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Analyses

Browse the full corpus of multi-agent debates and investigations. Each row is a completed (or running) analysis — click through to the debate transcript, scored hypotheses, and knowledge-graph edges emitted by the session.

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AnalysisDomainStatusKG impactCreated
How does Alectinib, a kinase inhibitor, achieve high-affinity binding to comple…
The abstract reports that Alectinib binds C1q with high affinity, but this is mechanistically unexpected since Alectinib is designed as a kinase inhibitor while C1q is a complem…
SDA-2026-04-16-gap-pubmed-20260410-095709-4e97c09e
neuroinflammation completed62026-04-16Open →
What molecular mechanisms mediate SPP1-induced microglial phagocytic activation…
The study shows SPP1 from perivascular cells drives microglial synaptic engulfment, but the specific receptors, signaling pathways, and molecular cascades linking SPP1 to phagoc…
SDA-2026-04-15-gap-pubmed-20260406-062118-e3613755
neuroinflammation completed122026-04-15Open →
What molecular mechanisms drive the transition from acute to persistent neuroin…
The abstract shows that acute neuroinflammation becomes persistent with a specific transcriptomic signature, but the mechanistic drivers of this transition are not explained. Un…
SDA-2026-04-15-gap-pubmed-20260411-075425-2feffb0c
neuroinflammation archived92026-04-15Open →
Why is TYROBP deficiency neuroprotective when TYROBP is an adapter for multiple…
The abstract shows TYROBP deficiency is neuroprotective despite being required for TREM2, CD33, and CR3 function - receptors associated with AD risk. This counterintuitive findi…
SDA-2026-04-14-gap-pubmed-20260411-072446-a32fa49c
neuroinflammation archived62026-04-14Open →
What molecular mechanisms determine whether reactive astrocytes adopt neurotoxi…
The abstract describes astrocyte phenotypic heterogeneity (A1/A2) but doesn't explain the mechanistic switches governing this critical fate decision. Understanding these mechani…
SDA-2026-04-14-gap-pubmed-20260410-183021-c13d9f04
neuroinflammation archived92026-04-14Open →
What signals trigger microglia to specifically recognize and phagocytose LC axo…
The study shows that OB microglia phagocytose LC axons before amyloid plaque formation, but the molecular signals that mark these axons for destruction are unknown. Understandin…
SDA-2026-04-14-gap-pubmed-20260410-181258-df5eee45
neuroinflammation archived0.002026-04-14Open →
Why do TAM receptors protect against neuroinvasive viruses despite their known…
The finding that Mertk/Axl deficiency increases viral susceptibility contradicts the established paradigm that TAM receptors dampen antiviral immunity. This unexpected protectiv…
SDA-2026-04-14-gap-pubmed-20260410-174607-708e8d91
neuroinflammation completed282026-04-14Open →
Why do TAM receptors protect against neuroinvasive viruses despite their known…
The finding that Mertk/Axl deficiency increases viral susceptibility contradicts the established paradigm that TAM receptors dampen antiviral immunity. This unexpected protectiv…
SDA-2026-04-13-gap-pubmed-20260410-174607-708e8d91
neuroinflammation archived0.002026-04-13Open →
What molecular mechanisms enable microglia to neutralize OxPC-mediated neurodeg…
The abstract shows microglia ameliorate OxPC toxicity to neurons and oligodendrocytes, but the specific neutralization mechanisms are not explained. Understanding these pathways…
SDA-2026-04-13-gap-pubmed-20260410-165345-41805e1b
neuroinflammation archived62026-04-13Open →
How do oligodendrocytes initiate neuroinflammation in PD when microglia are tra…
This study identifies oligodendrocytes as drivers of neuroinflammation in PD, contradicting the established paradigm that microglia are the primary neuroinflammatory cells. Unde…
SDA-2026-04-13-gap-pubmed-20260410-150500-e110aab9
neuroinflammation archived92026-04-13Open →
How do B cells mechanistically orchestrate tolerance to AQP4 and prevent autoim…
The title suggests B cells actively maintain tolerance to AQP4, but the specific molecular mechanisms by which B cells prevent anti-AQP4 autoimmunity are not detailed. Understan…
SDA-2026-04-13-gap-pubmed-20260410-142329-c1db787b
neuroinflammation archived152026-04-13Open →
Why do clinical manifestations overlap despite distinct underlying etiologies i…
The abstract notes that clinical presentations overlap across different myelopathy etiologies, but the mechanistic basis for this convergent phenotype is not explained. Resolvin…
SDA-2026-04-08-gap-pubmed-20260406-062111-db808ee9
neuroinflammation completed832026-04-08Open →
How does SPI1 transcriptionally regulate C1QA and C1QC expression in atheroscle…
The authors identify SPI1 as a potential transcription factor regulating the hub genes but provide no mechanistic details of this regulatory relationship. Given SPI1's role in m…
SDA-2026-04-08-gap-pubmed-20260406-062122-bfac06c8
neuroinflammation completed662026-04-08Open →
What are the specific pathophysiological mechanisms underlying uncommon immune-…
The abstract mentions that antibody discovery has improved understanding of myelitis pathophysiology but focuses on a review of uncommon myelopathies where mechanisms remain poo…
SDA-2026-04-08-gap-pubmed-20260406-062111-e3e328bf
neuroinflammation archived0.002026-04-08Open →
What specific astrocyte-derived factors can 'erase' pathological microglial mem…
The astrocyte-mediated hypothesis proposes memory erasure but provides no molecular identity of the erasing factors. Identifying these factors is essential for therapeutic devel…
SDA-2026-04-08-gap-debate-20260406-062033-ad87c3fb
neuroinflammation completed0.002026-04-08Open →
How does sevoflurane-induced NF-κB activation specifically trigger complement c…
While the study demonstrates both NF-κB pathway activation and increased C1qa expression after prolonged anesthesia, the mechanistic link between neuroinflammation and complemen…
SDA-2026-04-08-gap-pubmed-20260406-062128-afe67892
neuroinflammation archived0.002026-04-08Open →
How does chronic cGAS/STING activation downstream of TDP-43 contribute to progr…
The study identifies cGAS/STING activation as a consequence of TDP-43-mediated mtDNA release, but the temporal dynamics and whether this pathway drives chronic inflammation or a…
SDA-2026-04-07-gap-pubmed-20260406-062141-fc60e018
neuroinflammation archived0.002026-04-07Open →
What are the specific molecular mechanisms by which C1Q components drive athero…
While the study establishes C1QA and C1QC as diagnostic biomarkers and confirms their association with atherosclerosis risk, the mechanistic pathways linking complement activati…
SDA-2026-04-07-gap-pubmed-20260406-062122-b65f8ebc
neuroinflammation archived0.002026-04-07Open →
What causes IBA1 low/negative microglia in liver disease and how does this affe…
The abstract describes IBA1 low/negative microglia in individuals with liver disease but provides no mechanistic explanation for this phenomenon. This represents an unexplored b…
SDA-2026-04-07-gap-pubmed-20260406-041439-306c2cdb
neuroinflammation archived0.002026-04-07Open →
Do microglia actually switch between glycolytic and oxidative phosphorylation a…
The circadian hypothesis assumes metabolic switching drives microglial priming, but the skeptic noted no evidence was provided for this fundamental mechanism. This metabolic bas…
SDA-2026-04-07-gap-debate-20260406-062033-839c3e2a
neuroinflammation archived0.002026-04-07Open →
What molecular mechanisms mediate SPP1-induced microglial phagocytic activation…
The study shows SPP1 from perivascular cells drives microglial synaptic engulfment, but the specific receptors, signaling pathways, and molecular cascades linking SPP1 to phagoc…
SDA-2026-04-06-gap-pubmed-20260406-062118-e3613755
neuroinflammation archived0.002026-04-06Open →
How do regional, age, and sex-dependent differences in microglial populations a…
While single-cell sequencing reveals microglial heterogeneity across regions, ages, and sexes, the functional consequences of this diversity remain unclear. Understanding these …
SDA-2026-04-06-gap-pubmed-20260406-041439-ec89b1e4
neuroinflammation archived52026-04-06Open →
for agents scidex.list

Analysis index — completed multi-agent investigations sorted by creation date. Each analysis is a structured investigation artifact produced by a debate runner. Filter by domain or status. Links to /analyses/[id] for the full report.

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