Serum copper and zinc levels in individuals with autism spectrum disorders

Li, Siou; Wang, Jialiang; Bjørklund, Geir; Zhao, Weina; Yin, Changhao

doi:10.1097/wnr.0000000000000251

Cited by 87 publications

(50 citation statements)

References 24 publications

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“…Clinical data have previously established that mean serum Zn 2+ levels are significantly lower in children diagnosed with ASD compared to unaffected children and that there exist disturbances in Zn 2+ metabolism in patients diagnosed with ASD [10-12]. hDAT T356M is the first de novo DAT mutation found in a patient with ASD, and hDAT T356M functional deficits can partially be rescued by Zn 2+ .…”

Section: Discussionmentioning

confidence: 99%

Zn2+ reverses functional deficits in a de novo dopamine transporter variant associated with autism spectrum disorder

et al. 2015

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Our laboratory recently characterized a novel autism spectrum disorder (ASD)-associated de novo missense mutation in the human dopamine transporter (hDAT) gene SLC6A3 (hDAT T356M). This hDAT variant exhibits dysfunctional forward and reverse transport properties that may contribute to DA dysfunction in ASD. Here, we report that Zn2+ reverses, at least in part, the functional deficits of ASD-associated hDAT variant T356M. These data suggest that the molecular mechanism targeted by Zn2+ to restore partial function in hDAT T356M may be a novel therapeutic target to rescue functional deficits in hDAT variants associated with ASD.

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Section: Discussionmentioning

confidence: 99%

Zn2+ reverses functional deficits in a de novo dopamine transporter variant associated with autism spectrum disorder

et al. 2015

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“…Low levels of zinc have been measured in the infant hair of individuals with ASD [170], and in mouse models zinc deficiency during development leads to alterations in social behavior [171]. Disruptions in fetal copper homeostasis during brain development might contribute to ASD risk, with both elevated and decreased copper levels linked with autism [172–174]. Employing a validated tooth matrix in a twin–cotwin design with monozygotic and dizygotic twins discordant for ASD, a study tested whether fetal and postnatal metal dysregulation increases ASD risk.…”

Section: Environmental Factorsmentioning

confidence: 99%

The contribution of environmental exposure to the etiology of autism spectrum disorder

Bölte

Girdler

Marschik

2018

Cell. Mol. Life Sci.

343

246

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Autism spectrum disorder (ASD) is a neurodevelopmental condition of heterogeneous etiology. While it is widely recognized that genetic and environmental factors and their interactions contribute to autism phenotypes, their precise causal mechanisms remain poorly understood. This article reviews our current understanding of environmental risk factors of ASD and their presumed adverse physiological mechanisms. It comprehensively maps the significance of parental age, teratogenic compounds, perinatal risks, medication, smoking and alcohol use, nutrition, vaccination, toxic exposures, as well as the role of extreme psychosocial factors. Further, we consider the role of potential protective factors such as folate and fatty acid intake. Evidence indicates an increased offspring vulnerability to ASD through advanced maternal and paternal age, valproate intake, toxic chemical exposure, maternal diabetes, enhanced steroidogenic activity, immune activation, and possibly altered zinc–copper cycles and treatment with selective serotonin reuptake inhibitors. Epidemiological studies demonstrate no evidence for vaccination posing an autism risk. It is concluded that future research needs to consider categorical autism, broader autism phenotypes, as well as autistic traits, and examine more homogenous autism variants by subgroup stratification. Our understanding of autism etiology could be advanced by research aimed at disentangling the causal and non-causal environmental effects, both founding and moderating, and gene–environment interplay using twin studies, longitudinal and experimental designs. The specificity of many environmental risks for ASD remains unknown and control of multiple confounders has been limited. Further understanding of the critical windows of neurodevelopmental vulnerability and investigating the fit of multiple hit and cumulative risk models are likely promising approaches in enhancing the understanding of role of environmental factors in the etiology of ASD.

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“…A recent study suggests that increased levels of BPb in some children with ASD may trigger the production of serum anti-ribosomal P antibodies (Mostafa et al 2016b). It has been reported that ASD children often have a lower zinc (Zn)-to-copper (Cu) ratio in blood compared to healthy controls (Faber et al 2009, Li et al 2014, Crăciun et al 2016) and children with other neurological disorders (Macedoni-Lukšič et al 2015). It has been suggested that metallothionein (MT) dysfunction may occur as a cause of Hg accumulation in children with ASD, and the same dysfunction may also lead to Zn deficiency (Bjørklund 2013).…”

Section: Autoantibodiesmentioning

confidence: 99%