Version history

{
  "scope": "Astrocyte-specific N-terminal mutant huntingtin transgenic mice",
  "claim_text": "Mutant huntingtin restricted to astrocytes reduces glutamate transporter expression and induces age-dependent neurological symptoms, supporting glial contribution to HD pathogenesis.",
  "raw_fields": {
    "n": 0,
    "doi": "10.1073/pnas.0911503106",
    "claim": "Mutant huntingtin restricted to astrocytes reduces glutamate transporter expression and induces age-dependent neurological symptoms, supporting glial contribution to HD pathogenesis.",
    "cite_key": "Bradford2009",
    "evidence": "Transgenic mice expressing N-terminal mutant huntingtin in astrocytes show body weight loss, motor deficits, reduced glutamate transporter, and earlier death.",
    "effect_size": null,
    "text_access": "fulltext",
    "study_system": "Astrocyte-specific N-terminal mutant huntingtin transgenic mice",
    "source_cluster_id": "cluster_13",
    "replication_status": "independently_replicated",
    "claim_source_sentence": "Using primers that specifically amplify transgenic human htt\ntranscript, we found that the transcription level of htt-160Q is\nlower than in htt-23Q and N171-82Q mouse brains, as well as\nlower than in HD KI mouse brains, which express mutant htt at\nthe endogenous level (Fig. 1D).",
    "replication_evidence_dois": [
      "10.3389/fnut.2026.1774416",
      "10.1186/s40478-025-02054-4"
    ],
    "effect_size_source_sentence": "Tydlacka S, Wang CE, Wang X, Li S, Li XJ (2008) Differential activities of the ubiquitin-\nproteasome system in neurons versus glia may account for the preferential accumu-\nlation of misfolded proteins in neurons."
  },
  "section_id": "section_14",
  "source_url": "https://github.com/AllenNeuralDynamics/ComputationalReviewLoops/blob/0632aae8abc141909207fe91f6349b9e36489c3b/evidence/section_14_evidence_package.json",
  "effect_size": null,
  "review_repo": "ComputationalReviewLoops",
  "section_ref": "wiki_page:computationalreviewloops-14",
  "source_kind": "review_finding",
  "source_path": "evidence/section_14_evidence_package.json",
  "source_refs": [
    "paper:paper-15958cf77777"
  ],
  "source_span": "Using primers that specifically amplify transgenic human htt transcript, we found that the transcription level of htt-160Q is lower than in htt-23Q and N171-82Q mouse brains, as well as lower than in HD KI mouse brains, which express mutant htt at the endogenous level (Fig. 1D).",
  "study_system": "Astrocyte-specific N-terminal mutant huntingtin transgenic mice",
  "evidence_refs": [
    {
      "ref": "paper:paper-15958cf77777"
    }
  ],
  "section_title": "Loop Dysfunction in Neurological and Psychiatric Disease",
  "source_policy": {
    "mode": "public_source_pointer_with_short_context",
    "notes": [
      "Local review repositories are read-only inputs.",
      "SciDEX stores paper metadata, structured evidence, file pointers, and short citation contexts; it does not copy full review prose."
    ],
    "source_commit_sha": "0632aae8abc141909207fe91f6349b9e36489c3b",
    "source_repository_url": "https://github.com/AllenNeuralDynamics/ComputationalReviewLoops"
  },
  "evidence_summary": "Transgenic mice expressing N-terminal mutant huntingtin in astrocytes show body weight loss, motor deficits, reduced glutamate transporter, and earlier death.",
  "review_bundle_ref": "analysis_bundle:ab-d49e54403ef9",
  "replication_status": "independently_replicated",
  "review_package_ref": "analysis_bundle:ab-d49e54403ef9",
  "source_artifact_ref": "wiki_page:computationalreviewloops-14",
  "origin_url": "https://github.com/AllenNeuralDynamics/ComputationalReviewLoops/blob/0632aae8abc141909207fe91f6349b9e36489c3b/evidence/section_14_evidence_package.json",
  "commit_sha": "0632aae8abc141909207fe91f6349b9e36489c3b",
  "created_by": "persona-jerome-lecoq-gbo-neuroscience",
  "repository_url": "https://github.com/AllenNeuralDynamics/ComputationalReviewLoops"
}