Maternal Immune Activation and Autism Spectrum Disorder: From Rodents to Nonhuman and Human Primates.
Maternal Immune Activation and Autism Spectrum Disorder: From Rodents to Nonhuman and Human Primates.
复制标题
DOI：
10.1016/j.biopsych.2016.10.020
复制
发表时间：
2017-03-01
影响因子：
10.6
通讯作者：
Bauman MD
中科院分区：
文献类型：
--
作者：
Careaga M;Murai T;Bauman MD
在怀孕期间暴露于感染的一部分妇女生下一个孩子的风险增加，这个孩子后来被诊断患有神经发育或神经精神障碍。虽然流行病学研究主要集中在母亲感染和后代精神分裂症（SZ）风险增加之间的关联，越来越多的证据表明，母亲感染也可能增加自闭症谱系障碍（ASD）的风险。许多因素，包括遗传易感性，感染的强度和时间，以及暴露于额外的令人厌恶的产后事件，可能会影响母体感染改变胎儿脑发育的程度和疾病表型（ASD; SZ;其他神经发育障碍）的表达。临床前动物模型提供了一个测试平台，以系统地评估母体感染对胎儿脑发育的影响，确定与人类CNS疾病的相关性，并评估新的预防和治疗策略。小鼠、大鼠和非人灵长类动物的母体免疫激活（MIA）模型表明，母体免疫应答是妊娠期间暴露于感染与随后后代大脑和行为发育变化之间的关键联系。然而，产前免疫激发的类型、严重程度和时间的差异以及行为表型分析方法的不一致性阻碍了临床前结果向人类研究的转化。在这里，我们强调了MIA模型作为研究ASD产前风险因素的临床前工具的承诺和局限性，并提出了具体的变化，以提高重现性和最大限度地提高翻译潜力。
A subset of women who are exposed to infection during pregnancy have an increased risk of giving birth to a child who will later be diagnosed with a neurodevelopmental or neuropsychiatric disorder. Although epidemiology studies have primarily focused on the association between maternal infection and an increased risk of offspring schizophrenia (SZ), mounting evidence indicates that maternal infection may also increase the risk of autism spectrum disorder (ASD). A number of factors, including genetic susceptibility, the intensity and timing of the infection, and exposure to additional aversive postnatal events, may influence the extent to which maternal infection alters fetal brain development and which disease phenotype (ASD; SZ; other neurodevelopmental disorders) is expressed. Preclinical animal models provide a test bed to systematically evaluate the effects of maternal infection on fetal brain development, determine the relevance to human CNS disorders, and to evaluate novel preventative and therapeutic strategies. Maternal immune activation (MIA) models in mice, rats, and nonhuman primates suggest that the maternal immune response is the critical link between exposure to infection during pregnancy and subsequent changes in brain and behavioral development of offspring. However, differences in the type, severity, and timing of prenatal immune challenge paired with inconsistencies in behavioral phenotyping approaches have hindered the translation of preclinical results to human studies. Here we highlight the promises and limitations of the MIA model as a preclinical tool to study prenatal risk factors for ASD, and suggest specific changes to improve reproducibility and maximize translational potential.
登录
查看更多内容
DOI：
10.1186/2045-5380-1-9
发表时间：
2011-11-07
期刊：
Biology of mood & anxiety disorders
影响因子：
--
作者：
Belzung C;Lemoine M
通讯作者：
Lemoine M
DOI：
10.1126/science.1198469
发表时间：
2011-01-21
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Atarashi K;Tanoue T;Shima T;Imaoka A;Kuwahara T;Momose Y;Cheng G;Yamasaki S;Saito T;Ohba Y;Taniguchi T;Takeda K;Hori S;Ivanov II;Umesaki Y;Itoh K;Honda K
通讯作者：
Honda K
影响因子：
9.3
作者：
Boris, Marvin;Kaiser, Claudia C.;Feinstein, Douglas L.
通讯作者：
Feinstein, Douglas L.
影响因子：
10.6
作者：
Abazyan, Bagrat;Nomura, Jun;Kannan, Geetha;Ishizuka, Koko;Tamashiro, Kellie L.;Nucifora, Frederick;Pogorelov, Vladimir;Ladenheim, Bruce;Yang, Chunxia;Krasnova, Irina N.;Cadet, Jean Lud;Pardo, Carlos;Mori, Susumu;Kamiya, Atsushi;Vogel, Michael W.;Sawa, Akira;Ross, Christopher A.;Pletnikov, Mikhail V.
通讯作者：
Pletnikov, Mikhail V.
DOI：
10.1073/pnas.1301213110
发表时间：
2013-06-18
影响因子：
11.1
作者：
Chang, Steve W. C.;Brent, Lauren J. N.;Platt, Michael L.
通讯作者：
Platt, Michael L.