| gap-pubmed-20260411- | What determines the transition from acute protective P2Y2R signaling to chronic | open | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does P2Y2R activation simultaneously promote both neuroprotective and pro-in | open | 0.85 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | Do the 432 differentially expressed proteins represent cause or consequence of A | open | 0.85 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What are the functional roles and pathogenic mechanisms of novel AD-associated p | open | 0.83 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What are the clinical limitations of A2AR antagonists and GLP1R agonists that re | open | 0.74 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How do GLP1R agonists mechanistically reduce neuroinflammation in PD brain tissu | open | 0.77 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | What are the precise molecular mechanisms underlying A2AR-D2R antagonistic inter | open | 0.79 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What molecular features determine which nuclear import receptors can rescue TDP- | resolved | 0.77 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does the NLS-independent KPNB1 mechanism reconcile with established nuclear | resolved | 0.76 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What determines the specificity of KPNB1 recruitment to pathological vs. physiol | resolved | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What are the specific therapeutic targets within AQP1 ion channel function for t | resolved | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How do specific neurotransmitters and neuropeptides mechanistically modulate CSF | open | 0.79 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What are the molecular mechanisms that regulate AQP1 ion channel gating in choro | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does the hydrophobic lubricant coating maintain electrical insulation while | open | 0.78 | 0.00 | 2026-04-11 | 0 | | neural-engineering |
| gap-pubmed-20260411- | What specific molecular mechanisms enable lubricant coatings to reduce neuroinfl | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | Can selective orexin receptor antagonists modulate ischemic outcomes and establi | resolved | 0.83 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does increased cortical OX1R expression contribute to ischemic cell death me | open | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What mechanisms drive selective OX1R upregulation while OX2R remains unchanged a | open | 0.77 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What downstream circuit targets mediate the opposing effects of ACC CaMKII+ vers | resolved | 0.76 | 0.00 | 2026-04-11 | 0 | | pain-neuroscience |
| gap-pubmed-20260411- | How do PV+ and SST+ interneuron subtypes mechanistically segregate social prefer | open | 0.79 | 0.00 | 2026-04-11 | 0 | | social-neuroscience |
| gap-pubmed-20260411- | What mechanisms explain the functional 'conflict' whereby ACC GABAergic activati | resolved | 0.80 | 0.00 | 2026-04-11 | 0 | | pain-neuroscience |
| gap-pubmed-20260411- | Why has Nurr1's role in autophagy-lysosomal regulation been overlooked despite i | open | 0.79 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does Nurr1 mechanistically regulate autophagy-lysosomal pathway function thr | resolved | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What therapeutic targets can be derived from understanding FTD pathogenic mechan | open | 0.74 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why do 50-70% of FTD cases occur sporadically without identifiable genetic mutat | open | 0.76 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What mechanisms determine the correlation between clinical FTD phenotypes and sp | open | 0.79 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does the NEB-PVALB vagal pathway integrate with central respiratory networks | open | 0.74 | 0.00 | 2026-04-11 | 0 | | respiratory-neurobiology |
| gap-pubmed-20260411- | What determines the anatomical specificity of PVALB+ vagal neurons for NEBs vers | open | 0.73 | 0.00 | 2026-04-11 | 0 | | developmental-neurobiology |
| gap-pubmed-20260411- | How do NEBs mechanistically distinguish airway closure from other mechanical sti | open | 0.80 | 0.00 | 2026-04-11 | 0 | | sensory-neurobiology |
| gap-pubmed-20260411- | What determines the phenotypic spectrum boundaries between ALS and other neurode | open | 0.75 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does the exposome interact with genetic risk factors through the gene-time-e | open | 0.72 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How do mutations in different ALS genes converge on the same dysregulated pathwa | resolved | 0.85 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Is collateral degradation a general mechanism across other protein aggregation d | open | 0.76 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What determines whether sequestered ESCRT-III proteins undergo collateral degrad | open | 0.75 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How do α-synuclein aggregates specifically recognize and bind the conserved α-he | open | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Is targeting α-synuclein therapeutically viable given its physiological function | open | 0.78 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does α-synuclein accumulation in peripheral tissues mechanistically contribu | open | 0.76 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What are the specific mechanisms by which pathological α-synuclein promotes neur | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | What determines disease-specific vulnerability despite shared Nrf2-Keap1 dysfunc | open | 0.81 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does hydrogen sulfide mechanistically modulate Nrf2-Keap1 signaling in neuro | open | 0.79 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What are the broader implications of dysregulated lysosomal TBK1 signaling for l | open | 0.75 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does constitutive lysosomal TBK1 accumulation in ALS-FTD mutants cause neuro | open | 0.85 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What is the molecular mechanism by which amino acids recruit TBK1 to lysosomes? | open | 0.80 | 0.00 | 2026-04-11 | 0 | | cellular-metabolism |
| gap-pubmed-20260411- | What structural features of α-synuclein PFF confer high-affinity binding to LAG3 | open | 0.85 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does LAG3-mediated α-synuclein transmission relate to other proposed cellula | open | 0.79 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What molecular mechanisms mediate LAG3-dependent α-synuclein PFF endocytosis and | open | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why do current therapies focus primarily on aggregate clearance rather than prev | resolved | 0.79 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How do loss-of-function and gain-of-function TDP-43 mechanisms interact to drive | resolved | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What upstream mechanisms initially trigger TDP-43 nuclear clearance and cytoplas | resolved | 0.85 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How do RCD-released DAMPs specifically sustain the inflammation-cell death ampli | open | 0.79 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |