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The Impact of Neuroimmune Alterations in Autism Spectrum Disorder.

Gottfried C, Bambini-Junior V, Francis F, Riesgo R, Savino W - Front Psychiatry (2015)

Bottom Line: In the past decade, studies of ASD have substantially increased, in both humans and animal models.Moreover, the use of animal models to study ASD is providing increasing information on the relationship between the immune system and the pathophysiology of ASD.Herein, we will discuss the accumulating literature for ASD, giving special attention to the relevant aspects of factors that may be related to the neuroimmune interface in the development of ASD, including changes in neuroplasticity.

View Article: PubMed Central - PubMed

Affiliation: Translational Research Group in Autism Spectrum Disorder (GETTEA), Federal University of Rio Grande do Sul , Porto Alegre , Brazil ; Research Group in Neuroglial Plasticity, Department of Biochemistry, Federal University of Rio Grande do Sul , Porto Alegre , Brazil.

ABSTRACT
Autism spectrum disorder (ASD) involves a complex interplay of both genetic and environmental risk factors, with immune alterations and synaptic connection deficiency in early life. In the past decade, studies of ASD have substantially increased, in both humans and animal models. Immunological imbalance (including autoimmunity) has been proposed as a major etiological component in ASD, taking into account increased levels of pro-inflammatory cytokines observed in postmortem brain from patients, as well as autoantibody production. Also, epidemiological studies have established a correlation of ASD with family history of autoimmune diseases; associations with major histocompatibility complex haplotypes and abnormal levels of immunological markers in the blood. Moreover, the use of animal models to study ASD is providing increasing information on the relationship between the immune system and the pathophysiology of ASD. Herein, we will discuss the accumulating literature for ASD, giving special attention to the relevant aspects of factors that may be related to the neuroimmune interface in the development of ASD, including changes in neuroplasticity.

No MeSH data available.


Related in: MedlinePlus

Hypothesis for neuroimmune interactions in triggering the development of ASD. This hypothesis considers the presence of environmental risk factors during pregnancy, followed by immunoneuroendocrine response from the mother to the developing embryo/fetus. The risk factors (such as VPA) would influence central and peripheral neural responses in the context of a crosstalk with the immune system, followed by gradual changes in neural plasticity and function, resulting in behavioral impairment during development, ultimately leading to ASD.
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Figure 2: Hypothesis for neuroimmune interactions in triggering the development of ASD. This hypothesis considers the presence of environmental risk factors during pregnancy, followed by immunoneuroendocrine response from the mother to the developing embryo/fetus. The risk factors (such as VPA) would influence central and peripheral neural responses in the context of a crosstalk with the immune system, followed by gradual changes in neural plasticity and function, resulting in behavioral impairment during development, ultimately leading to ASD.

Mentions: Since the first descriptions of autism, 70 years of investigation have passed, with great efforts mainly in the last decade, bringing important information and knowledge on the mechanisms underlying ASD. Nevertheless, even with these advances, the etiology of ASD remains largely unknown and we are still searching for specific clinical marker(s) able to improve early diagnosis. We work on the hypothesis that integrating maternal–embryo systems will contribute to the understanding of ASD. One possibility, which was summarized here, concerns the hypothesis of neuroimmune interactions being involved in triggering ASD development, as schematically depicted in Figure 2. The presence of environmental risk factors during critical periods of embryonic/fetal development may influence the immune system in the mother, promoting localized or systemic inflammatory responses with the release of cytokines and hormonal molecules, which in turn, via neuroimmunomodulatory responses and crosstalk between circulatory and neural systems, may impair circuitry development, neuronal plasticity, and neuroglial function in the embryo/fetus. As immunological factors interfere with neural development since the embryonic period, and considering that inflammation or immune response may arise due to abnormal environmental interactions in utero, a better understanding of the neuroimmune changes that may underlie the pathogenesis or pathophysiology of ASD will hopefully have a large impact on the development of new clinical and therapeutic strategies to better deal with ASD.


The Impact of Neuroimmune Alterations in Autism Spectrum Disorder.

Gottfried C, Bambini-Junior V, Francis F, Riesgo R, Savino W - Front Psychiatry (2015)

Hypothesis for neuroimmune interactions in triggering the development of ASD. This hypothesis considers the presence of environmental risk factors during pregnancy, followed by immunoneuroendocrine response from the mother to the developing embryo/fetus. The risk factors (such as VPA) would influence central and peripheral neural responses in the context of a crosstalk with the immune system, followed by gradual changes in neural plasticity and function, resulting in behavioral impairment during development, ultimately leading to ASD.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4563148&req=5

Figure 2: Hypothesis for neuroimmune interactions in triggering the development of ASD. This hypothesis considers the presence of environmental risk factors during pregnancy, followed by immunoneuroendocrine response from the mother to the developing embryo/fetus. The risk factors (such as VPA) would influence central and peripheral neural responses in the context of a crosstalk with the immune system, followed by gradual changes in neural plasticity and function, resulting in behavioral impairment during development, ultimately leading to ASD.
Mentions: Since the first descriptions of autism, 70 years of investigation have passed, with great efforts mainly in the last decade, bringing important information and knowledge on the mechanisms underlying ASD. Nevertheless, even with these advances, the etiology of ASD remains largely unknown and we are still searching for specific clinical marker(s) able to improve early diagnosis. We work on the hypothesis that integrating maternal–embryo systems will contribute to the understanding of ASD. One possibility, which was summarized here, concerns the hypothesis of neuroimmune interactions being involved in triggering ASD development, as schematically depicted in Figure 2. The presence of environmental risk factors during critical periods of embryonic/fetal development may influence the immune system in the mother, promoting localized or systemic inflammatory responses with the release of cytokines and hormonal molecules, which in turn, via neuroimmunomodulatory responses and crosstalk between circulatory and neural systems, may impair circuitry development, neuronal plasticity, and neuroglial function in the embryo/fetus. As immunological factors interfere with neural development since the embryonic period, and considering that inflammation or immune response may arise due to abnormal environmental interactions in utero, a better understanding of the neuroimmune changes that may underlie the pathogenesis or pathophysiology of ASD will hopefully have a large impact on the development of new clinical and therapeutic strategies to better deal with ASD.

Bottom Line: In the past decade, studies of ASD have substantially increased, in both humans and animal models.Moreover, the use of animal models to study ASD is providing increasing information on the relationship between the immune system and the pathophysiology of ASD.Herein, we will discuss the accumulating literature for ASD, giving special attention to the relevant aspects of factors that may be related to the neuroimmune interface in the development of ASD, including changes in neuroplasticity.

View Article: PubMed Central - PubMed

Affiliation: Translational Research Group in Autism Spectrum Disorder (GETTEA), Federal University of Rio Grande do Sul , Porto Alegre , Brazil ; Research Group in Neuroglial Plasticity, Department of Biochemistry, Federal University of Rio Grande do Sul , Porto Alegre , Brazil.

ABSTRACT
Autism spectrum disorder (ASD) involves a complex interplay of both genetic and environmental risk factors, with immune alterations and synaptic connection deficiency in early life. In the past decade, studies of ASD have substantially increased, in both humans and animal models. Immunological imbalance (including autoimmunity) has been proposed as a major etiological component in ASD, taking into account increased levels of pro-inflammatory cytokines observed in postmortem brain from patients, as well as autoantibody production. Also, epidemiological studies have established a correlation of ASD with family history of autoimmune diseases; associations with major histocompatibility complex haplotypes and abnormal levels of immunological markers in the blood. Moreover, the use of animal models to study ASD is providing increasing information on the relationship between the immune system and the pathophysiology of ASD. Herein, we will discuss the accumulating literature for ASD, giving special attention to the relevant aspects of factors that may be related to the neuroimmune interface in the development of ASD, including changes in neuroplasticity.

No MeSH data available.


Related in: MedlinePlus