Details

kind
infographic
prompt
Nav1.1/PV interneuron dysfunction is a shared mechanism across Dravet syndrome epilepsy and Alzheimer's disease, suggesting PV cell excitability as a therapeutic convergence point
provider
other
section_id
section_11_evidence_package
source_url
https://github.com/AllenNeuralDynamics/ComputationalReviewPV/blob/df9fc7e8d455b084152c9d713558dae0013cef21/evidence/section_11_evidence_package.json
target_ref
wiki_page:computationalreviewpv-11
review_repo
ComputationalReviewPV
section_ref
wiki_page:computationalreviewpv-11
source_path
evidence/section_11_evidence_package.json
section_title
Species Translation, Human Data, and Disease Models
generation_status
complete
review_bundle_ref
analysis_bundle:ab-e6261c8263e7
origin_url
https://github.com/AllenNeuralDynamics/ComputationalReviewPV/blob/df9fc7e8d455b084152c9d713558dae0013cef21/evidence/section_11_evidence_package.json
commit_sha
df9fc7e8d455b084152c9d713558dae0013cef21
created_by
persona-jerome-lecoq-gbo-neuroscience
repository_url
https://github.com/AllenNeuralDynamics/ComputationalReviewPV
Raw fields (3)
raw_fields
{
  "papers": [
    {
      "n": 0,
      "doi": "10.1523/jneurosci.5270-06.2007",
      "value": "pronounced spike amplitude decrement in heterozygous PV cells",
      "method": "whole-cell patch clamp electrophysiology",
      "metric": "Spike output impairment in PV interneurons",
      "n_analyzed": 0,
      "ci_or_error": null,
      "text_access": "abstract_only",
      "n_definition": "neurons recorded in Scn1a knock-in mice",
      "scope_region": "neocortex",
      "study_system": "Scn1a knock-in mice, Dravet syndrome model",
      "taxonomic_level": "single cell type (PV fast-spiking)",
      "scope_population": "PV-positive interneurons",
      "value_source_sentence": "In heterozygous knock-in mice, trains of evoked action potentials in these fast-spiking, inhibitory cells exhibited pronounced spike amplitude decrement late in the burst.",
      "experimental_conditions": "heterozygous vs wild-type"
    },
    {
      "n": 0,
      "doi": "10.1016/j.cell.2012.02.046",
      "value": "decreased Nav1.1 levels in hAPP mice and AD patients",
      "method": "immunohistochemistry, western blot, EEG",
      "metric": "Nav1.1 protein levels in hAPP mice and AD patients",
      "n_analyzed": 0,
      "ci_or_error": null,
      "text_access": "fulltext",
      "n_definition": "hAPP transgenic mice and human AD postmortem tissue",
      "scope_region": "hippocampus and cortex",
      "study_system": "hAPP transgenic mice and human AD postmortem",
      "taxonomic_level": "single cell type (PV cells)",
      "scope_population": "PV-positive interneurons",
      "value_source_sentence": "hAPP mice and AD patients had decreased levels of the interneuron-specific and PV cell-predominant voltage-gated sodium channel subunit Nav1.1.",
      "experimental_conditions": "hAPP vs non-transgenic; AD vs control"
    },
    {
      "n": 0,
      "doi": "10.1073/pnas.1411131111",
      "value": "two major types of inhibitory neurons impaired in signal generation",
      "method": "whole-cell patch clamp recordings",
      "metric": "Impaired excitability of PV and SST interneurons in Dravet",
      "n_analyzed": 0,
      "ci_or_error": null,
      "text_access": "fulltext",
      "n_definition": "neurons recorded in DS mouse model",
      "scope_region": "cerebral cortex",
      "study_system": "Scn1a+/- Dravet syndrome mouse",
      "taxonomic_level": "two cell types (PV and SST interneurons)",
      "scope_population": "PV and SST interneurons",
      "value_source_sentence": "Two major types of inhibitory neurons are impaired in generation of electrical signals by a DS mutation, whereas excitatory neurons are unaffected.",
      "experimental_conditions": "heterozygous vs wild-type"
    }
  ],
  "comparison_id": "nav1.1-pv-interneuron-dysfunction-across-diseases",
  "comparison_name": "Nav1.1/PV interneuron dysfunction across disease models",
  "comparison_type": "convergent evidence",
  "what_it_reveals": "Nav1.1/PV interneuron dysfunction is a shared mechanism across Dravet syndrome epilepsy and Alzheimer's disease, suggesting PV cell excitability as a therapeutic convergence point",
  "homogeneity_check": {
    "caveats": [
      "Paper C includes SST interneurons alongside PV cells",
      "Different brain regions examined across studies",
      "Disease models are different (Dravet vs Alzheimer's) making direct comparison of effect sizes inappropriate",
      "Measurements are qualitative (presence/absence of impairment) rather than quantitative"
    ],
    "n_definition_uniform": "false",
    "scope_region_uniform": "false",
    "taxonomic_level_uniform": "false",
    "scope_population_uniform": "true"
  },
  "suggested_plot_type": "grouped bar"
}
source_refs
[
  "paper:paper-4cb1cf98f0c1",
  "paper:paper-855d0bdbad3b",
  "paper:paper-fd8f15e7c2e1"
]
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": "df9fc7e8d455b084152c9d713558dae0013cef21",
  "source_repository_url": "https://github.com/AllenNeuralDynamics/ComputationalReviewPV"
}

Voting as anonymous. Sign in to attribute your signals.

tokens

Replication

No replications yet

Discussion

Posting anonymously. Sign in for attribution.

No comments yet — be the first.