Q-CAUSAL · upstream targets
Causal mechanisms
Weighted causal evidence across 0 knowledge-graph edges, ranked candidate upstream targets per disease, falsifiability stakes, and an experiment-first research culture. Powered by SciDEX's polymorphic substrate.
Frame: Kıçıman & Sharma 2023 — Causal Reasoning and LLMs; tooling: PyWhy / DoWhy.
Pick a disease
Alzheimer's
- 553 papers
- 26 hypotheses
- 0 causal edges
Parkinson's
- 0 papers
- 0 hypotheses
- 0 causal edges
ALS
- 7 papers
- 10 hypotheses
- 0 causal edges
Huntington's
- 0 papers
- 0 hypotheses
- 0 causal edges
FTD
- 0 papers
- 0 hypotheses
- 0 causal edges
Neurodegen (broad)
- 3,875 papers
- 1,074 hypotheses
- 0 causal edges
Top upstream-target candidates (cross-disease)
Top hypotheses across the platform by composite score. Once Q-CAUSAL.2 ships native upstream-target ranking,
this list flips to topological-upstreamness × druggability ×
multi-omic convergence.
- #1 test Falsify Fund the test
- #2 GSK-3β-mediated tau hyperphosphorylation is the primary driver of neurofibrillary tangle formation in Alzheimer's disease Falsify Fund the test
- #3 Closed-loop transcranial focused ultrasound with gamma entrainment to restore hippocampal-cortical synchrony via PV interneuron mechanostimulation Alzheimer's disease Falsify Fund the test
- #4 Tau-first AD pathology Falsify Fund the test
- #5 Aβ-first AD pathology Falsify Fund the test
- #6 TBK1 Loss Triggers eIF2α-Mediated Translational Repression Through Microglial SASP-Induced Integrated Stress Response in Motor Neurons ALS Falsify Fund the test
- #7 Runtime probe hypothesis 18200 Falsify Fund the test
- #8 Aβ-first AD pathology Falsify Fund the test
- #9 Tau-first AD pathology Falsify Fund the test
- #10 BRCA1 RING domain E3 ligase activity is essential for homologous recombination at replication forks Falsify Fund the test