| gap-pubmed-20260410- | How do astrocytic surface receptors (P2Y1/P2Y2, mGLUR5, α7nAChR, NMDARs) mechani | open | 0.83 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does sulfatide loss cause cognitive impairment and peripheral bladder dysfun | open | 0.70 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why do females show more severe sulfatide deficiency-induced phenotypes compared | open | 0.75 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What mechanisms drive astrogliosis and myelin lipid disruption independently of | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | Why does increased TDP-43 aggregation propensity lead to reduced neurotoxicity c | resolved | 0.86 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does a partial loss-of-function TDP-43 variant with high aggregation propens | resolved | 0.82 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What molecular mechanisms determine tissue-specific TDP-43 pathology (muscle vs. | resolved | 0.85 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What mechanisms explain how multiple toxic metals converge as a unified upstream | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How do transgenerational exposures to toxic metals influence neurodegeneration r | open | 0.78 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does antigen-inducible cytokine production compare to constitutive expressio | open | 0.73 | 0.00 | 2026-04-10 | 0 | | cancer-immunotherapy |
| gap-pubmed-20260410- | What mechanisms underlie IL18's enhancement of CAR T cell cytolytic function aga | open | 0.80 | 0.00 | 2026-04-10 | 0 | | cancer-immunotherapy |
| gap-pubmed-20260410- | How does mitophagy selectively regulate DHODH/FSP1-CoQ10-NADH versus other ferro | open | 0.76 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why does BNIP3-mediated mitophagy bypass the canonical GPX4-GSH ferroptosis resi | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why does OPTN loss specifically cause dysmyelination alongside axonal degenerati | open | 0.79 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What triggers the transition from RIPK1/RIPK3 activation to downstream axonal de | open | 0.79 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does optineurin mechanistically regulate RIPK1 turnover to suppress necropto | resolved | 0.84 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What determines the optimal timing and dosing for gene suppression to achieve di | open | 0.79 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How can gene suppression approaches be effectively translated from monogenic dis | open | 0.76 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What would be the therapeutic efficacy and safety of modulating clusterin levels | open | 0.78 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How do intracellular versus secreted clusterin forms differentially interact wit | open | 0.76 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What mechanisms explain why clusterin increases associate with Aβ and tau but no | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why does TREM2 isoform upregulation occur consistently across mouse models and h | open | 0.77 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | How do the identified novel isoforms functionally contribute to tau pathology de | open | 0.76 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What mechanisms drive differential isoform expression in tau pathology despite u | resolved | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How do the molecular profiles of iPSC-derived pericytes compare to native brain | open | 0.79 | 0.00 | 2026-04-10 | 0 | | vascular-neurobiology |
| gap-pubmed-20260410- | What molecular mechanisms enable iPSC-derived pericytes to maintain BBB and phag | open | 0.82 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What are the shared pathophysiological mechanisms between normal cognitive aging | open | 0.82 | 0.00 | 2026-04-10 | 0 | | cognitive-aging |
| gap-pubmed-20260410- | How can translational animal models be developed to better align with human ADRD | open | 0.80 | 0.00 | 2026-04-10 | 0 | | translational-neuroscience |
| gap-pubmed-20260410- | Which specific aging processes are differentially regulated in ADRD versus norma | open | 0.85 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What mechanisms allow sensory neuronal STAT3 to contribute to IL-31-independent | open | 0.77 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | How does IL-31 enhance itch responses to mechanistically distinct pruritogens li | open | 0.78 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | What are the molecular mechanisms by which STAT3 regulates IL-31 receptor expres | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | What determines the specificity and efficiency of peroxidated lipid sequestratio | open | 0.78 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How does ROS enhancement of Aβ42 phenotypes mechanistically relate to the lipid | open | 0.82 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What are the molecular mechanisms by which AD risk genes regulate ROS-induced ne | resolved | 0.85 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What determines the specificity of N protein for disrupting cGAS-G3BP1 versus ot | open | 0.73 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | How does SARS-CoV-2 N protein phase separation specifically disrupt cGAS-G3BP1 a | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | Do other chemotherapeutic agents show similar astrocyte-mediated resistance thro | open | 0.74 | 0.00 | 2026-04-10 | 0 | | neuro-oncology |
| gap-pubmed-20260410- | How does CX43-mediated intercellular communication specifically activate STAT1 i | open | 0.76 | 0.00 | 2026-04-10 | 0 | | neuro-oncology |
| gap-pubmed-20260410- | What are the downstream molecular targets of CX43-dependent STAT1 signaling that | open | 0.82 | 0.00 | 2026-04-10 | 0 | | neuro-oncology |
| gap-pubmed-20260410- | How does the timing of STING activation during ischemia versus reperfusion phase | open | 0.76 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What are the specific molecular mechanisms by which STING activation leads to I/ | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neuroinflammation |
| gap-pubmed-20260410- | Why do GBA mutations cause earlier onset and distinct cognitive decline patterns | open | 0.74 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What are the exact molecular mechanisms underlying the bidirectional pathogenic | open | 0.85 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why does senolytic treatment improve pre-injury cognition but fail to rescue pos | open | 0.75 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What cellular/molecular mechanisms explain how senescent cells increase seizure | open | 0.80 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why do UbBD mutants specifically impair autophagosome maturation rather than ear | open | 0.79 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | What determines the differential disease outcomes (glaucoma vs ALS) from distinc | open | 0.85 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | How do OPTN UbBD mutants retain interaction with wild-type OPTN despite losing u | open | 0.83 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |
| gap-pubmed-20260410- | Why does the Christchurch mutation phenocopy ApoE2 protection despite different | open | 0.79 | 0.00 | 2026-04-10 | 0 | | neurodegeneration |