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本文引用的文献

1
Early intervention combined with targeted treatment promotes cognitive and behavioral improvements in young children with fragile x syndrome.早期干预结合针对性治疗可促进脆性X综合征幼儿的认知和行为改善。
Case Rep Genet. 2012;2012:280813. doi: 10.1155/2012/280813. Epub 2012 Mar 26.
2
Effects of STX209 (arbaclofen) on neurobehavioral function in children and adults with fragile X syndrome: a randomized, controlled, phase 2 trial.STX209(阿巴洛芬)对脆性 X 综合征儿童和成人神经行为功能的影响:一项随机、对照、2 期试验。
Sci Transl Med. 2012 Sep 19;4(152):152ra127. doi: 10.1126/scitranslmed.3004214.
3
Matrix metalloproteinases and minocycline: therapeutic avenues for fragile X syndrome.基质金属蛋白酶和米诺环素:脆性 X 综合征的治疗途径。
Neural Plast. 2012;2012:124548. doi: 10.1155/2012/124548. Epub 2012 May 20.
4
De novo gene disruptions in children on the autistic spectrum.自闭症谱系儿童中的新生基因缺失。
Neuron. 2012 Apr 26;74(2):285-99. doi: 10.1016/j.neuron.2012.04.009.
5
Negative allosteric modulation of the mGluR5 receptor reduces repetitive behaviors and rescues social deficits in mouse models of autism.负变构调节 mGluR5 受体可减少自闭症小鼠模型的重复行为并改善社交缺陷。
Sci Transl Med. 2012 Apr 25;4(131):131ra51. doi: 10.1126/scitranslmed.3003501.
6
Enriched experience and recovery from amblyopia in adult rats: impact of motor, social and sensory components.丰富的经验和成年大鼠弱视的恢复:运动、社会和感觉成分的影响。
Neuropharmacology. 2012 Jun;62(7):2388-97. doi: 10.1016/j.neuropharm.2012.02.010.
7
Chronic pharmacological mGlu5 inhibition corrects fragile X in adult mice.慢性药理学 mGlu5 抑制可纠正成年小鼠的脆性 X 。
Neuron. 2012 Apr 12;74(1):49-56. doi: 10.1016/j.neuron.2012.03.009.
8
The pathophysiology of fragile X (and what it teaches us about synapses).脆性 X 症的病理生理学(及其对突触的启示)。
Annu Rev Neurosci. 2012;35:417-43. doi: 10.1146/annurev-neuro-060909-153138. Epub 2012 Apr 5.
9
Amblyopia: background to the special issue on stroke recovery.弱视:脑卒中康复特刊背景介绍。
Dev Psychobiol. 2012 Apr;54(3):224-38. doi: 10.1002/dev.21022.
10
Pharmacological treatment of fragile X syndrome with GABAergic drugs in a knockout mouse model.使用 GABA 能药物治疗脆性 X 综合征的药物治疗。
Behav Brain Res. 2012 Apr 1;229(1):244-9. doi: 10.1016/j.bbr.2012.01.031. Epub 2012 Jan 21.

成人神经发育障碍的治疗。

Treatment of neurodevelopmental disorders in adulthood.

机构信息

Neuroscience Center, University of Helsinki, 00014 Helsinki, Finland.

出版信息

J Neurosci. 2012 Oct 10;32(41):14074-9. doi: 10.1523/JNEUROSCI.3287-12.2012.

DOI:10.1523/JNEUROSCI.3287-12.2012
PMID:23055475
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3500763/
Abstract

Brain development in neurodevelopmental disorders has been considered to comprise a sequence of critical periods, and abnormalities occurring during early development have been considered irreversible in adulthood. However, findings in mouse models of neurodevelopmental disorders, including fragile X, Rett syndrome, Down syndrome, and neurofibromatosis type I suggest that it is possible to reverse certain molecular, electrophysiological, and behavioral deficits associated with these disorders in adults by genetic or pharmacological manipulations. Furthermore, recent studies have suggested that critical period-like plasticity can be reactivated in the adult brain by environmental manipulations or by pharmacotherapy. These studies open up a tantalizing possibility that targeted pharmacological treatments in combination with regimes of training or rehabilitation might alleviate or reverse the symptoms of neurodevelopmental disorders even after the end of critical developmental periods. Even though translation from animal experimentation to clinical practice is challenging, these results suggest a rational basis for treatment of neurodevelopmental disorders in adulthood.

摘要

神经发育障碍中的大脑发育被认为包含一系列关键期,并且早期发育过程中的异常在成年后被认为是不可逆转的。然而,神经发育障碍的小鼠模型研究,包括脆性 X 综合征、雷特综合征、唐氏综合征和神经纤维瘤病 I 型,表明通过遗传或药物操作,有可能逆转与这些疾病相关的某些分子、电生理和行为缺陷。此外,最近的研究表明,通过环境操作或药物治疗,成人大脑中的类似关键期可塑性可以被重新激活。这些研究提出了一个诱人的可能性,即靶向药物治疗与训练或康复方案相结合,即使在关键发育期结束后,也可能减轻或逆转神经发育障碍的症状。尽管从动物实验到临床实践的转化具有挑战性,但这些结果为成年期神经发育障碍的治疗提供了合理的依据。