| gap-pubmed-20260410- | How does GDNF overexpression increase reactive astrocyte proliferation after str | open | 0.77 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | What molecular mechanisms drive GDNF-mediated suppression of mitochondrial fissi | resolved | 0.83 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Does TDP-43-mediated HK1 sequestration occur in other neurodegenerative diseases | resolved | 0.75 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What determines the specificity of TDP-43 binding to HK1 versus other glycolytic | resolved | 0.78 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does HK1 compensation reduce cytoplasmic TDP-43 and ubiquitin accumulation? | resolved | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does intrinsic thalamic P/Q channel function regulate embryonic neurogenesis | open | 0.84 | 0.00 | 2026-04-10 | 0 | | neurodevelopment |
| gap-pubmed-20260410- | What transsynaptic signaling mechanisms coordinate T-type calcium and BK channel | open | 0.82 | 0.00 | 2026-04-10 | 0 | | synaptic-biology |
| gap-pubmed-20260410- | How do P/Q channel deficits paradoxically increase thalamic excitability despite | partially_addressed | 0.89 | 0.00 | 2026-04-10 | 0 | | synaptic-biology |
| gap-pubmed-20260410- | Why does GM1 selectively restore only 261 of the total BMAA-induced differential | open | 0.75 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What is the translational relevance of zebrafish embryo findings to human BMAA n | open | 0.72 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does GM1 specifically modulate MAPK pathway components to achieve neuroprote | open | 0.83 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does LCA's metabolic protection (downregulating GLUT4/P-AKT) relate to its n | open | 0.77 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What are the specific molecular mechanisms by which LCA regulates M1/M2 microgli | open | 0.83 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | How can biomarkers predict which cell death pathways are active in individual PD | open | 0.79 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What mechanisms drive the self-amplifying vicious cycle linking oxidative stress | partially_addressed | 0.87 | 0.00 | 2026-04-10 | 1 | 2026-04-25 | neurodegeneration |
| gap-pubmed-20260410- | How do multiple cell death pathways interact spatiotemporally during PD progress | open | 0.85 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why does astrocyte-specific APOE3Ch expression provide superior amyloid protecti | open | 0.79 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does astrocytic APOE3Ch expression lead to broad downregulation of immune an | open | 0.82 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | What molecular mechanisms enable APOE3Ch to shift amyloid aggregation toward les | open | 0.85 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why have antiglutamatergic and antioxidant therapies shown limited clinical effi | resolved | 0.82 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How do glutamate excitotoxicity and oxidative stress mechanistically interact in | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does brain ischemia signal to peripheral NK cells to suppress STAT3 expressi | resolved | 0.81 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | What are the downstream molecular mechanisms by which STAT3 activation restores | open | 0.83 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | How do different exercise modalities (cardiovascular vs resistance) differential | open | 0.81 | 0.00 | 2026-04-10 | 0 | | neuroplasticity |
| gap-pubmed-20260410- | What are the specific biophysical mechanisms by which muscle-derived exerkines c | open | 0.82 | 0.00 | 2026-04-10 | 0 | | synaptic-biology |
| gap-pubmed-20260410- | What are the optimal therapeutic targets for preventing TDP-43 neurotoxicity ver | resolved | 0.86 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why is TDP-43 pathology particularly associated with hippocampal sclerosis and s | resolved | 0.78 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does TDP-43 pathology mechanistically interact with Aβ plaques, tau tangles, | resolved | 0.85 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What is the relative therapeutic efficacy of isolated Ginsenoside Ro versus whol | open | 0.81 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does Ginsenoside Ro specifically modulate IBA1/GFAP-MAPK signaling to reduce | open | 0.84 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | What alternative pathways drive tau hyperphosphorylation if major tau kinases ar | resolved | 0.81 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What molecular mechanisms enable CDK5/p25 to protect working memory and reduce t | open | 0.82 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why does CDK5/p25 activation reduce tau phosphorylation when it's considered a m | open | 0.85 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What are the optimal mitochondrial targets and intervention strategies for enhan | open | 0.82 | 0.00 | 2026-04-10 | 0 | | therapeutic-development |
| gap-pubmed-20260410- | How do mitochondrial metabolism, dynamics, and ROS production coordinately regul | open | 0.79 | 0.00 | 2026-04-10 | 0 | | stem-cell-biology |
| gap-pubmed-20260410- | What are the specific molecular mechanisms by which mitochondrial dysfunction co | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How do disrupted neuron-microglia interactions amplify neurotoxicity beyond dire | open | 0.74 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What determines the cell-type specificity of APOE4's most pronounced effects occ | open | 0.76 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | How does APOE4-induced microglial lipid dysregulation specifically impair cleara | resolved | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why does flotillin remain unchanged in vascular dementia but decrease specifical | open | 0.76 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What mechanism causes Aβ to attenuate flotillin release from exosomes in Alzheim | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How should simultaneous tau and Aβ clearance strategies be optimized for therape | open | 0.79 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What mechanisms explain how elevated BACE1 levels contribute to AD pathogenesis | resolved | 0.82 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why do BACE1 inhibitors fail to improve cognition despite successfully reducing | resolved | 0.85 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What functional consequences result from the distinct microglial phenotype obser | open | 0.72 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | How do conflicting findings on microglial activation in MDD post-mortem studies | open | 0.73 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | Why do microglia show enhanced homeostatic markers but no inflammatory activatio | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | What cellular insults trigger acetylation at K82 in sporadic ALS patients? | open | 0.72 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What determines which post-translational modifications lead to irreversible vs r | resolved | 0.76 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does importin α1/β exert anti-aggregation activity beyond nuclear transport? | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |