| gap-pubmed-20260411- | How do retinal tau pathology patterns compare to brain tau pathology in the same | open | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What molecular mechanisms link 4R tau isoform imbalance to delayed retinal cell | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Can lithium's anti-aging effects extend beyond kidney to other organ systems via | open | 0.72 | 0.00 | 2026-04-11 | 0 | | aging-biology |
| gap-pubmed-20260411- | What drives age-related GSK3β overexpression and hyperactivation in podocytes? | open | 0.77 | 0.00 | 2026-04-11 | 0 | | aging-biology |
| gap-pubmed-20260411- | How does GSK3β mechanistically regulate p16INK4A and p53 to drive senescence sig | open | 0.82 | 0.00 | 2026-04-11 | 0 | | cellular-senescence |
| gap-pubmed-20260411- | What determines the content specificity of CBS hallucinations (predominantly fac | resolved | 0.78 | 0.00 | 2026-04-11 | 0 | | visual-neuroscience |
| gap-pubmed-20260411- | Why do CBS hallucinations follow specific temporal patterns (3-5 minutes, 3 epis | open | 0.75 | 0.00 | 2026-04-11 | 0 | | neural-networks |
| gap-pubmed-20260411- | What neural mechanisms generate complex visual hallucinations in CBS patients wi | resolved | 0.80 | 0.00 | 2026-04-11 | 0 | | visual-neuroscience |
| gap-pubmed-20260411- | What mechanism links increased type I IFN-stimulated gene expression to worse ou | open | 0.79 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | Why does IL-1 signaling have protective rather than inflammatory effects in MAV- | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | Do CD11c+ cells actively uptake alpha-synuclein aggregates or acquire them throu | open | 0.82 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | What is the mechanism by which CD11c+ cells transport alpha-synuclein from brain | open | 0.85 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Can retromer-stabilizing compounds like R55 prevent neurodegeneration in vivo? | investigating | 0.87 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does impaired retromer function mechanistically lead to α-synuclein aggregat | open | 0.85 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What molecular mechanism explains why R524W but not P316S Vps35 mutations cause | open | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How do decreased BSCL2 and CDK5 protein levels causally contribute to dopaminerg | open | 0.76 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What molecular mechanisms link BSCL2 and CDK5 to circadian rhythm disruption in | resolved | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How do PV+ and SST+ interneurons differentially contribute to excitation-inhibit | resolved | 0.83 | 0.00 | 2026-04-11 | 0 | | synaptic-biology |
| gap-pubmed-20260411- | What molecular mechanisms cause interneuron dysfunction to occur upstream of amy | open | 0.85 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What mechanisms underlie vascular pathology's contribution to neurodegenerative | open | 0.78 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How do disease-specific pathological proteins differentially disrupt distinct NV | open | 0.76 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What are the specific mechanisms by which immune-mediated BBB disruption induces | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | Why does dopamine loss specifically predispose neurons to ferroptotic vulnerabil | open | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does oligomeric α-synuclein mechanistically trigger ferroptosis in dopaminer | open | 0.85 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why does Aβ42 integration only minimally improve p-tau217 diagnostic performance | open | 0.72 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What mechanisms cause kidney dysfunction to elevate plasma p-tau217 levels in no | resolved | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How do non-canonical APP processing pathways contribute to Aβ pathogenesis compa | open | 0.74 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What determines the cellular compartment-specific balance between amyloidogenic | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How do genetic polymorphisms in CHEMR23 affect ligand bias and disease susceptib | open | 0.74 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | What molecular mechanisms determine ligand-specific biased agonism at CHEMR23? | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | What mechanisms underlie TYROBP's role as a potential hub protein in AD pathogen | resolved | 0.82 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | Why is TYROBP deficiency neuroprotective when TYROBP is an adapter for multiple | partially_addressed | 0.89 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | How does the R152H GPX4 mutation cause fatal neurological defects in Sedaghatian | open | 0.72 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does GPX4 interaction with autophagy modulate neuronal fate under oxidative | open | 0.79 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What determines whether GPX4 loss triggers ferroptosis versus other cell death p | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What accounts for the safety-efficacy profile differences between tau immunother | open | 0.76 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why do broad-based tau therapies show greater promise than targeted approaches l | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does CTS specifically promote ADAM10 maturation at the molecular level? | open | 0.75 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Does CTS-mediated ADAM10/PKC-α activation translate to neuroprotection in primar | open | 0.85 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What upstream signaling pathways trigger CTS-induced PKC-α phosphorylation and a | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What upstream signals cause GRAMD1B upregulation in FTLD and AD neurons? | open | 0.72 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does GRAMD1B regulate tau phosphorylation - directly or through autophagy/li | open | 0.85 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What molecular mechanisms link GRAMD1B-mediated cholesterol transport to autopha | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How can cell-autonomous gene therapy treatments be designed to address epilepsy' | open | 0.72 | 0.00 | 2026-04-11 | 0 | | neurotherapeutics |
| gap-pubmed-20260411- | What mechanisms determine why some epilepsy gene therapies succeed in preclinica | open | 0.78 | 0.00 | 2026-04-11 | 0 | | translational-neuroscience |
| gap-pubmed-20260411- | How can gene therapy expression be precisely controlled on-demand for the delica | open | 0.85 | 0.00 | 2026-04-11 | 0 | | neurotherapeutics |
| gap-pubmed-20260411- | How do different opsin variants and stimulation parameters affect circuit-level | open | 0.77 | 0.00 | 2026-04-11 | 0 | | synaptic-biology |
| gap-pubmed-20260411- | What are the long-term safety and off-target effects of chronic optogenetic stim | resolved | 0.80 | 0.00 | 2026-04-11 | 0 | | neuroscience-methodology |
| gap-pubmed-20260411- | Will the cognitive benefits of JAK inhibition in HAND translate from mouse model | open | 0.87 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | How does baricitinib simultaneously reduce HIV reservoir maintenance while cross | open | 0.76 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |