PFOA exposure cause the observed decrease in RNA translational efficien | open | 0.79 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What molecular mechanisms link pre-differentiation PFOA exposure to persistent t | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does gallic acid prevent α-synuclein aggregation - through direct protein in | open | 0.78 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What molecular mechanisms mediate gallic acid's simultaneous inhibition of both | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What determines tissue-specific vulnerability to SPRTN deficiency-induced premat | open | 0.76 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How do DPC-induced micronuclei specifically trigger cGAS-STING activation versus | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | Does electroacupuncture preconditioning versus post-stroke intervention differ i | open | 0.81 | 0.00 | 2026-04-10 | 0 | | stroke-therapy |
| gap-pubmed-20260410- | What determines the directionality and selectivity of astrocyte-to-neuron mitoch | open | 0.77 | 0.00 | 2026-04-10 | 0 | | cellular-communication |
| gap-pubmed-20260410- | How does electroacupuncture specifically activate the CD38-cADPR-Ca2+ pathway to | open | 0.79 | 0.00 | 2026-04-10 | 0 | | neuroprotection |
| gap-pubmed-20260410- | Why does Ang-1, typically neuroprotective in vascular contexts, accelerate Alzhe | open | 0.76 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does Ang-1 mechanistically drive Aβ accumulation through the FOXA2/PEN2/APP | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why does CMA hyperactivation occur broadly across cancers despite tissue-specifi | open | 0.75 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does CMA-mediated TET3 degradation mechanistically silence the cGAS-STING pa | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | What mechanisms drive MST4-mediated LAMP2A phosphorylation specifically in gliob | resolved | 0.83 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Are there additional DJ-1-independent pathways through which miRNA-122-5p promot | open | 0.79 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What mechanisms cause miRNA-122-5p upregulation specifically under hyperglycemic | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What biological mechanisms account for the additional predictive value when comb | open | 0.76 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why do plasma p-tau217 and tau-PET show equivalent predictive performance despit | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Which specific DUBs are therapeutically targetable for treating neurodegenerativ | open | 0.76 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does oxidative stress-mediated DUB inhibition contribute to neurodegeneratio | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How can TRPML1-mediated signaling modulation be translated into effective therap | resolved | 0.82 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What are the specific molecular mechanisms by which TRPML1-mediated lysosomal ca | resolved | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What determines selective vulnerability of somatostatin inhibitory neuron subtyp | open | 0.75 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does coordinated upregulation of cohesin complex and DNA damage response fac | open | 0.78 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What molecular mechanisms enable specific inhibitory neuron subtypes to confer r | open | 0.85 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-20260410-172514 | RNA binding protein dysregulation across ALS FTD AD | partially_addressed | 0.90 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why do glial endfeet show Ca2+ responses at capillaries but not arterioles durin | open | 0.78 | 0.00 | 2026-04-10 | 0 | | glial-biology |
| gap-pubmed-20260410- | What are the relative contributions of capillaries versus arterioles to overall | open | 0.85 | 0.00 | 2026-04-10 | 0 | | cerebrovascular-physiology |
| gap-pubmed-20260410- | What are the molecular mechanisms by which glial Ca2+ signaling triggers capilla | open | 0.82 | 0.00 | 2026-04-10 | 0 | | neurovascular-coupling |
| gap-pubmed-20260410- | How does SH3BP2 expression become upregulated specifically in spinal cord injury | open | 0.75 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | What are the direct molecular targets through which SH3BP2 activates the JAK/STA | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | Why do some AD GWAS hits affect inflammatory cluster proportions while others on | open | 0.74 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | How does MS4A6A mechanistically regulate the disease-associated microglia (DAM) | open | 0.79 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | What is the shared molecular conversion point by which disparate AD GWAS hits (I | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | Why have no current interventions successfully modified underlying AD disease me | resolved | 0.82 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What mechanisms underlie the 20-year preclinical phase before cognitive symptoms | open | 0.78 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why do >95% of AD cases fail to clear Aβ peptides while <5% develop disease from | open | 0.85 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What role does altered microglial inflammation play in DLK pathway activation du | open | 0.74 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | How does remyelination mechanistically prevent DLK pathway activation in damaged | open | 0.76 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |