ArticleMolecular therapy. Methods & clinical development2023
AAV-BDNF gene therapy ameliorates a hypothalamic neuroinflammatory signature in the
Article in Molecular therapy. Methods & clinical development, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Low dose systemic AAV-exendin-4 gene therapy for Prader-Willi syndrome and dietary obesity.Molecular therapy. Advances · 2026Article
- Stimulus-Dependent Expression ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Environmental Enrichment Normalizes Metabolic Function in the Murine Model of Prader-Willi Syndrome Magel2-Null Mice.Endocrinology · 2025Article
- MAGEL2 (patho-)physiology and Schaaf-Yang syndrome.Developmental medicine and child neurology · 2025Review
- Precision medicine to identify, prevent, and treat pediatric obesity.Pharmacotherapy · 2024Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Individuals with Prader-Willi syndrome (PWS) exhibit several metabolic and behavioral abnormalities associated with excessive food-seeking activity. PWS is thought to be driven in part by dysfunctional hypothalamic circuitry and blunted responses to peripheral signals of satiety. Previous work described a hypothalamic transcriptomic signature of individuals with PWS. Notably, PWS patients exhibited downregulation of genes involved in neuronal development and an upregulation of neuroinflammatory genes. Deficiencies of brain-derived neurotrophic factor (BDNF) and its receptor were identified as potential drivers of PWS phenotypes. Our group recently applied an adeno-associated viral (AAV)-BDNF gene therapy within a preclinical PWS model,
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.