The influence of neuroinflammation in Autism Spectrum Disorder

Matta, Samantha M; Hill‐Yardin, Elisa L.; Crack, Peter J

doi:10.1016/j.bbi.2019.04.037

Cited by 273 publications

(184 citation statements)

References 197 publications

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“…Interestingly, the composition of exosomes secreted from mesenchymal stem cells could be manipulated by the treatment of several interleukins [274]. Recently, neuroinflammation induced by proinflammatory cytokines was suggested as a novel pathogenesis of ASD, particularly in irritability and socialization problems [275]. As a therapeutic approach, stem-cell-derived exosomes containing anti-inflammatory molecules could be used as efficient carriers for delivering anti-inflammatory molecules across the blood-brain barrier [276].…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Genetic and Epigenetic Etiology Underlying Autism Spectrum Disorder

Yoon

Choi

Lee

et al. 2020

JCM

105

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Autism spectrum disorder (ASD) is a pervasive neurodevelopmental disorder characterized by difficulties in social interaction, language development delays, repeated body movements, and markedly deteriorated activities and interests. Environmental factors, such as viral infection, parental age, and zinc deficiency, can be plausible contributors to ASD susceptibility. As ASD is highly heritable, genetic risk factors involved in neurodevelopment, neural communication, and social interaction provide important clues in explaining the etiology of ASD. Accumulated evidence also shows an important role of epigenetic factors, such as DNA methylation, histone modification, and noncoding RNA, in ASD etiology. In this review, we compiled the research published to date and described the genetic and epigenetic epidemiology together with environmental risk factors underlying the etiology of the different phenotypes of ASD.

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Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Genetic and Epigenetic Etiology Underlying Autism Spectrum Disorder

Yoon

Choi

Lee

et al. 2020

JCM

105

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“…A large proportion of children with ASD have been reported to have co-occurring behavioural, medical and biological conditions [2][3][4]. Furthermore, growing evidence suggest an ongoing immune dysfunction in the brain and the peripheral immune system of a subset of individuals with ASD [5,6]. Several peripheral markers of inflammation (interleukin-1 beta (IL-1β), IL-6 and tumour necrosis factor-alpha (TNF-α)) have been found to be elevated in children with ASD [7][8][9][10][11].…”

Section: Introductionmentioning

confidence: 99%

“…Several reports from human studies also suggest that gestational vitamin D and/or omega-3 LCPUFA deficiency is associated with the development of ASD [38][39][40][41] and other psychological and neurodevelopmental disorders [42]. Furthermore, children with ASD have been shown to have inadequate intakes of vitamin D and omega-3 LCPUFA [11][12][13][14][15], as is reflected in significantly lower vitamin D and/or omega-3 LCPUFA status than their healthy counterparts [5,16].…”

Section: Introductionmentioning

confidence: 99%

Inflammation (IL-1β) Modifies the Effect of Vitamin D and Omega-3 Long Chain Polyunsaturated Fatty Acids on Core Symptoms of Autism Spectrum Disorder—An Exploratory Pilot Study

et al. 2020

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Background: The role of vitamin D and omega-3 long chain polyunsaturated fatty acids (omega-3 LCPUFA) in improving core symptoms of autism spectrum disorder (ASD) in children has been investigated by a few randomised controlled trials and the results are mixed and inconclusive. The response to treatment with these nutrients is heterogenous and may be influenced by inflammatory state. As an exploratory analysis, we investigated whether inflammatory state would modulate the effect of these nutrients on core symptoms of ASD. Methods: Seventy-three New Zealand children with ASD (2.5-8.0 years) completed a 12-month randomised, double-blind, placebo-controlled trial of vitamin D (VID, 2000 IU/day), omega-3 LCPUFA; (OM, 722 mg/day docosahexaenoic acid), or both (VIDOM). Non-fasting baseline plasma interleukin-1β (IL-1β) was available for 67 children (VID = 15, OM = 21, VIDOM = 15, placebo = 16). Children were categorised as having undetectable/normal IL-1β (<3.2 pg/ml, n = 15) or elevated IL-1β (≥3.2 pg/mL, n = 52). The Social Responsiveness Scale (SRS) questionnaire was used to assess core symptoms of ASD (baseline, 12-month). Mixed model repeated measure analyses (including all children or only children with elevated IL-1β) were used. Results: We found evidence for an interaction between baseline IL-1β and treatment response for SRS-total, SRS-social communicative functioning, SRS-awareness and SRS-communication (all P interaction < 0.10). When all children were included in the analysis, two outcome comparisons (treatments vs. placebo) showed greater improvements: VID, no effect (all P > 0.10); OM and VIDOM (P = 0.01) for SRS-awareness. When only children with elevated IL-1β were included, five outcomes showed greater improvements: OM (P = 0.01) for SRS-total; OM (P = 0.03) for SRS-social communicative Nutrients 2020, 12, 661 2 of 17 functioning; VID (P = 0.01), OM (P = 0.003) and VIDOM (P = 0.01) for SRS-awareness. Conclusion: Inflammatory state may have modulated responses to vitamin D and omega-3 LCPUFA intervention in children with ASD, suggesting children with elevated inflammation may benefit more from daily vitamin D and omega-3 LCPUFA supplementation.

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“…Although its etiology remains largely unknown and complex, a growing body of evidence implicates the disturbance in the immune system as a mechanism of psychiatric disorders, including ASD (3)(4)(5). Alterations in the peripheral innate and adaptive immune responses, as well as prominent in ammation in the brain, have been reported in patients with ASD (6,7). In the periphery, increased expression of pro-in ammatory cytokines, including interleukin-1 beta (IL-1β), IL-6, tumor necrosis factor alpha (TNF-α), transforming growth factor beta, IL-8, and IL-17 has been observed in the plasma, serum, and peripheral blood mononuclear cells (PBMCs) of patients with ASD (7,8).…”

Section: Introductionmentioning

confidence: 99%

“…Alterations in the peripheral innate and adaptive immune responses, as well as prominent in ammation in the brain, have been reported in patients with ASD (6,7). In the periphery, increased expression of pro-in ammatory cytokines, including interleukin-1 beta (IL-1β), IL-6, tumor necrosis factor alpha (TNF-α), transforming growth factor beta, IL-8, and IL-17 has been observed in the plasma, serum, and peripheral blood mononuclear cells (PBMCs) of patients with ASD (7,8). Antioxidant networks (e.g., superoxidase dismutase expression and activity) and the responses to innate immunity stimuli (e.g., lipopolysaccharide and zymosan) have been found to be dysregulated in the monocytes of ASD patients (9)(10)(11).…”

Section: Introductionmentioning

confidence: 99%

TNF-α expression ratio of M1/M2 macrophages is a potential adjunctive tool for the diagnosis of autism spectrum disorder

Yamauchi¹,

Makinodan²,

Toritsuka³

et al. 2020

Preprint

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Background The etiology of autism spectrum disorder (ASD) is complex. Its pathobiology is characterized by enhanced inflammatory activities; however, the exact ASD pathobiology remains unclear. Some cases of ASD are difficult to diagnose using existing psychological assessments because the careful exclusion of other psychiatric disorders is challenging. To distinguish between the appropriate targets for interventions and research, the demand for identifying efficient diagnostic biomarkers is increasing. This study aimed to find an inflammatory indicator beneficial for the diagnosis of ASD.Methods Cytokine mRNA expression, including tumor necrosis factor-α (TNF-α), was measured in the differentiated M1 and M2 macrophages of ASD patients (n = 29) and typically developed (TD) individuals (n = 30). TNF-α expression was also measured in the monocytes of ASD patients (n = 7) and TD individuals (n = 6).Results TNF-α expression in M1 macrophages and TNF-α expression ratio of M1/M2 macrophages were markedly higher in ASD patients than in TD subjects; however, this difference was not observed in M2 macrophages (M1: p < 0.01; ratio of M1/M2: p < 0.0001; M2: p > 0.05), suggesting that this indicator could be a useful tool for diagnosing ASD (M1: sensitivity = 34.5%, specificity = 96.7%, area under the curve (AUC) = 0.74, positive likelihood ratio (PLR) = 10.34; ratio of M1/M2: sensitivity = 55.2%, specificity = 96.7%, AUC = 0.79, PLR = 16.55). However, there was no significant difference in the TNF-α expression in monocytes between ASD and TD individuals (p > 0.05).Conclusion These findings suggest that TNF-α expression in differentiated macrophages represents a novel adjunctive tool for the diagnosis of ASD.

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The influence of neuroinflammation in Autism Spectrum Disorder

Cited by 273 publications

References 197 publications

Genetic and Epigenetic Etiology Underlying Autism Spectrum Disorder

Genetic and Epigenetic Etiology Underlying Autism Spectrum Disorder

Inflammation (IL-1β) Modifies the Effect of Vitamin D and Omega-3 Long Chain Polyunsaturated Fatty Acids on Core Symptoms of Autism Spectrum Disorder—An Exploratory Pilot Study

TNF-α expression ratio of M1/M2 macrophages is a potential adjunctive tool for the diagnosis of autism spectrum disorder

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