Autism Spectrum Disorders (ASD) Characterization in Children by Decomposing MRI Brain Regions with Zernike Moments

Author(s):  
Nicolás Múnera ◽  
Javier Almeida ◽  
Charlems Álvarez ◽  
Nelson Velasco ◽  
Eduardo Romero
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jason L. He ◽  
Georg Oeltzschner ◽  
Mark Mikkelsen ◽  
Alyssa Deronda ◽  
Ashley D. Harris ◽  
...  

AbstractIndividuals on the autism spectrum are often reported as being hyper- and/or hyporeactive to sensory input. These sensory symptoms were one of the key observations that led to the development of the altered excitation-inhibition (E-I) model of autism, which posits that an increase ratio of excitatory to inhibitory signaling may explain certain phenotypical expressions of autism spectrum disorders (ASD). While there has been strong support for the altered E-I model of autism, much of the evidence has come from animal models. With regard to in-vivo human studies, evidence for altered E-I balance in ASD come from studies adopting magnetic resonance spectroscopy (MRS). Spectral-edited MRS can be used to provide measures of the levels of GABA + (GABA + macromolecules) and Glx (glutamate + glutamine) in specific brain regions as proxy markers of inhibition and excitation respectively. In the current study, we found region-specific elevations of Glx in the primary sensorimotor cortex (SM1) in ASD. There were no group differences of GABA+ in either the SM1 or thalamus. Higher levels of Glx were associated with more parent reported difficulties of sensory hyper- and hyporeactivity, as well as reduced feed-forward inhibition during tactile perception in children with ASD. Critically, the finding of elevated Glx provides strong empirical support for increased excitation in ASD. Our results also provide a clear link between Glx and the sensory symptoms of ASD at both behavioral and perceptual levels.


Author(s):  
C. Sue Carter ◽  
Suma Jacob

The effects of oxytocin and vasopressin on the brain and behavior can be sexually dimorphic, especially during the course of development (Bales, Kim, et al., 2004; Bales, Pfeifer, et al., 2004; Bales, Plotsky, et al., 2007; Bielsky et al., 2005a; Carter, 2003; Thompson et al., 2006; Yamamoto et al., 2005; Yamamoto et al., 2004). Given the sexual discrepancy observed in autism spectrum disorders (ASDs), these two neuropeptides, oxytocin (OT) and arginine vasopressin (AVP), have received attention for their potential role in ASDs (Green and Hollander, 2010; Insel et al., 1999; Leckman & Herman, 2002; Welch et al., 2005; Winslow, 2005; Young et al., 2002). Changes in either OT or AVP and their receptors could be capable of influencing symptom domains or behaviors associated with ASDs. Arginine vasopressin is androgen dependent in some brain regions (De Vries & Panzica, 2006), and males are more sensitive to AVP, especially during development. We hypothesize here that AVP, which has a unique role in males, must be present in optimal levels to be protective against ASDs. Either excess AVP or disruptions in the AVP system could play a role in development of the traits found in ASDs. In contrast, OT may possibly be secreted in response to adversity, especially in females, serving as a protective factor.


2019 ◽  
Vol 8 (4) ◽  
pp. 487 ◽  
Author(s):  
Billeci ◽  
Calderoni ◽  
Conti ◽  
Lagomarsini ◽  
Narzisi ◽  
...  

Autism Spectrum Disorders (ASD) is a group of neurodevelopmental disorders that is characterized by an altered brain connectivity organization. Autistic traits below the clinical threshold (i.e., the broad autism phenotype; BAP) are frequent among first-degree relatives of subjects with ASD; however, little is known regarding whether subthreshold behavioral manifestations of ASD mirror also at the neuroanatomical level in parents of ASD probands. To this aim, we applied advanced diffusion network analysis to MRI of 16 dyads consisting of a child with ASD and his father in order to investigate: (i) the correlation between structural network organization and autistic features in preschoolers with ASD (all males; age range 1.5–5.2 years); (ii) the correlation between structural network organization and BAP features in the fathers of individuals with ASD (fath-ASD). Local network measures significantly correlated with autism severity in ASD children and with BAP traits in fath-ASD, while no significant association emerged when considering the global measures of brain connectivity. Notably, an overlap of some brain regions that are crucial for social functioning (cingulum, superior temporal gyrus, inferior temporal gyrus, middle frontal gyrus, frontal pole, and amygdala) in patients with ASD and fath-ASD was detected, suggesting an intergenerational transmission of these neural substrates. Overall, the results of this study may help in elucidating the neurostructural endophenotype of ASD, paving the way for bridging connections between underlying genetic and ASD symptomatology.


2020 ◽  
Author(s):  
Jinglun Li ◽  
Xiu Chen ◽  
Ruwen Zheng ◽  
Ai Chen ◽  
Yan Zhou ◽  
...  

Abstract BackgroundAutism Spectrum Disorders (ASD) is a neurodevelopment disorder. The cerebellum has been reported to be one of the key regions involved in ASD. However, the associations between the cerebellum and clinical traits remain unclear. MethodsHere we performed Amplitude of Low Frequency Fluctuations (ALFF) analysis to detect the alterations of brain spontaneous activity in ASDs and explore the associations between spontaneous brain activity and clinical traits. ResultsCompared with normal controls, cerebellum crus 2 showed significantly weaker average ALFF values. Other regions such as left cerebellum 6, cerebellum vermis 4 5, putamen, SMA and thalamus showed increased mean ALFF values. In ASD patients with SRS total score T above 59, the mean ALFF values of cerebellum vermis 4 5 was significantly correlated with SRS total score T (r=0.175, P=0.031), SRS cognition score T (r=0.169, P=0.036) and SRS motivation score T (r=0.176, P=0.028).ConclusionsThese findings were not observed in other brain regions and in normal controls. Our study suggests a role of cerebellum in cognitive impairments in ASD and supports a mechanistic basis for the targeted treatment of ASD disorders.Trial registrationNot applicable.


2016 ◽  
Vol 16 (2) ◽  
pp. 283-292 ◽  
Author(s):  
Giusy Olivito ◽  
Silvia Clausi ◽  
Fiorenzo Laghi ◽  
Anna Maria Tedesco ◽  
Roberto Baiocco ◽  
...  

Author(s):  
Natacha Akshoomoff ◽  
Catherine Lord ◽  
Alan J. Lincoln ◽  
Rachel Y. Courchesne ◽  
Ruth A. Carper ◽  
...  

2020 ◽  
Vol 25 (41) ◽  
pp. 4344-4356 ◽  
Author(s):  
Moonsang Seo ◽  
George Anderson

Background: Autism Spectrum Disorders (ASD) have long been conceived as developmental disorder. A growing body of data highlights a role for alterations in the gut in the pathoetiology and/or pathophysiology of ASD. Recent work shows alterations in the gut microbiome to have a significant impact on amygdala development in infancy, suggesting that the alterations in the gut microbiome may act to modulate not only amygdala development but how the amygdala modulates the development of the frontal cortex and other brain regions. Methods: This article reviews wide bodies of data pertaining to the developmental roles of the maternal and foetal gut and immune systems in the regulation of offspring brain development. Results: A number of processes seem to be important in mediating how genetic, epigenetic and environmental factors interact in early development to regulate such gut-mediated changes in the amygdala, wider brain functioning and inter-area connectivity, including via regulation of microRNA (miR)-451, 14-3-3 proteins, cytochrome P450 (CYP)1B1 and the melatonergic pathways. As well as a decrease in the activity of monoamine oxidase, heightened levels of in miR-451 and CYP1B1, coupled to decreased 14-3-3 act to inhibit the synthesis of N-acetylserotonin and melatonin, contributing to the hyperserotonemia that is often evident in ASD, with consequences for mitochondria functioning and the content of released exosomes. These same factors are likely to play a role in regulating placental changes that underpin the association of ASD with preeclampsia and other perinatal risk factors, including exposure to heavy metals and air pollutants. Such alterations in placental and gut processes act to change the amygdala-driven biological underpinnings of affect-cognitive and affect-sensory interactions in the brain. Conclusion : Such a perspective readily incorporates previously disparate bodies of data in ASD, including the role of the mu-opioid receptor, dopamine signaling and dopamine receptors, as well as the changes occurring to oxytocin and taurine levels. This has a number of treatment implications, the most readily applicable being the utilization of sodium butyrate and melatonin.


2008 ◽  
Vol 20 (4) ◽  
pp. 1231-1250 ◽  
Author(s):  
Christopher S. Monk

AbstractDisturbances in the detection of, response to, and interpretation of emotion are common in many forms of psychopathology. The amygdala, striatum, and structures within the prefrontal cortex are highly involved in mediating these stages of emotion processing, and evidence indicates that these regions show structural and functional alterations in different types of psychopathology, including anxiety, depression, and autism spectrum disorders. However, we do not know how genes and the environment interact to alter development of these brain regions in ways that give rise to emotion-related psychopathology. This review discusses the current understanding of brain regions that are involved in emotional functioning, how they develop, and how they are altered in three forms of psychopathology: anxiety, depression, and autism spectrum disorders. Following this, a framework is described that may facilitate the integration of investigations of genetic variation and brain function with symptom and diagnostic measures. The framework involves three components: (a) a greater emphasis on simultaneously analyzing multiple levels (genes, brain function, behavior, symptoms, and diagnoses); (b) further integration of developmental considerations, including timing of environmental events, adaptations (or maladaptations), and disorder-related trajectories that guide some children toward atypical experiences; and (c) greater cross-talk between animal and human investigations to take advantage of biological measures that cannot be acquired in humans.


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