| gap-pubmed-20260411- | Do BIN1 heterozygous and homozygous knockouts show dose-dependent effects on neu | open | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why does BIN1 show cell-type specific expression in oligodendrocytes versus glut | resolved | 0.75 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does BIN1 interaction with L-type calcium channels mechanistically regulate | resolved | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What are the specific molecular mechanisms by which BIN1 inhibits DNM2 activity? | open | 0.79 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How do AD risk-associated BIN1 polymorphisms mechanistically increase BIN1 expre | resolved | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What molecular mechanisms determine how ESCRT-III specifically holds BIN1 at aut | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does M. oleifera simultaneously reduce AChE activity while enhancing choline | open | 0.73 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Which specific bioactive compounds in M. oleifera mediate the neuroprotective ef | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Which specific phenylpropanoid compounds in ESP are responsible for the anti-AD | open | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does ESP binding to Mst1 mechanistically regulate the Nrf2/Sirt3 pathway? | open | 0.84 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does sumatriptan modulate nociceptive transmission within the trigeminovascu | open | 0.77 | 0.00 | 2026-04-11 | 0 | | pain-neurobiology |
| gap-pubmed-20260411- | Why does sumatriptan prevent migraine attacks without reducing overall headache | open | 0.79 | 0.00 | 2026-04-11 | 0 | | pain-neurobiology |
| gap-pubmed-20260411- | What criteria determine which protein-protein interactions should be prioritized | open | 0.76 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How do multiple protein-protein interactions (Drp1-Aβ, PrPC-Aβ, Mint2-PDZ) mecha | open | 0.78 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What determines which autophagy pathway defects are primary versus secondary in | open | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How do multiple autophagy targets (AMPK, mTORC1, ULK1, LRRK2, etc.) interact to | resolved | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does DJ-1-mediated gut microbiome dysbiosis influence brain pathology in Par | resolved | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What mechanisms link DJ-1 deficiency to specific gut microbiome changes (Alistip | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does the proteostasis-first adaptation mechanism fail in Alzheimer's disease | resolved | 0.85 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why does MAPT transcription decrease during proteasome but not autophagy inhibit | resolved | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Which specific transcription factors mediate MAPT suppression during proteostati | partially_addressed | 0.87 | 0.00 | 2026-04-11 | 1 | 2026-04-25 | neurodegeneration |
| gap-pubmed-20260411- | How does sphingomyelin content alter membrane lipid distribution to affect APP p | open | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why is sphingomyelin synthase elevation specific to hippocampus but not cerebell | open | 0.76 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What molecular mechanisms link elevated sphingomyelin synthase activity to incre | partially_addressed | 0.89 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What determines the heterogeneity between OPC-like and differentiated malignant | open | 0.77 | 0.00 | 2026-04-11 | 0 | | neuro-oncology |
| gap-pubmed-20260411- | How does PDGFRA signaling sustain OPC-like cells and what drives the block in di | open | 0.83 | 0.00 | 2026-04-11 | 0 | | neuro-oncology |
| gap-pubmed-20260411- | What mechanisms drive the selective vulnerability of midline CNS regions to H3K2 | open | 0.78 | 0.00 | 2026-04-11 | 0 | | neuro-oncology |
| gap-pubmed-20260411- | What is the optimal timing and duration of neurosteroid treatment for maximal ne | open | 0.81 | 0.00 | 2026-04-11 | 0 | | therapeutic-intervention |
| gap-pubmed-20260411- | Why are children disproportionately vulnerable to organophosphate neurotoxicity | open | 0.79 | 0.00 | 2026-04-11 | 0 | | neurodevelopment |
| gap-pubmed-20260411- | What molecular mechanisms underlie ganaxolone's neuroprotection against organoph | open | 0.82 | 0.00 | 2026-04-11 | 0 | | neuroprotection |
| gap-pubmed-20260411- | What triggers the neuroinflammatory response in HuR-deficient neurons and how do | open | 0.79 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | How does HuR regulate the identified target genes to prevent neuronal apoptosis | open | 0.83 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What molecular mechanisms link HuR deficiency to selective vulnerability of moto | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Will these combination therapies translate effectively from rotenone-induced PD | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How do the multiple signaling pathways (Nrf2/HO-1, NF-κB, AMPK/SIRT-1, AKT/GSK-3 | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What molecular mechanisms explain why cocoa and vinpocetine combinations showed | resolved | 0.83 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How do blood transcriptome changes in SHS relate to brain-specific neurodegenera | open | 0.74 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What mechanisms link ABC transporter dysfunction to neurodegeneration in subopti | open | 0.79 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What is the causal relationship between P2Y12R expression patterns and epilepsy | open | 0.72 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does P2Y12R nanoclustering mechanistically regulate microglial surveillance | open | 0.74 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | What mechanisms explain the discordance between ex vivo and in vivo P2Y12R micro | open | 0.79 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | What determines P2X7's dual role in both cell death and cell proliferation pathw | open | 0.76 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | How do P2X7 receptor polymorphisms mechanistically influence therapeutic respons | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why does LRRK2 modulation correct firing patterns without providing neuroprotect | open | 0.76 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What molecular mechanisms link LRRK2 kinase activity to α-synuclein-induced aber | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Do the functionally reprogrammed pericyte-derived neurons integrate into existin | open | 0.83 | 0.00 | 2026-04-11 | 0 | | stroke-recovery |
| gap-pubmed-20260411- | How does the sequential AMPK inhibition-activation protocol overcome barriers to | open | 0.79 | 0.00 | 2026-04-11 | 0 | | cellular-reprogramming |
| gap-pubmed-20260411- | What determines the distinct lineage commitment of NG2+ vs Tbx18+ pericyte subty | open | 0.82 | 0.00 | 2026-04-11 | 0 | | neuroregeneration |
| gap-pubmed-20260411- | How does divergence of epigenetic cell type identities with aging contribute to | open | 0.76 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | Why are highly cell-type-differentiated CpGs more susceptible to age-related met | open | 0.79 | 0.00 | 2026-04-11 | 0 | | epigenetic-aging |