Neuroanatomy of autism

Amaral, David G.; Schumann, Cynthia M.; Nordahl, Christine Wu

doi:10.1016/j.tins.2007.12.005

Cited by 1,365 publications

(1,197 citation statements)

References 70 publications

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“…This is in accord with many previous VBM studies (Abell et al 1999;Boddaert et al 2004;Brieber et al 2007;Salmond et al 2007;Ke et al 2009;Dziobek et al 2010;Kosaka et al 2010;Toal et al 2010;Riva et al 2011;Via et al 2011;Yu et al 2011). However, other studies have found gray matter increases in some of these and other regions in ASD, making the current picture on structural brain differences in ASD somewhat inconsistent (Amaral et al 2008). These inconsistencies may be related to the recently often discussed heterogeneity in the spectrum, as well as between-study differences with respect to functionality and age of the ASD group (Brambilla et al 2003;Nordahl et al 2007;Amaral et al 2008;Nickl-Jockschat et al 2011).…”

Section: Regional Gray Matter Abnormalities and Their Correlation Witsupporting

confidence: 88%

“…Moreover, our data provide the first anatomical evidence of a compromised structure of the temporoparietal cortex predicting social dysfunctions in ASD, highlighting the behavioral significance of ASD-related structural changes. Regional gray matter changes in ASD, however, might vary, for example as a function of age or diagnostic subgroup (Brambilla et al 2003;Nordahl et al 2007;Amaral et al 2008). Here we only investigated adult highfunctioning individuals with ASD, and our conclusions are limited by a rather small sample size.…”

Section: Discussionmentioning

confidence: 99%

“…However, other studies have found gray matter increases in some of these and other regions in ASD, making the current picture on structural brain differences in ASD somewhat inconsistent (Amaral et al 2008). These inconsistencies may be related to the recently often discussed heterogeneity in the spectrum, as well as between-study differences with respect to functionality and age of the ASD group (Brambilla et al 2003;Nordahl et al 2007;Amaral et al 2008;Nickl-Jockschat et al 2011). …”

Section: Regional Gray Matter Abnormalities and Their Correlation Witmentioning

confidence: 99%

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Right Temporoparietal Gray Matter Predicts Accuracy of Social Perception in the Autism Spectrum

David

Schultz

Milne

et al. 2013

J Autism Dev Disord

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Individuals with an autism spectrum disorder (ASD) show hallmark deficits in social perception. These difficulties might also reflect fundamental deficits in integrating visual signals. We contrasted predictions of a social perception and a spatialndash;temporal integration deficit account. Participants with ASD and matched controls performed two tasks: the first required spatiotemporal integration of global motion signals without social meaning, the second required processing of socially relevant local motion. The ASD group only showed differences to controls in social motion evaluation. In addition, gray matter volume in the temporalndash;parietal junction correlated positively with accuracy in social motion perception in the ASD group. Our findings suggest that socialndash;perceptual difficulties in ASD cannot be reduced to deficits in spatialndash;temporal integration

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Section: Regional Gray Matter Abnormalities and Their Correlation Witsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Section: Regional Gray Matter Abnormalities and Their Correlation Witmentioning

confidence: 99%

See 1 more Smart Citation

Right Temporoparietal Gray Matter Predicts Accuracy of Social Perception in the Autism Spectrum

David

Schultz

Milne

et al. 2013

J Autism Dev Disord

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“…Alterations in the volume, activity, and/ or connectivity of the amygdala (features influenced by the gut microbiota) [16,[35][36][37] have been reported in individuals diagnosed with schizophrenia, [38,39] attention deficit hyperactivity disorder (ADHD), [40] and autism spectrum disorders (ASD). [41,42] In particular, functional dysregulation of the amygdala is considered central to the social deficits observed in individuals with ASD. [43] Although this "amygdala theory of autism" has been challenged by some, [44] there is certainly evidence that the amygdala has relevance for the development of social behavior and socio-emotional processing across species.…”

Section: Mood Disorders and Amygdala Functionmentioning

confidence: 99%

Gutsy Moves: The Amygdala as a Critical Node in Microbiota to Brain Signaling

et al. 2017

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The amygdala is a key brain area regulating responses to stress and emotional stimuli, so improving our understanding of how it is regulated could offer novel strategies for treating disturbances in emotion regulation. As we review here, a growing body of evidence indicates that the gut microbiota may contribute to a range of amygdala-dependent brain functions from pain sensitivity to social behavior, emotion regulation, and therefore, psychiatric health. In addition, it appears that the microbiota is necessary for normal development of the amygdala at both the structural and functional levels. While further investigations are needed to elucidate the exact mechanisms of microbiota-to-amygdala communication, ultimately, this work raises the intriguing possibility that the gut microbiota may become a viable treatment target in disorders associated with amygdala dysregulation, including visceral pain, post-traumatic stress disorder, and beyond. Also see the video abstract here: https://youtu.be/O5gvxVJjX18

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“…Frequently, comorbid conditions include intellectual disability (65 %), seizures (30 %), and different forms of sleep problems [49][50][51]; less recognized, but equally impairing, are frequent psychiatric comorbidities, that include anxiety disorders, obsessive-compulsive disorders, and depression [52]. Altered neurodevelopment during early pregnancy represents the neuropathological cause of ASD [53,54]. Postmortem studies have unveiled neuroanatomical and cytoarchitectonic abnormalities in the cerebellum, inferior olivary complex, deep cerebellar nuclei, hippocampus, amygdala, entorhinal cortex, fusiform gyrus, and anterior and posterior cingulate cortex, with thinner cortical minicolumns, excessive growth of the frontal lobes, and excessive dendritic spine density [55].…”

Section: Autism Spectrum Disorder: Clinical Traits Neuropsychologicamentioning

confidence: 99%

Endocannabinoid Signaling in Autism

et al. 2015

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Autism spectrum disorder (ASD) is a complex behavioral condition with onset during early childhood and a lifelong course in the vast majority of cases. To date, no behavioral, genetic, brain imaging, or electrophysiological test can specifically validate a clinical diagnosis of ASD. However, these medical procedures are often implemented in order to screen for syndromic forms of the disorder (i.e., autism comorbid with known medical conditions). In the last 25 years a good deal of information has been accumulated on the main components of the Bendocannabinoid (eCB) system^, a rather complex ensemble of lipid signals (Bendocannabinoids^), their target receptors, purported transporters, and metabolic enzymes. It has been clearly documented that eCB signaling plays a key role in many human health and disease conditions of the central nervous system, thus opening the avenue to the therapeutic exploitation of eCB-oriented drugs for the treatment of psychiatric, neurodegenerative, and neuroinflammatory disorders. Here we present a modern view of the eCB system, and alterations of its main components in human patients and animal models relevant to ASD. This review will thus provide a critical perspective necessary to explore the potential exploitation of distinct elements of eCB system as targets of innovative therapeutics against ASD.Key Words Autism spectrum disorder . endocannabinoid system . fragile X syndrome . metabolic regulation . reward system The Endocannabinoid SystemTwenty-five years after the cloning and expression of a complementary DNA that encoded a G protein-coupled receptor, named type-1 cannabinoid (CB 1 ) receptor [1], there is a good deal of information on the main components of the so-called Bendocannabinoid (eCB) system^, as well as on its role in controlling cannabinergic signaling in human health and disease [2][3][4]. Anandamide (AEA) and 2-arachidonoylglycerol (2-AG) are the most active eCBs as yet identified, although this family of bioactive lipids includes other arachidonic acid (AA) derivatives with cannabimimetic properties (i.e., noladin ether, virodhamine, N-arachidonoyldopamine, to name but a few). The classical dogma that eCBs are synthesized and released Bon demand^upon (patho)physiological stimuli has been recently revisited on the basis of unexpected evidence for intracellular reservoirs and transporters of eCBs. These new entities have been shown to drive intracellular trafficking of eCBs, adding a new dimension to the regulation of their biological activity [5]. To date, several metabolic routes have B. Chakrabarti, A. Persico and N. Battista are equal first authors.

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Neuroanatomy of autism

Cited by 1,365 publications

References 70 publications

Right Temporoparietal Gray Matter Predicts Accuracy of Social Perception in the Autism Spectrum

Right Temporoparietal Gray Matter Predicts Accuracy of Social Perception in the Autism Spectrum

Gutsy Moves: The Amygdala as a Critical Node in Microbiota to Brain Signaling

Endocannabinoid Signaling in Autism

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