| gap-pubmed-20260412- | How does disrupted phosphatidylcholine metabolism mechanistically link to impair | open | 0.76 | 0.00 | 2026-04-12 | 0 | | neurodegeneration |
| gap-pubmed-20260412- | What determines the cell-type specificity of ABCA7 variant effects despite wides | open | 0.77 | 0.00 | 2026-04-12 | 0 | | neurodegeneration |
| gap-pubmed-20260412- | How does ABCA7 dysfunction specifically cause neuronal hyperexcitability in Alzh | open | 0.84 | 0.00 | 2026-04-12 | 0 | | neurodegeneration |
| gap-pubmed-20260412- | What are the specific downstream targets and pathways through which MIR27A and M | open | 0.76 | 0.00 | 2026-04-12 | 0 | | neurodegeneration |
| gap-pubmed-20260412- | How do MIR27A and MIR146A polymorphisms mechanistically alter miRNA-target inter | open | 0.80 | 0.00 | 2026-04-12 | 0 | | neurodegeneration |
| gap-pubmed-20260412- | Does Orai1 regulation of astrocyte reactivity apply to chronic neurodegeneration | open | 0.74 | 0.00 | 2026-04-12 | 0 | | neurodegeneration |
| gap-pubmed-20260412- | What downstream signaling pathways link astrocyte Orai1 to inhibitory neurotrans | open | 0.76 | 0.00 | 2026-04-12 | 0 | | neuroinflammation |
| gap-pubmed-20260412- | How does Orai1-mediated calcium signaling mechanistically control astrocyte meta | open | 0.80 | 0.00 | 2026-04-12 | 0 | | neuroinflammation |
| gap-pubmed-20260412- | What are the long-term consequences of STOP dysfunction for mitotic fidelity and | open | 0.71 | 0.00 | 2026-04-12 | 0 | | neurodegeneration |
| gap-pubmed-20260412- | How does calmodulin regulate STOP protein function in microtubule stabilization? | resolved | 0.74 | 0.00 | 2026-04-12 | 0 | | cellular-neuroscience |
| gap-pubmed-20260412- | What molecular mechanisms determine tissue-specific STOP protein association pat | resolved | 0.77 | 0.00 | 2026-04-12 | 0 | | cellular-neuroscience |
| gap-pubmed-20260412- | Does crosstalk between functional and pathological amyloids represent a general | open | 0.72 | 0.00 | 2026-04-12 | 0 | | neurodegeneration |
| gap-pubmed-20260412- | How do functional amyloids like SST influence pathological amyloid aggregation i | open | 0.77 | 0.00 | 2026-04-12 | 0 | | neurodegeneration |
| gap-pubmed-20260412- | What molecular mechanisms govern crosstalk between Aβ and somatostatin amyloid a | open | 0.80 | 0.00 | 2026-04-12 | 0 | | neurodegeneration |
| gap-pubmed-20260412- | Can adenine nucleotide translocase enhancement rescue VCP mutation-induced neuro | resolved | 0.82 | 0.00 | 2026-04-12 | 0 | | neurodegeneration |
| gap-pubmed-20260412- | How do VCP mutations mechanistically cause adenine nucleotide translocase dysreg | open | 0.80 | 0.00 | 2026-04-12 | 0 | | neurodegeneration |
| gap-debate-20260412- | Can cross-disease biomarkers distinguish primary pathology from secondary cross- | open | 0.68 | 0.70 | 2026-04-12 | 0 | | neurodegeneration |
| gap-debate-20260412- | How do endolysosomal membrane damage patterns influence protein aggregation spec | open | 0.71 | 0.68 | 2026-04-12 | 0 | | cell-biology |
| gap-debate-20260412- | What biochemical properties enable certain proteins to act as cross-seeding temp | open | 0.78 | 0.70 | 2026-04-12 | 0 | | molecular-biology |
| gap-debate-20260412- | Does galectin-3 catalyze amyloid cross-nucleation or merely co-localize with agg | open | 0.82 | 0.69 | 2026-04-12 | 0 | | neurodegeneration |
| gap-debate-20260412- | Do tunneling nanotubes exist and function for mitochondrial transfer in vivo und | open | 0.75 | 0.64 | 2026-04-12 | 0 | | neurobiology |
| gap-debate-20260412- | Why do P2X7 knockout mice show enhanced rather than impaired CNS recovery if P2X | open | 0.80 | 0.70 | 2026-04-12 | 0 | | neurodegeneration |
| gap-debate-20260412- | Can mitochondria within extracellular vesicles retain respiratory competence aft | open | 0.85 | 0.65 | 2026-04-12 | 0 | | cell-biology |
| gap-debate-20260412- | Do astrocytes functionally express TRIM46, and can PKCα phosphorylate it to driv | partially_addressed | 0.90 | 0.65 | 2026-04-12 | 0 | | molecular-biology |
| gap-debate-20260412- | What is the therapeutic window for blocking tau propagation before irreversible | open | 0.75 | 0.72 | 2026-04-12 | 0 | | translational-medicine |
| gap-debate-20260412- | Which synaptic adhesion molecules are necessary and sufficient for tau uptake? | open | 0.79 | 0.70 | 2026-04-12 | 0 | | molecular-biology |
| gap-debate-20260412- | How do extracellular vesicle and trans-synaptic pathways interact in vivo? | open | 0.82 | 0.66 | 2026-04-12 | 0 | | cell-biology |
| gap-debate-20260412- | What distinguishes seed-competent from non-pathogenic tau in trans-synaptic tran | partially_addressed | 0.87 | 0.72 | 2026-04-12 | 1 | 2026-04-26 | neurodegeneration |
| gap-debate-20260412- | How do aging-related PTM changes distinguish from disease-specific modifications | resolved | 0.75 | 0.71 | 2026-04-12 | 0 | | neurodegeneration |
| gap-debate-20260412- | Can O-GlcNAcase inhibitors achieve therapeutic selectivity for pathological tau | open | 0.85 | 0.71 | 2026-04-12 | 0 | | neurodegeneration |
| gap-debate-20260412- | Does K280 acetylation causally drive mitochondrial dysfunction or merely correla | open | 0.80 | 0.69 | 2026-04-12 | 0 | | molecular-biology |
| gap-debate-20260412- | Which tau PTMs are both disease-specific and druggable with selective small mole | partially_addressed | 0.90 | 0.70 | 2026-04-12 | 0 | | neurodegeneration |
| gap-debate-20260412- | What determines tissue-specific distribution of pathogenic tau PTMs across brain | open | 0.75 | 0.71 | 2026-04-12 | 0 | | neurodegeneration |
| gap-debate-20260412- | Which caspase isoforms specifically cleave tau at Asp-421 in human AD brain tiss | open | 0.80 | 0.62 | 2026-04-12 | 0 | | molecular-biology |
| gap-debate-20260412- | How does the reversibility of tau acetylation reconcile with stable prion-like p | open | 0.85 | 0.71 | 2026-04-12 | 0 | | neurodegeneration |
| gap-debate-20260412- | What is the atomic-resolution structure of K280-acetylated tau and how does it t | partially_addressed | 0.90 | 0.69 | 2026-04-12 | 0 | | structural-biology |
| gap-pubmed-20260411- | What are the causal relationships between epigenetic changes and neurotoxic dama | open | 0.74 | 0.00 | 2026-04-11 | 0 | | neurotoxicology |
| gap-pubmed-20260411- | How do epigenetic modifications contribute to addiction and psychopathology at t | open | 0.76 | 0.00 | 2026-04-11 | 0 | | neuropsychiatry |
| gap-pubmed-20260411- | What specific epigenetic mechanisms underlie learned behavior and cognition in t | resolved | 0.80 | 0.00 | 2026-04-11 | 0 | | cognitive-neuroscience |
| gap-pubmed-20260411- | Why do some L1CAM-negative EVs still contain neuronal proteins, and what is thei | open | 0.79 | 0.00 | 2026-04-11 | 0 | | biomarker-validation |
| gap-pubmed-20260411- | What mechanisms determine the variable co-expression of neuronal proteins (30-63 | open | 0.77 | 0.00 | 2026-04-11 | 0 | | extracellular-vesicle-biology |
| gap-pubmed-20260411- | Why do MS macrophages specifically lose the ability to upregulate peroxisomal β- | open | 0.80 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | What are the specific downstream targets of class I HDAC inhibition that mediate | open | 0.81 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | What mechanisms explain why tefinostat is less potent than entinostat in promoti | open | 0.83 | 0.00 | 2026-04-11 | 0 | | neuroinflammation |
| gap-pubmed-20260411- | Why do GFM1 mutations cause tissue-specific neurodegeneration despite ubiquitous | open | 0.79 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does GFM1 loss mechanistically link mitochondrial translation defects to enh | resolved | 0.81 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What molecular mechanisms drive the compensatory upregulation of electron transp | resolved | 0.83 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What is the causal relationship between astrocyte senescence reduction and α-syn | resolved | 0.82 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | How does engineered C. butyricum cross the blood-brain barrier to directly bind | partially_addressed | 0.89 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |
| gap-pubmed-20260411- | What determines the variable phenotypic expression of CHCHD10 mutations across d | open | 0.76 | 0.00 | 2026-04-11 | 0 | | neurodegeneration |