| gap-pubmed-20260410- | What biological mechanisms explain how unhealthful plant-based diets specificall | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What determines the specificity of BYHW for vertebral versus other arterial terr | open | 0.76 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does BYHW achieve multi-target modulation of AGE-RAGE/NF-κB beyond simple pa | open | 0.79 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | Can aquaporin modulation provide therapeutic benefit for epilepsy and brain swel | open | 0.76 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | How do aquaporins mediate neural signal transduction in the central nervous syst | open | 0.85 | 0.00 | 2026-04-10 | 0 | | synaptic-biology |
| gap-pubmed-20260410- | What molecular mechanisms enable aquaporins to facilitate cell migration in neur | open | 0.79 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What determines which synapses become the 'strongest unpaired synapses' that und | open | 0.75 | 0.00 | 2026-04-10 | 0 | | synaptic-biology |
| gap-pubmed-20260410- | How do cell-specific E-I balance set points relate to cortical circuit function | resolved | 0.76 | 0.00 | 2026-04-10 | 0 | | circuit-neuroscience |
| gap-pubmed-20260410- | What molecular mechanisms compute dendritic Ca2+ signaling to determine heterosy | open | 0.80 | 0.00 | 2026-04-10 | 0 | | synaptic-biology |
| gap-pubmed-20260410- | How does the JNK/CDK5/GSK-3β pathway connect acetate signaling to tau hyperphosp | open | 0.77 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What mechanisms enable acetate to cross the blood-brain barrier and accumulate i | resolved | 0.79 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does CBM588 selectively increase acetate-producing bacteria without altering | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What drives the tight co-expression relationship between Abi3 and Gngt2 in AD pa | open | 0.78 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does the S209F mutation alter ABI3 phosphorylation and what are the function | open | 0.82 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What mechanisms explain why inflammatory gliosis has opposing effects on amyloid | open | 0.85 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | What are the optimal dosing regimens and treatment duration for metformin's neur | open | 0.83 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What are the specific molecular mechanisms by which metformin prevents neurodege | resolved | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What drives the temporal progression from EAAT4 loss to delayed GLAST dysfunctio | open | 0.74 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why are posterior cerebellar Purkinje cells selectively vulnerable to glutamate | open | 0.76 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What mechanisms cause GLAST loss in β-III spectrin deficiency independent of EAA | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How do sex differences in steroid biosynthesis genes contribute to ADNP syndrome | open | 0.76 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What is the causal relationship between brain atrophy seen in ASD/ID neuroimagin | open | 0.82 | 0.00 | 2026-04-10 | 0 | | neurodevelopment |
| gap-pubmed-20260410- | How does tauopathy develop in young brains with ADNP mutations versus age-relate | open | 0.85 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What determines artemether's brain penetration and bioavailability for cerebrova | open | 0.82 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does artemether specifically activate CAMKK2 to initiate the neuroprotective | open | 0.79 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How can HSF1-NLRP3 pathway modulation be translated to clinical septic brain inj | open | 0.75 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | Why is brain tissue particularly vulnerable to HSF1 deficiency-induced pyroptosi | open | 0.73 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | What is the direct molecular mechanism by which HSF1 inhibits NLRP3 in brain tis | open | 0.82 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | Which specific neurodegenerative diseases are driven by ADEPT and what determine | open | 0.79 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does the shift toward homologous-directed repair in aged neurons create vuln | open | 0.76 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What molecular mechanisms determine which transposable elements successfully hij | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Can therapeutic agents be designed to replicate β-synuclein's multi-domain inhib | open | 0.75 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How do environmental perturbations overcome β-synuclein's inherent resistance to | open | 0.79 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What are the molecular mechanisms underlying β-synuclein's multi-pronged inhibit | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How do oligodendroglia regulate lactate production versus transport to support a | open | 0.83 | 0.00 | 2026-04-10 | 0 | | cellular-metabolism |
| gap-pubmed-20260410- | Why is oligodendroglial MCT1 specifically reduced in ALS, and is this cause or c | resolved | 0.82 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What is the molecular mechanism by which oligodendroglial MCT1 disruption causes | partially_addressed | 0.89 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why do periodontal disease associations with dementia vary by age and sex? | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What mechanisms link periodontal bacterial infections to Alzheimer's disease pat | resolved | 0.85 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why do current treatment guidelines lack evidence-based recommendations for psyc | resolved | 0.76 | 0.00 | 2026-04-10 | 0 | | clinical-neuroscience |
| gap-pubmed-20260410- | What neurobiological mechanisms underlie differential drug efficacy in psychotic | open | 0.79 | 0.00 | 2026-04-10 | 0 | | neuropsychiatry |
| gap-pubmed-20260410- | How does peripheral neutrophil LRRK2 activity correlate with brain LRRK2 pathway | resolved | 0.85 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why do neutrophils express higher LRRK2 levels than other peripheral blood cells | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What is the mechanism by which fedratinib causes Wernicke's encephalopathy in ~1 | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does disrupted MCL-1/ACSL1 interaction contribute to cardiac toxicity of MCL | open | 0.82 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What is the detailed molecular mechanism by which MCL-1 binding to ACSL1 enhance | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does the gut-brain axis specifically transport butyric acid signals to regul | resolved | 0.74 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What are the specific molecular mechanisms by which butyric acid regulates HDAC4 | open | 0.83 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why does microbiota transplantation improve behavior but fail to restore butyric | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How can electrical stimulation delivery parameters be optimized for different ty | open | 0.76 | 0.00 | 2026-04-10 | 0 | | peripheral-nerve-injury |