🧫
Anti-ASC antibody intracerebroventricular injection in APP/PS1 mice
active
experiment
Created: 2026-04-10T22:44:55
By: etl-v1-backfill
Quality:
50%
✓ SciDEX
ID: exp-dca68e10-7729-4ca8-b2b0-6a7a9f71188e
🧫 Experiment Protocol
ValidationAlzheimer's diseaseASCAPP/PS1 transgenic mice (8 months old)proposed
This experiment evaluated the therapeutic potential of ASC-targeting antibodies in vivo using eight-month-old APP/PS1 transgenic mice, which are an established mouse model of Alzheimer's disease. The mice received intracerebroventricular (lateral ventricle) injections of either anti-ASC N-terminal antibodies or anti-ASC C-terminal antibodies. The study comprehensively assessed cognitive function through behavioral testing and examined multiple aspects of AD-like pathology including amyloid-β deposition, tau hyperphosphorylation, and neuroinflammation. This experiment aimed to determine whether the neuroprotective effects observed in cell culture could translate to improved outcomes in a living animal model, and whether targeting different domains of ASC would have differential therapeutic effects.
PRIMARY OUTCOME
Cognitive function and AD-like pathology markers
EXPECTED OUTCOMES
1. The intervention targeting ASC shifts Cognitive function and AD-like pathology markers in the predicted direction relative to the matched control arm.
2. Secondary disease-relevant readouts in Alzheimer's disease remain directionally concordant with the primary endpoint rather than showing isolated single-assay effects.
3. The effect persists after adjustment for baseline covariates, batch effects, or repeated-measures structure used in the study design.
SUCCESS CRITERIA
Significant improvement in cognitive performance and reduction in Aβ plaques, tau pathology, and neuroinflammation compared to control mice
PROTOCOL
1. Establish APP/PS1 transgenic mice (8 months old) cohorts for Alzheimer's disease and predefine inclusion, exclusion, and quality-control criteria before intervention. 2. Apply the experimental manipulation described for ASC, alongside matched control or comparator arms, and document dose, exposure window, and sample timing in a locked protocol log. 3. Measure Cognitive function and AD-like pathology markers together with orthogonal secondary readouts such as molecular, imaging, behavioral, or safety endpoints that are appropriate to the title and study design. 4. Use blinded outcome assessment where feasible, prespecified statistical analysis, and replicate the core readout across biological replicates or an independent validation subset. 5. Interpret results against the baseline study rationale: This experiment evaluated the therapeutic potential of ASC-targeting antibodies in vivo using eight-month-old APP/PS1 transgenic mice, which are an established mouse model of Alzheimer's disease. The mice received intracerebroventricular (lateral ventricle) in
LINKED HYPOTHESES
h_seaad_004· OPC differentiation blockade contributes to white matter degeneration in early-stage ADh-seaad-51323624· Cell-Type Specific TREM2 Upregulation in DAM Microgliah-4dd0d19b· LRP1-Dependent Tau Uptake Disruptionh-b234254c· TREM2-mediated microglial tau clearance enhancementh-55ef81c5· Extracellular Vesicle Biogenesis Modulation
Source: PMID 41707905 ↗
🧫 Experiment Extras
PATHWAY
ASC-mediated inflammasome pathway, amyloid processing pathway, tau phosphorylation pathway
MARKET PRICE
$0.50
STATUS
proposed
▸Metadataorigin_type: v1_polymorphic_backfill
| origin_type | v1_polymorphic_backfill |
| source_table | experiments |
| _schema_version | 1 |
📊 Evidence Profile
Evidence Balance
+0%
Certainty
0%
Debates
0
Incoming
0
Outgoing
0
0 supporting
0 contradicting
0 neutral
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