Epothilone D Modulates Autism-like Behaviors in the BTBR Mouse Model of Autism Spectrum Disorder.


Journal

Neuroscience
ISSN: 1873-7544
Titre abrégé: Neuroscience
Pays: United States
ID NLM: 7605074

Informations de publication

Date de publication:
10 05 2022
Historique:
received: 04 12 2021
revised: 17 02 2022
accepted: 21 02 2022
pubmed: 2 3 2022
medline: 27 4 2022
entrez: 1 3 2022
Statut: ppublish

Résumé

Autism spectrum disorder (ASD) is a neurodevelopmental disorder, characterized by impaired social communication, abnormal repetitive behaviors and restricted interests and/or sensory behaviors. It has been widely accepted that ASD involves a complex interplay of both genetic and environmental risk factors. Existing medications are only symptomatic treatments, there are no effective treatments that can improve these core social behavior deficits. Recent studies indicated that synaptic development and abnormal myelination are linked to the pathogenesis of ASD. The stable tubule only polypeptide (STOP) protein, also known as microtubule-associated protein 6, plays an important role in neuronal development and synaptic plasticity. Our previous studies showed that STOP protein was significantly reduced in the plasma of autistic subjects and in the cortex of BTBR T

Identifiants

pubmed: 35227832
pii: S0306-4522(22)00095-1
doi: 10.1016/j.neuroscience.2022.02.025
pii:
doi:

Substances chimiques

Epothilones 0
Myelin Proteins 0
desoxyepothilone B T0358E0YUF
Dimethyl Sulfoxide YOW8V9698H

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

171-181

Informations de copyright

Copyright © 2022 IBRO. Published by Elsevier Ltd. All rights reserved.

Auteurs

Min Zhao (M)

Department of Neurology, Shanxi Provincial People's Hospital, Affiliate of Shanxi Medical University, Taiyuan 030012, China.

Qiaoqiao Chang (Q)

Department of Neurology, Shanxi Provincial People's Hospital, Affiliate of Shanxi Medical University, Taiyuan 030012, China; Department of Neurology, The First Affiliated Hospital of Northwest University, Xi'an, Shaanxi 710002, China.

Hua Yang (H)

Department of Neurology, Shanxi Provincial People's Hospital, Affiliate of Shanxi Medical University, Taiyuan 030012, China.

Min Wang (M)

Department of Neurology, Shanxi Provincial People's Hospital, Affiliate of Shanxi Medical University, Taiyuan 030012, China; Department of Neurology, Nanchong Central Hospital, The Second Clinical College of North Sichuan Medical College, Nanchong 637000, Sichuan, China.

Yongfeng Liu (Y)

Department of Neurology, Shanxi Provincial People's Hospital, Affiliate of Shanxi Medical University, Taiyuan 030012, China.

Na Lv (N)

Department of Neurology, Shanxi Provincial People's Hospital, Affiliate of Shanxi Medical University, Taiyuan 030012, China.

Qiang Lei (Q)

Department of Neurology, Shanxi Provincial People's Hospital, Affiliate of Shanxi Medical University, Taiyuan 030012, China.

Hongen Wei (H)

Department of Neurology, Shanxi Provincial People's Hospital, Affiliate of Shanxi Medical University, Taiyuan 030012, China; Shanxi Key Laboratory of Brain Disease Control, Shanxi Provincial People's Hospital, Taiyuan, China. Electronic address: hongen.wei@sxmu.edu.cn.

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Classifications MeSH