| gap-pubmed-20260411- | What are the developmental-specific vulnerabilities that make pediatric brains m | open | 0.81 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | How does sustained microgliosis mechanistically cause myelination defects and wh | open | 0.86 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | What molecular mechanisms drive the transition from acute to persistent neuroinf | partially_addressed | 0.89 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | How does TREM2 regulate immunometabolic switching between protective and damagin | open | 0.79 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | What determines TREM2's substrate specificity for myelin debris, amyloid beta, a | resolved | 0.82 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | How do TREM2 receptor proximal and distal signaling alterations mechanistically | resolved | 0.85 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How do the unique ADME properties of protein degraders affect their safety profi | open | 0.72 | 0.00 | 2026-04-11 | 0 | | drug-development |
| gap-pubmed-20260411- | What mechanisms underlie the unique hemotoxicity and thrombocytopenia associated | open | 0.77 | 0.00 | 2026-04-11 | 0 | | drug-development |
| gap-pubmed-20260411- | What determines the temporal progression from monocyte infiltration to irreversi | open | 0.75 | 0.00 | 2026-04-11 | 0 | | vascular-dementia |
| gap-pubmed-20260411- | How do peripheral cardiac events trigger specific monocyte chemoattractant prote | open | 0.77 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | What molecular mechanisms mediate crosstalk between brain myeloid cells and olig | open | 0.82 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | How does calpain-mediated LAMP2 cleavage specifically cause lysosome membrane pe | open | 0.81 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What determines whether neurons form autophagosomes or undergo apoptosis during | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why does autophagy inhibition improve neuronal survival when autophagy is typica | partially_addressed | 0.89 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What mechanisms control the selective packaging of misfolded proteins and altere | open | 0.78 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How do findings from cell culture and animal models translate to human neurodege | open | 0.75 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Do extracellular vesicles play a causal role in neurodegeneration pathogenesis o | open | 0.85 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why does FB1 cause opposite effects on ceramide levels in lung versus liver? | open | 0.62 | 0.00 | 2026-04-11 | 0 | | neurotoxicology |
| gap-pubmed-20260411- | What molecular mechanism explains how FB1 inhibits ceramide synthases? | open | 0.64 | 0.00 | 2026-04-11 | 0 | | neurotoxicology |
| gap-pubmed-20260411- | What are the specific epigenetic targets regulated by neuronal HDAC9? | open | 0.86 | 0.00 | 2026-04-11 | 0 | | epigenetics |
| gap-pubmed-20260411- | Why does HDAC9 expression specifically decline with age in neurons? | open | 0.80 | 0.00 | 2026-04-11 | 0 | | aging-biology |
| gap-pubmed-20260411- | What molecular mechanisms mediate HDAC9's effects on Aβ deposition and synaptic | partially_addressed | 0.89 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does the timing and intensity of exercise affect the magnitude of stress res | open | 0.79 | 0.00 | 2026-04-11 | 0 | | exercise-neuroscience |
| gap-pubmed-20260411- | What are the specific molecular mechanisms by which exercise preconditioning con | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neuroplasticity |
| gap-pubmed-20260411- | How do disease-specific intracellular environments alter TFEB post-translational | resolved | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What determines whether TFEB post-translational modifications are protective or | open | 0.85 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How do engineered microbial systems compare to natural plant compounds for AD me | open | 0.72 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What mechanisms control the bidirectional interactions between plant compounds a | open | 0.76 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How do individual microbiota profiles determine therapeutic efficacy of plant-de | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why do NfL levels not correlate with seizure burden or neurodegeneration markers | open | 0.75 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why does plasma NfL elevation resolve in chronic epilepsy while brain tissue dam | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What determines the relative therapeutic efficacy of targeting different mHTT in | open | 0.76 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why do promising preclinical peptide therapeutics for HD fail to translate to ef | open | 0.85 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why do intervention protocol variations cause high heterogeneity in electroacupu | open | 0.83 | 0.00 | 2026-04-11 | 0 | | neuromodulation |
| gap-pubmed-20260411- | What specific mechanisms link electroacupuncture's diverse molecular effects to | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neuroplasticity |
| gap-pubmed-20260411- | What drives the weak correlation between plasma GFAP and tau accumulation rates? | open | 0.70 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | Do GFAP-pathology relationships differ between typical and atypical AD variants? | open | 0.79 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why does plasma GFAP lose correlation with AD pathology in advanced disease stag | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | What determines the transition from nuclear ASC specks to cytosolic specks and I | open | 0.79 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | How does LRRK2-G2019S mechanistically intersect with NLRP3 inflammasome signalin | resolved | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What mechanisms drive nuclear ASC speck formation in microglia and how does this | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | Can therapeutic restoration of HSJ1 function rescue polyQ-induced proteostasis d | open | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Does HSJ1 sequestration by polyQ aggregates affect proteostasis of proteins beyo | open | 0.79 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What determines the selectivity of HSJ1 sequestration by different polyQ protein | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What molecular mechanisms prevent cGAS oligomerization on chromatin during mitos | open | 0.75 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | Why does cGAS selectively lose chromatin sensing ability but retain mitochondria | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | How does proteopathic tau specifically damage lysosomes to trigger this calcium- | open | 0.83 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What determines cell fate decisions between survival and death following lysosom | open | 0.76 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How do stress granules mechanistically repair damaged lysosomes beyond promoting | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What drives the formation of stress granules specifically in tau-mutant retinal | open | 0.75 | 0.00 | 2026-04-11 | 0 | | cellular-stress-response |