Author Correction: Altered cerebellar connectivity in autism and cerebellar-mediated rescue of autism-related behaviors in mice

Stoodley, Catherine J.; D’Mello, Anila M.; Ellegood, Jacob; Jakkamsetti, Vikram; Liu, Pei; Nebel, Mary Beth; Gibson, Jennifer M.; Kelly, Elyza; Meng, Fantao; Cano, Christopher A.; Pascual, Juan M.; Mostofsky, Stewart H.; Lerch, Jason P.; Tsai, Peter T.

doi:10.1038/s41593-018-0096-2

Cited by 11 publications

(8 citation statements)

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“…Therefore, low‐frequency force oscillations may be associated with low‐frequency fluctuations of activity in visuomotor brain regions activated during grip‐force tracking. Right Crus I and left IPL are interconnected brain areas activated during precision‐grip force tracking [Neely et al, 2013; Vaillancourt et al, 2006] and are implicated in core ASD social and communication deficits [Stoodley et al, 2018]. Future studies should examine whether the low frequency oscillations (<0.25 Hz) observed during visuomotor force tracking are associated with anomalous connectivity within the visuomotor network, including right Crus I and left IPL, in children with ASD.…”

Section: Discussionmentioning

confidence: 99%

Children with Autism Spectrum Disorder Show Impairments During Dynamic Versus Static Grip‐force Tracking

et al. 2020

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Impairments in visuomotor integration (VMI) may contribute to anomalous development of motor, as well as socialcommunicative, skills in children with autism spectrum disorder (ASD). However, it is relatively unknown whether VMI impairments are specific to children with ASD versus children with other neurodevelopmental disorders. As such, this study addressed the hypothesis that children with ASD, but not those in other clinical control groups, would show greater deficits in high-VMI dynamic grip-force tracking versus low-VMI static presentation. Seventy-nine children, aged 7-17 years, participated: 22 children with ASD, 17 children with fetal alcohol spectrum disorder (FASD), 18 children with Attention-Deficit Hyperactivity Disorder (ADHD), and 22 typically developing (TD) children. Two grip-force tracking conditions were examined: (1) a low-VMI condition (static visual target) and (2) a high-VMI condition (dynamic visual target). Low-frequency force oscillations <0.5 Hz during the visuomotor task were also examined. Twoway ANCOVAs were used to examine group x VMI and group x frequency effects (α = 0.05). Children with ASD showed a difficulty, above that seen in the ADHD/FASD groups, tracking dynamic, but not static, visual stimuli as compared to TD children. Low-frequency force oscillations <0.25 Hz were also significantly greater in the ASD versus the TD group. This study is the first to report VMI deficits during dynamic versus static grip-force tracking and increased proportion of force oscillations <0.25 Hz during visuomotor tracking in the ASD versus TD group. Dynamic VMI impairments may be a core psychophysiologic feature that could contribute to impaired development of motor and socialcommunicative skills in ASD.

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Section: Discussionmentioning

confidence: 99%

Children with Autism Spectrum Disorder Show Impairments During Dynamic Versus Static Grip‐force Tracking

et al. 2020

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“…4a). Using a combination of recently developed technologies such as optogenetics, chemogenetics, trans-synaptic tracers and single-cell sequencing in both animal models and human cells [76][77][78][79] , we now have the ability to determine the effect of genetic variants on specific cells and networks with unprecedented detail.…”

Section: Identifying the Circuitsmentioning

confidence: 99%

A framework for the investigation of rare genetic disorders in neuropsychiatry

Sanders

Şahin

Hostyk

et al. 2019

Nat Med

105

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“…In addition to epilepsy and complications to tuber formation throughout the body, approximately 50% of TSC patients meet the criteria for diagnosis of ASD, with a substantial portion of others suffering more subtle neuropsychiatric disturbances (Sundberg and Sahin, 2015; Gipson and Johnston, 2017). Though a previous study linked cerebellar tuber formation to the development of ASD (Weber et al, 2000), more recent efforts have been made to investigate how Purkinje cell function is specifically disrupted through targeted knock-out of TSC1 in Purkinje cells (Tsai et al, 2012; Stoodley et al, 2018). Initial analysis showed that when TSC1 is knocked out of Purkinje cells, there are substantial morphological and neurophysiological changes in Purkinje cells (Tsai et al, 2012).…”

Section: Mouse Models Of Cerebellar Cognitive Disordersmentioning

confidence: 99%

“…These changes were sufficient to cause behavioral anomalies consistent with what is observed in patients with ASD, including aberrant social interactions, increased repetitive behaviors, and changes in vocalizations (Tsai et al, 2012). Subsequent studies showed that genetically altering TSC1 in vivo also induced structural connectivity defects within cortical areas that have been suspected to be dysfunctional in patients with ASD (Stoodley et al, 2018). These studies were among the first to mechanistically link Purkinje cell dysfunction with specific neurobehavioral outcomes in ASD and support the interesting hypothesis that dysfunction in cerebellar computations, that are perhaps localized to specific lobules such as right CrusI/II, could lead to motor as well as cognitive dysfunction.…”

Section: Mouse Models Of Cerebellar Cognitive Disordersmentioning

confidence: 99%

Functional Outcomes of Cerebellar Malformations

Gill

Sillitoe

2019

Front. Cell. Neurosci.

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The cerebellum is well-established as a primary center for controlling sensorimotor functions. However, recent experiments have demonstrated additional roles for the cerebellum in higher-order cognitive functions such as language, emotion, reward, social behavior, and working memory. Based on the diversity of behaviors that it can influence, it is therefore not surprising that cerebellar dysfunction is linked to motor diseases such as ataxia, dystonia, tremor, and Parkinson’s disease as well to non-motor disorders including autism spectrum disorders (ASD), schizophrenia, depression, and anxiety. Regardless of the condition, there is a growing consensus that developmental disturbances of the cerebellum may be a central culprit in triggering a number of distinct pathophysiological processes. Here, we consider how cerebellar malformations and neuronal circuit wiring impact brain function and behavior during development. We use the cerebellum as a model to discuss the expanding view that local integrated brain circuits function within the context of distributed global networks to communicate the computations that drive complex behavior. We highlight growing concerns that neurological and neuropsychiatric diseases with severe behavioral outcomes originate from developmental insults to the cerebellum.

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Author Correction: Altered cerebellar connectivity in autism and cerebellar-mediated rescue of autism-related behaviors in mice

Abstract: In the version of this article initially published, the Simons Foundation was missing from the list of sources of support to P.T.T. in the Acknowledgments. The error has been corrected in the HTML and PDF versions of the article.

Cited by 11 publications

References 0 publications

Children with Autism Spectrum Disorder Show Impairments During Dynamic Versus Static Grip‐force Tracking

Children with Autism Spectrum Disorder Show Impairments During Dynamic Versus Static Grip‐force Tracking

A framework for the investigation of rare genetic disorders in neuropsychiatry

Functional Outcomes of Cerebellar Malformations

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