scholarly journals Correction to: Absence of parvalbumin increases mitochondria volume and branching of dendrites in inhibitory Pvalb neurons in vivo: a point of convergence of autism spectrum disorder (ASD) risk gene phenotypes

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Lucia Janickova ◽  
Karin Farah Rechberger ◽  
Lucas Wey ◽  
Beat Schwaller

An amendment to this paper has been published and can be accessed via the original article.

Neuroscience ◽  
2010 ◽  
Vol 168 (3) ◽  
pp. 797-810 ◽  
Author(s):  
K.L. Eagleson ◽  
M.C. Gravielle ◽  
L.J. Schlueter McFadyen-Ketchum ◽  
S.J. Russek ◽  
D.H. Farb ◽  
...  

Author(s):  
Derek Sayre Andrews ◽  
Thomas A. Avino ◽  
Maria Gudbrandsen ◽  
Eileen Daly ◽  
Andre Marquand ◽  
...  

2019 ◽  
Vol 83 (3) ◽  
pp. 301-325 ◽  
Author(s):  
Bianca M. Marro ◽  
Erin Kang ◽  
Kathryn M. Hauschild ◽  
Karys M. Normansell ◽  
Tamara M. Abu-Ramadan ◽  
...  

Youth with autism spectrum disorder (ASD) experience deficits in social knowledge. It has long been theorized that these youth must learn these skills explicitly, and social skills interventions (SSIs) have followed suit. Recently, performance-based SSIs have emerged, which promote in vivo opportunities for social engagement without explicit instruction. Effects of performance-based SSIs on social knowledge have not been examined. This study employs two discrete samples (one lab-based, one community-based) of youth with ASD to examine the effects of performance-based interventions on social knowledge. Results largely support the efficacy and effectiveness of improving social knowledge by performance-based interventions without explicit teaching. This indicates that youth with ASD may be able to learn these aspects of social cognition implicitly, rather than exclusively explicitly. The results of the current study also suggest that SSI content, dosage, and intensity may relate to these outcomes, which are important considerations in clinical practice and future studies.


2009 ◽  
Vol 20 (6) ◽  
pp. 1332-1340 ◽  
Author(s):  
Armin Raznahan ◽  
Roberto Toro ◽  
Eileen Daly ◽  
Dene Robertson ◽  
Clodagh Murphy ◽  
...  

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Faye McKenna ◽  
Laura Miles ◽  
Jeffrey Donaldson ◽  
F. Xavier Castellanos ◽  
Mariana Lazar

AbstractPrior ex vivo histological postmortem studies of autism spectrum disorder (ASD) have shown gray matter microstructural abnormalities, however, in vivo examination of gray matter microstructure in ASD has remained scarce due to the relative lack of non-invasive methods to assess it. The aim of this work was to evaluate the feasibility of employing diffusional kurtosis imaging (DKI) to describe gray matter abnormalities in ASD in vivo. DKI data were examined for 16 male participants with a diagnosis of ASD and IQ>80 and 17 age- and IQ-matched male typically developing (TD) young adults 18–25 years old. Mean (MK), axial (AK), radial (RK) kurtosis and mean diffusivity (MD) metrics were calculated for lobar and sub-lobar regions of interest. Significantly decreased MK, RK, and MD were found in ASD compared to TD participants in the frontal and temporal lobes and several sub-lobar regions previously associated with ASD pathology. In ASD participants, decreased kurtosis in gray matter ROIs correlated with increased repetitive and restricted behaviors and poor social interaction symptoms. Decreased kurtosis in ASD may reflect a pathology associated with a less restrictive microstructural environment such as decreased neuronal density and size, atypically sized cortical columns, or limited dendritic arborizations.


2019 ◽  
Vol 20 (17) ◽  
pp. 4071 ◽  
Author(s):  
Ibuki Ueoka ◽  
Hang Thi Nguyet Pham ◽  
Kinzo Matsumoto ◽  
Masamitsu Yamaguchi

Whole exome analyses have identified a number of genes associated with autism spectrum disorder (ASD) and ASD-related syndromes. These genes encode key regulators of synaptogenesis, synaptic plasticity, cytoskeleton dynamics, protein synthesis and degradation, chromatin remodeling, transcription, and lipid homeostasis. Furthermore, in silico studies suggest complex regulatory networks among these genes. Drosophila is a useful genetic model system for studies of ASD and ASD-related syndromes to clarify the in vivo roles of ASD-associated genes and the complex gene regulatory networks operating in the pathogenesis of ASD and ASD-related syndromes. In this review, we discuss what we have learned from studies with vertebrate models, mostly mouse models. We then highlight studies with Drosophila models. We also discuss future developments in the related field.


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