🧫
Adoptive transfer of TCRAβ-Tregs in AD mouse model
active
experiment
Created: 2026-04-10T22:51:28
By: etl-v1-backfill
Quality:
50%
✓ SciDEX
ID: exp-94b13181-2a62-4f75-ae37-d0983058aa76
🧫 Experiment Protocol
ValidationAlzheimer's diseaseAPP, PSEN1transgenic mice expressing chimeric mouse-human APP and mutant human presenilin-1proposed
This experiment tested the therapeutic efficacy of engineered TCRAβ-Tregs in a transgenic mouse model of Alzheimer's disease. Mice expressing chimeric mouse-human amyloid precursor protein and mutant human presenilin-1 received adoptive transfer of the engineered TCRAβ-Tregs. The study measured multiple outcomes including behavioral performance, immune responses, and immunohistochemical markers. Key findings included sustained immune suppression, reduced microglial activation, decreased amyloid loads, and improved cognitive functions. 18F-fluorodeoxyglucose labeling was used to track the TCRAβ-Tregs, demonstrating their ability to home to the brain and provide antigen-specific targeting. The results showed that TCRAβ-Tregs could reduce amyloid burden, restore brain homeostasis, and improve learning and memory compared to controls.
PRIMARY OUTCOME
amyloid load reduction and cognitive improvement
EXPECTED OUTCOMES
1. The intervention targeting APP, PSEN1 shifts amyloid load reduction and cognitive improvement 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
- Prespecified primary endpoint (amyloid load reduction and cognitive improvement) improves versus control with p < 0.05 or an equivalent corrected threshold used by the study.
- The effect size is biologically meaningful and reproduced across technical/biological replicates or the validation subset.
- Safety, data quality, and missingness remain within protocol-defined bounds so the result is interpretable rather than driven by attrition or assay failure.
PROTOCOL
1. Establish transgenic mice expressing chimeric mouse-human APP and mutant human presenilin-1 cohorts for Alzheimer's disease and predefine inclusion, exclusion, and quality-control criteria before intervention. 2. Apply the experimental manipulation described for APP, PSEN1, alongside matched control or comparator arms, and document dose, exposure window, and sample timing in a locked protocol log. 3. Measure amyloid load reduction and cognitive improvement 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 tested the therapeutic efficacy of engineered TCRAβ-Tregs in a transgenic mouse model of Alzheimer's disease. Mice expressing chimeric mouse-human amyloid precursor protein and mutant human presenilin-1 received adoptive transfer of the enginee
LINKED HYPOTHESES
Source: PMID 38111016 ↗
🧫 Experiment Extras
PATHWAY
amyloid processing pathway, neuroinflammation, T cell regulation
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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