Abnormal development pattern of the amygdala and hippocampus from childhood to adulthood with autism

Xu, Qin; Zuo, Chenyi; Liao, Shuirong; Long, Yang; Wang, Yanpei

doi:10.1016/j.jocn.2020.03.049

Cited by 40 publications

(39 citation statements)

References 24 publications

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“…ASD and ID are brain-wide disorders, and while neocortex is thought to be important for ASD/ID etiology, it is not affected in isolation. A wealth of studies have highlighted the importance of other key circuits, including basal ganglia, amygdala, hippocampus, and cerebellum [87,[347][348][349][350][351][352][353][354][355][356][357][358][359][360][361][362][363][364][365]. Importantly, many of the concepts discussed above, including the mechanisms supporting dendritic nonlinearities, are relevant across these structures.…”

Section: Discussionmentioning

confidence: 99%

Dendritic Integration Dysfunction in Neurodevelopmental Disorders

Nelson¹,

Bender²

2021

Dev Neurosci

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Neurodevelopmental disorders (NDDs) that affect cognition, social interaction, and learning, including autism spectrum disorder (ASD) and intellectual disability (ID), have a strong genetic component. Our current understanding of risk genes highlights two main groups of dysfunction: those in genes that act as chromatin modifiers and those in genes that encode for proteins localized at or near synapses. Understanding how dysfunction in these genes contributes to phenotypes observed in ASD and ID remains a major question in neuroscience. In this review, we highlight emerging evidence suggesting that dysfunction in dendrites – regions of neurons that receive synaptic input – may be key to understanding features of neuronal processing affected in these disorders. Dendritic integration plays a fundamental role in sensory processing, cognition, and conscious perception, processes hypothesized to be impaired in NDDs. Many high-confidence ASD genes function within dendrites where they control synaptic integration and dendritic excitability. Further, increasing evidence demonstrates that several ASD/ID genes, including chromatin modifiers and transcription factors, regulate the expression or scaffolding of dendritic ion channels, receptors, and synaptic proteins. Therefore, we discuss how dysfunction of subsets of NDD-associated genes in dendrites leads to defects in dendritic integration and excitability and may be one core phenotype in ASD and ID.

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Section: Discussionmentioning

confidence: 99%

Dendritic Integration Dysfunction in Neurodevelopmental Disorders

Nelson¹,

Bender²

2021

Dev Neurosci

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“…This hyperactivity of the amygdala was suggested to lead to suppression of normal development of social behaviour ( Tinbergen and Tinbergen, 1976 ) hence warranting further investigation of amygdala morphology and function. Amygdalar volumes as well as amygdalar neuron numbers in autistic vs. control children (6.5–12.0 years) demonstrate early relative increases ( Avino et al, 2018 ; Xu et al, 2020 ) that dissipate by adolescence (13–19 years). By early adulthood (20–27 years), the early increase in amygdala volume and neuron numbers has been reversed.…”

Section: Update - Abnormal Dorsal Stream Development and Connectivity In Autismmentioning

confidence: 97%

Neural Mechanisms of Visual Motion Anomalies in Autism: A Two-Decade Update and Novel Aetiology

Spiteri

Crewther

2021

Front. Neurosci.

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The 21st century has seen dramatic changes in our understanding of the visual physio-perceptual anomalies of autism and also in the structure and development of the primate visual system. This review covers the past 20 years of research into motion perceptual/dorsal stream anomalies in autism, as well as new understanding of the development of primate vision. The convergence of this literature allows a novel developmental hypothesis to explain the physiological and perceptual differences of the broad autistic spectrum. Central to these observations is the development of motion areas MT+, the seat of the dorsal cortical stream, central area of pre-attentional processing as well as being an anchor of binocular vision for 3D action. Such development normally occurs via a transfer of thalamic drive from the inferior pulvinar → MT to the anatomically stronger but later-developing LGN → V1 → MT connection. We propose that autistic variation arises from a slowing in the normal developmental attenuation of the pulvinar → MT pathway. We suggest that this is caused by a hyperactive amygdala → thalamic reticular nucleus circuit increasing activity in the PIm → MT via response gain modulation of the pulvinar and hence altering synaptic competition in area MT. We explore the probable timing of transfer in dominance of human MT from pulvinar to LGN/V1 driving circuitry and discuss the implications of the main hypothesis.

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“…In addition, studies have implicated the habenula in bipolar disorder (BD) 33 – 35 , obsessive–compulsive disorder (OCD) 36 , 37 as well as schizophrenia 38 , 39 and altered habenula volume has been reported in subjects diagnosed with BD and schizophrenia 40 , 41 . Previous studies have reported altered amygdala volume in subjects with ASD compared to age matched controls 25 , 42 . While subsequent research showed these volume differences might only be apparent at certain ages, these point to an altered developmental trajectory of this important social brain area in ASD 21 , 23 , 25 , 42 , 43 .…”

Section: Introductionmentioning

confidence: 88%

“…Previous studies have reported altered amygdala volume in subjects with ASD compared to age matched controls 25 , 42 . While subsequent research showed these volume differences might only be apparent at certain ages, these point to an altered developmental trajectory of this important social brain area in ASD 21 , 23 , 25 , 42 , 43 . So while neuroimaging and brain stimulation techniques have provided some insight into the role of the habenula in psychiatric disorders further research is warranted to obtain a deeper understanding of the neurocircuitry of social behaviour and relate it to the differences found in human disorders 6 , 40 , 41 , 44 – 49 .…”

Section: Introductionmentioning

confidence: 88%

“…Affected individuals usually show symptoms of the disorder as early as 12 to 18 months of age 9 , 13 – 15 and multiple differences in functional and morphological brain phenotype have been reported in ASD 15 – 23 . In particular studies demonstrate that brain development is altered in individuals with ASD as exemplified by deviations from normal developmental trajectories in regional cortical thickness, surface area and structure volume 16 – 18 , 23 – 25 . Some of these brain changes are related to individual characteristics such as symptom severity and sex.…”

Section: Introductionmentioning

confidence: 99%

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Involvement of the habenula in the pathophysiology of autism spectrum disorder

Germann

Gouveia

Brentani

et al. 2021

Sci Rep

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The habenula is a small epithalamic structure with widespread connections to multiple cortical, subcortical and brainstem regions. It has been identified as the central structure modulating the reward value of social interactions, behavioral adaptation, sensory integration and circadian rhythm. Autism spectrum disorder (ASD) is characterized by social communication deficits, restricted interests, repetitive behaviors, and is frequently associated with altered sensory perception and mood and sleep disorders. The habenula is implicated in all these behaviors and results of preclinical studies suggest a possible involvement of the habenula in the pathophysiology of this disorder. Using anatomical magnetic resonance imaging and automated segmentation we show that the habenula is significantly enlarged in ASD subjects compared to controls across the entire age range studied (6–30 years). No differences were observed between sexes. Furthermore, support-vector machine modeling classified ASD with 85% accuracy (model using habenula volume, age and sex) and 64% accuracy in cross validation. The Social Responsiveness Scale (SRS) significantly differed between groups, however, it was not related to individual habenula volume. The present study is the first to provide evidence in human subjects of an involvement of the habenula in the pathophysiology of ASD.

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Abnormal development pattern of the amygdala and hippocampus from childhood to adulthood with autism

Cited by 40 publications

References 24 publications

Dendritic Integration Dysfunction in Neurodevelopmental Disorders

Dendritic Integration Dysfunction in Neurodevelopmental Disorders

Neural Mechanisms of Visual Motion Anomalies in Autism: A Two-Decade Update and Novel Aetiology

Involvement of the habenula in the pathophysiology of autism spectrum disorder

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