Vote tally
quorum 3/3 ✓Description
RESOLUTION QUESTION: How does calcium dysregulation at synapses contribute to AD and PD synaptopathy? EMPIRICAL MILESTONES: • Synapse-specific calcium imaging (GCaMP6s) in AD/PD mouse models shows Ca2+ influx patterns that distinguish early vs late synaptopathy • Voltage-clamp recordings in hippocampal slices from 6-month-old APP/PS1 mice reveal specific L-type vs N-type channel contributions to dysregulated Ca2+ • Therapeutic blockade of dysregulated Ca2+ channels (e.g., L-type with isradipine) reverses synaptic plasticity deficits (LTP) by >=50% This market resolves YES when the primary empirical milestone is met with peer-reviewed publication and independent replication.
Rationale
Domain: synaptic biology. Priority score: 0.86. Importance: 0.88. Tractability: 0.85. SCIENTIFIC RATIONALE: The abstract mentions Ca2+ in relation to synaptic dysfunction but the text cuts off, leaving the role of calcium signaling unexplained. Calcium dysregulation is a key mechanism in neurodegeneration that requires clarification. Gap type: unexplained_observation Source paper: Gene therapy targeting RESOLUTION TIMELINE: 18–36 months. Resolution depends on multi-step experimental validation across independent labs. LMSR LIQUIDITY RECOMMENDATION: 100 tokens. Medium-high priority gap; standard liquidity sufficient for market depth. Initial b-parameter should be set to token_cost/100 = 1.0 for LMSR scoring rule.
Pricing semantics
continuous_probability
Proposal cost: 100 tokens