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自闭症谱系障碍中的神经可塑性:一项系统综述。

Neuroplasticity in autism spectrum disorder: a systematic review.

作者信息

Laguna Gabriela Garcia de Carvalho, Gusmão Ana Beatriz Ferreira, Marques Breno Oliveira, Bragas Níkolas Brayan da Silva, Rodrigues Isadora Bagues, Melo Rafaela Souza, de Azevedo Katiene Rodrigues Menezes

机构信息

Universidade Federal da Bahia, Instituto Multidisciplinar em Saúde, Vitória da Conquista BA, Brazil.

Universidade Estadual de Santa Cruz, Vitória da Conquista BA, Brazil.

出版信息

Dement Neuropsychol. 2025 Jun 2;19:e20240182. doi: 10.1590/1980-5764-DN-2024-0182. eCollection 2025.

DOI:10.1590/1980-5764-DN-2024-0182
PMID:40469240
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12136586/
Abstract

UNLABELLED

The brain's ability to adapt in response to stimuli is called neuroplasticity.

OBJECTIVE

This study investigates neuroplasticity in autistic individuals, focusing on neurobiological aspects, clinical correlations, and therapeutic interventions.

METHODS

This systematic review, registered in the International Prospective Register of Systematic Reviews-PROSPERO (ID: CRD42024522425) and guided by Preferred Reporting Items for Systematic Reviews and Meta-Analyses-PRISMA (2020) criteria, searched databases like Web of Science, Scopus, United States National Library of Medicine/ Medical Literature Analysis and Retrieval System Online (PubMed/Medline), Latin American and Caribbean Health Sciences Literature (LILACS), and Scientific Electronic Library Online (SciELO) for original articles published in 2018-2023.

RESULTS

Of the 2,316 studies found, 11 were selected, involving 1,943 autistic individuals, both children and adults. Most studies were classified as high/moderate quality using the Newcastle-Ottawa and Jadad scales. Observations included variations in SHANK2 gene expression, lower concentrations of α-synuclein, higher β-synuclein in children with autism spectrum disorder (ASD), correlations between NCAM1 expression and motor skills, and higher brain-derived neurotrophic factor (BDNF) concentration compared to non-autistic children.

CONCLUSIONS

Alterations in SHANK2, α-synuclein, β-synuclein, NCAM1, and BDNF in ASD suggest biomarkers and therapeutic targets for more effective interventions, improving care for autistic individuals.

摘要

未标注

大脑对刺激做出适应性反应的能力被称为神经可塑性。

目的

本研究调查自闭症个体的神经可塑性,重点关注神经生物学方面、临床相关性和治疗干预措施。

方法

本系统评价在国际前瞻性系统评价注册库-PROSPERO(编号:CRD42024522425)注册,并遵循系统评价和Meta分析的首选报告项目-PRISMA(2020)标准,检索了科学网、Scopus、美国国立医学图书馆/医学文献分析与联机检索系统(PubMed/Medline)、拉丁美洲和加勒比卫生科学文献数据库(LILACS)以及科学电子图书馆在线数据库(SciELO)等数据库,以获取2018年至2023年发表的原创文章。

结果

在检索到的2316项研究中,筛选出11项,涉及1943名自闭症个体,包括儿童和成人。使用纽卡斯尔-渥太华量表和雅达量表,大多数研究被归类为高质量/中等质量。观察结果包括自闭症谱系障碍(ASD)儿童中SHANK2基因表达的变化、α-突触核蛋白浓度降低、β-突触核蛋白浓度升高、NCAM1表达与运动技能之间的相关性,以及与非自闭症儿童相比更高的脑源性神经营养因子(BDNF)浓度。

结论

ASD中SHANK2、α-突触核蛋白、β-突触核蛋白、NCAM1和BDNF的改变提示了生物标志物和治疗靶点,有助于采取更有效的干预措施,改善对自闭症个体的护理。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21d6/12136586/ae4e16bf481c/1980-5764-DN-19-e20240182-gf02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21d6/12136586/caeea99ea5f2/1980-5764-DN-19-e20240182-gf01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21d6/12136586/ae4e16bf481c/1980-5764-DN-19-e20240182-gf02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21d6/12136586/caeea99ea5f2/1980-5764-DN-19-e20240182-gf01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21d6/12136586/ae4e16bf481c/1980-5764-DN-19-e20240182-gf02.jpg

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本文引用的文献

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Validation of plasma protein glycation and oxidation biomarkers for the diagnosis of autism.血浆蛋白糖化和氧化生物标志物用于自闭症诊断的验证。
Mol Psychiatry. 2024 Mar;29(3):653-659. doi: 10.1038/s41380-023-02357-9. Epub 2023 Dec 22.
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Immunogenetics of autism spectrum disorder: A systematic literature review.自闭症谱系障碍的免疫遗传学:一项系统的文献综述。
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Autism Spectrum Disorder: Neurodevelopmental Risk Factors, Biological Mechanism, and Precision Therapy.
自闭症谱系障碍:神经发育风险因素、生物学机制与精准治疗
Int J Mol Sci. 2023 Jan 17;24(3):1819. doi: 10.3390/ijms24031819.
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Diminished Repetition Suppression Reveals Selective and Systems-Level Face Processing Differences in ASD.自闭症患者的重复抑制减少揭示了选择性和系统水平的面孔加工差异。
J Neurosci. 2023 Mar 15;43(11):1952-1962. doi: 10.1523/JNEUROSCI.0608-22.2023. Epub 2023 Feb 9.
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