Developmental Trajectories of the Corpus Callosum in Attention-Deficit/Hyperactivity Disorder

Gilliam, Mary; Stockman, Michael; Malek, Meaghan; Sharp, Wendy; Greenstein, Deanna; Lalonde, François; Clasen, Liv S.; Giedd, Jay N.; Rapoport, Judith L.; Shaw, Philip

doi:10.1016/j.biopsych.2010.11.024

Cited by 54 publications

(43 citation statements)

References 59 publications

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“…This could be seen as a parallel to the frequently described macrocephaly in human 16p11.2 deletion patients and other types of ASD (Courchesne et al, 2007). There is also an apparent decrease in the size of the corpus callosum, which has been repeatedly observed in ASD and ADHD (Giedd et al, 1994 and Gilliam et al, 2011), as well as mouse models for ASD (Ellegood et al, 2013 and Wahlsten et al, 2003). The 16p11+/− mice show hyperactivity, a potential correlate for ADHD observed in 16p11.2 patients (Shinawi et al, 2010).…”

Section: Discussionmentioning

confidence: 73%

Behavioral Abnormalities and Circuit Defects in the Basal Ganglia of a Mouse Model of 16p11.2 Deletion Syndrome

et al. 2014

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Summary A deletion on human chromosome 16p11.2 is associated with autism spectrum disorders. We deleted the syntenic region on mouse chromosome 7F3. MRI and high-throughput single-cell transcriptomics revealed anatomical and cellular abnormalities, particularly in cortex and striatum of juvenile mutant mice (16p11+/−). We found elevated numbers of striatal medium spiny neurons (MSNs) expressing the dopamine D2 receptor (Drd2+) and fewer dopamine-sensitive (Drd1+) neurons in deep layers of cortex. Electrophysiological recordings of Drd2+ MSN revealed synaptic defects, suggesting abnormal basal ganglia circuitry function in 16p11+/− mice. This is further supported by behavioral experiments showing hyperactivity, circling, and deficits in movement control. Strikingly, 16p11+/− mice showed a complete lack of habituation reminiscent of what is observed in some autistic individuals. Our findings unveil a fundamental role of genes affected by the 16p11.2 deletion in establishing the basal ganglia circuitry and provide insights in the pathophysiology of autism.

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Section: Discussionmentioning

confidence: 73%

Behavioral Abnormalities and Circuit Defects in the Basal Ganglia of a Mouse Model of 16p11.2 Deletion Syndrome

et al. 2014

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“…As noted above, links between prematurity and reduced birth weight with air pollution are increasingly reported [157,158]. Alterations in brain white matter are also observed in attention deficit hyperactivity disorder [164]. Disconnectivity, i.e., functional and/or anatomical damage to white matter axons in communicating pathways found in ASD and schizophrenia [107-109,188], is critical to language, social behavior and some cognitive functions.…”

Section: Discussionmentioning

confidence: 99%

Developmental neurotoxicity of inhaled ambient ultrafine particle air pollution: Parallels with neuropathological and behavioral features of autism and other neurodevelopmental disorders

et al. 2017

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Accumulating evidence from both human and animal studies show that brain is a target of air pollution. Multiple epidemiological studies have now linked components of air pollution to diagnosis of autism spectrum disorder (ASD), a linkage with plausibility based on the shared mechanisms of inflammation. Additional plausibility appears to be provided by findings from our studies in mice of exposures from postnatal day (PND) 4-7 and 10-13 (human 3rd trimester equivalent), to concentrated ambient ultrafine (UFP) particles, considered the most reactive component of air pollution, at levels consistent with high traffic areas of major U.S. cities and thus highly relevant to human exposures. These exposures, occurring during a period of marked neuro- and gliogenesis, unexpectedly produced a pattern of developmental neurotoxicity notably similar to multiple hypothesized mechanistic underpinnings of ASD, including its greater impact in males. UFP exposures induced inflammation/microglial activation, reductions in size of the corpus callosum (CC) and associated hypomyelination, aberrant white matter development and/or structural integrity with ventriculomegaly (VM), elevated glutamate and excitatory/inhibitory imbalance, increased amygdala astrocytic activation, and repetitive and impulsive behaviors. Collectively, these findings suggest the human 3rd trimester equivalent as a period of potential vulnerability to neurodevelopmental toxicity to UFP, particularly in males, and point to the possibility that UFP air pollution exposure during periods of rapid neuro- and gliogenesis may be a risk factor not only for ASD, but also for other neurodevelopmental disorders that share features with ASD, such as schizophrenia, attention deficit disorder, and periventricular leukomalacia.

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“…in cases of partial or complete agenesis of the corpus callosum, is associated with delayed and hampered interhemispheric integration (e.g., Bayard et al, 2004;Ocklenburg et al, 2015) and slowing of executive processing (Marco et al, 2012). Also, alterations during maturation of the corpus callosum have been linked to pediatric disorders or developmental disabilities, including attention/hyperactivity disorder (e.g., Gilliam et al, 2011, Dramsdahl et al, 2012 and dyslexia (e.g., von Plessen et al, 2002). These observations related to an altered callosal development also emphasize the importance of gaining a better understanding of the typical development of the corpus callosum during childhood.…”

Section: Introductionmentioning

confidence: 98%

Selective increase in posterior corpus callosum thickness between the age of 4 and 11 years

et al. 2016

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Developmental Trajectories of the Corpus Callosum in Attention-Deficit/Hyperactivity Disorder

Cited by 54 publications

References 59 publications

Behavioral Abnormalities and Circuit Defects in the Basal Ganglia of a Mouse Model of 16p11.2 Deletion Syndrome

Behavioral Abnormalities and Circuit Defects in the Basal Ganglia of a Mouse Model of 16p11.2 Deletion Syndrome

Developmental neurotoxicity of inhaled ambient ultrafine particle air pollution: Parallels with neuropathological and behavioral features of autism and other neurodevelopmental disorders

Selective increase in posterior corpus callosum thickness between the age of 4 and 11 years

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