Myélinisation précoce dans un modèle murin d'autisme

Titre original en anglais : Precocious myelination in a mouse model of autism

Cette publication est incluse dans le projet « Contributions académiques de personnes autistes sur l’autisme ». un auteur·ice de cette publication est identifié·e comme autiste dans le projet.

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Khanbabaei, M., Hughes, E., Ellegood, J., Qiu, L. R., Yip, R., Dobry, J., Murari, K., Lerch, J. P., Rho, J. M., & Cheng, N. (2019). Precocious myelination in a mouse model of autism. Translational Psychiatry, 9(1), 251-251. https://doi.org/10.1038/s41398-019-0590-7

Date de publication: 07/10/2019 Ajout dans AutiHub: 29/08/2026 Type: Article Langue de l’article: Anglais
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Auteurs

Auteur·ices des publications
10
Auteur·ices de la publication identifié·es comme autistes
1 / 10 (10,0 %)
  1. Maryam Khanbabaei
  2. Elizabeth Hughes *
  3. Jacob Ellegood
  4. Lily R. Qiu
  5. Raven Yip
  1. Jenna Dobry
  2. Kartikeya Murari
  3. Jason P. Lerch
  4. Jong M. Rho
  5. Ning Cheng

Résumé

Résumé Le trouble du spectre de l'autisme (TSA) a été supposé être le résultat d'une connectivité altérée dans le cerveau. Des études d'imagerie récentes suggèrent une maturation accélérée de la substance blanche chez les jeunes enfants atteints de TSA, dont les mécanismes sous-jacents sont inconnus. La myéline est une partie intégrante de la substance blanche et est essentielle à la connectivité ; cependant, son rôle dans le TSA reste largement incertain. Ici, nous avons étudié le développement de la myéline dans un modèle de TSA idiopathique, les souris BTBR. L'imagerie par résonance magnétique a révélé que les faisceaux de fibres dans le cerveau frontal des souris BTBR présentaient un volume accru au jour postnatal 6, mais que la différence diminuait au fil du temps, rappelant les observations chez les jeunes patients. Nous avons en outre identifié que la myélinisation dans le cerveau frontal de souris BTBR nouveau-nées mâles et femelles était accrue, associée à des niveaux élevés de protéine basique de la myéline. Cependant, le profil de myéline était inchangé chez les souris BTBR adultes, révélant une trajectoire développementale accélérée de la myélinisation. De manière cohérente, nous avons constaté que la signalisation du récepteur alpha du facteur de croissance dérivé des plaquettes (PDGFRα) était réduite dans le cerveau frontal de souris BTBR nouveau-nées. Toutefois, les niveaux d'espèces de microARN connues pour réguler la signalisation de PDGFRα et la myélinisation étaient inchangés. Ensemble, ces résultats suggèrent que la myélinisation précoce pourrait potentiellement contribuer à l'augmentation du volume et de la connectivité de la substance blanche observée chez les jeunes enfants atteints de TSA.

Abstract Autism spectrum disorder (ASD) has been hypothesized to be a result of altered connectivity in the brain. Recent imaging studies suggest accelerated maturation of the white matter in young children with ASD, with underlying mechanisms unknown. Myelin is an integral part of the white matter and critical for connectivity; however, its role in ASD remains largely unclear. Here, we investigated myelin development in a model of idiopathic ASD, the BTBR mice. Magnetic resonance imaging revealed that fiber tracts in the frontal brain of the BTBR mice had increased volume at postnatal day 6, but the difference reduced over time, reminiscent of the findings in young patients. We further identified that myelination in the frontal brain of both male and female neonatal BTBR mice was increased, associated with elevated levels of myelin basic protein. However, myelin pattern was unaltered in adult BTBR mice, revealing accelerated developmental trajectory of myelination. Consistently, we found that signaling of platelet-derived growth factor receptor alpha (PDGFRα) was reduced in the frontal brain of neonatal BTBR mice. However, levels of microRNA species known to regulate PDGFRα signaling and myelination were unaltered. Together, these results suggest that precocious myelination could potentially contribute to increased volume and connectivity of the white matter observed in young children with ASD.

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Références citées
105
Avec un DOI
102
Sans DOI, à partir du texte brut de la bibliographie
2
1 / 105 (1,0 %) références citées comprennent au moins une personne identifiée comme autiste.
Références avec données à compléter
2 / 105 (1,9 %)
Références avec noms d’auteurices détectés
105 / 105 (100,0 %)
Sans nom d’auteurice détecté
0
Sans titre structuré
2
Sans identifiant stable
2
Références avec noms bruts d’auteurices restant à vérifier
0
Références avec problème de récupération des métadonnées externes
1
Ces indicateurs portent sur les références citées affichées sur cette page, après fusion des doublons techniques. Une référence sans DOI peut quand même soutenir les statistiques d’auteurices lorsqu’un titre et des noms d’auteurices sont disponibles.
Noms d’auteurices détectés dans la bibliographie citée
680
À partir du DOI ou de métadonnées externes
680
À partir du texte brut validé de la bibliographie
0
Noms bruts déjà validés
0
Noms bruts restant à vérifier
0
51 / 680 (7,5 %) noms sont associés à un·e auteurice déjà présent·e dans AutiHub. 629 / 680 (92,5 %) noms ne sont pas encore associés.
Noms associés à une personne identifiée comme autiste
1 / 680 (0,1 %)
Calculé sur l’ensemble des noms d’auteurices détectés dans la bibliographie citée. Parmi les noms associés à un·e auteurice déjà présent·e dans AutiHub : 1 / 51 (2,0 %). Personnes distinctes identifiées comme autistes : 1 / 561 (0,2 %).
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