Brain structural abnormalities in young children with autism spectrum disorder

Sparks, Bobbi F.; Friedman, Seth D.; Shaw, Dennis; Aylward, Elizabeth H.; Echelard, Denise R.; Artru, Alan A.; Maravilla, K R; Giedd, Jay N.; Munson, Jeff; Dawson, Geraldine; Dager, Stephen R.

doi:10.1212/wnl.59.2.184

Cited by 840 publications

(746 citation statements)

References 39 publications

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“…Neuroanatomical observations, along with data from functional magnetic resonance imaging, have shown that a major pathological hallmark in autistic individuals may be a premature brain overgrowth affecting structures such as the cerebral cortex, the limbic system, including the hippocampal formation and the amygdala, and the cerebellum (Courchesne et al, 2001(Courchesne et al, , 2003Sparks et al, 2002;Schumann et al, 2004). Such overgrowth would happen early before clinical diagnosis is made consistent with the possibility that growth factors, which normally regulate cell differentiation, proliferation and survival, having a functional role in the disease.…”

Section: Wnt Signaling and Autismmentioning

confidence: 93%

The ups and downs of Wnt signaling in prevalent neurological disorders

2006

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In order to function properly, the brain must be wired correctly during critical periods in early development. Mistakes in this process are hypothesized to occur in disorders like autism and schizophrenia. Later in life, signaling pathways are essential in maintaining proper communication between neuronal and non-neuronal cells, and disrupting this balance may result in disorders like Alzheimer's disease. The Wnt/b-catenin pathway has a well-established role in cancer. Here, we review recent evidence showing the involvement of Wnt/b-catenin signaling in neurodevelopment as well as in neurodegenerative diseases. We suggest that the onset/development of such pathological conditions may involve the additive effect of genetic variation within Wnt signaling components and of molecules that modulate the activity of this signaling cascade.

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Section: Wnt Signaling and Autismmentioning

confidence: 93%

The ups and downs of Wnt signaling in prevalent neurological disorders

2006

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“…Whereas earlier postmortem studies on autistic patients indicated an increased number of cells with reduced cell size in the cortical, medial, and central nuclei of the amygdala (Kemper and Bauman, 1998), more recent and modern stereological counts of neurons in the amygdala revealed a reduced number of neurons, particularly in the lateral nucleus (Schumann and Amaral, 2006). The total amygdala volume is enlarged during early infancy (Sparks et al, 2002;Schumann et al, 2004), but can be reduced in adulthood (Aylward et al, 1999). Functionally, the amygdala has been linked to autism through its involvement in socio-emotional behavior.…”

Section: Introductionmentioning

confidence: 89%

“…Both microscopic and macroscopic studies reveal alterations in the morphology of the amygdala in autism (Kemper and Bauman, 1998;Aylward et al, 1999;Sparks et al, 2002;Schumann et al, 2004;Schumann and Amaral, 2006), indicating a dysfunction in this region that might possibly contribute to the autistic pathology. The current 'amygdala theory of autism' is based on the lost capability to evaluate socioemotional information and lost drive for social interaction derived from lesioning studies in monkeys and a few functional imaging studies in humans (Baron-Cohen et al, 2000;Sweeten et al, 2002;Pelphrey et al, 2004;Bachevalier and Loveland, 2006;Schultz, 2005), which implies that a hypofunctioning amygdala underlies autism.…”

Section: A Novel Role Suggested For the Amygdala In Autismmentioning

confidence: 99%

Abnormal Fear Conditioning and Amygdala Processing in an Animal Model of Autism

Markram

Rinaldi

Mendola

et al. 2007

Neuropsychopharmacol

337

262

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A core feature of autism spectrum disorders is the impairment in social interactions. Among other brain regions, a deficit in amygdala processing has been suggested to underlie this impairment, but whether the amygdala is processing fear abnormally in autism, is yet not clear. We used the valproic acid (VPA) rat model of autism to (a) screen for autism-like symptoms in rats, (b) test for alterations in amygdala-dependent fear processing, and (c) evaluate neuronal reactivity and synaptic plasticity in the lateral amygdala by means of in vitro single-cell electrophysiological recordings. VPA-treated animals displayed several symptoms common to autism, among them impaired social interactions and increased repetitive behaviors. Furthermore, VPA-treated rats were more anxious and exhibited abnormally high and longer lasting fear memories, which were overgeneralized and harder to extinguish. On the cellular level, the amygdala was hyperreactive to electrical stimulation and displayed boosted synaptic plasticity as well as a deficit in inhibition. We show for the first time enhanced, overgeneralized and resistant conditioned fear memories in an animal model of autism. Such hyperfear could be caused by the hyperreactivity and hyperplasticity found in the lateral amygdala, which may in turn be due to a deficit in the inhibitory system of the amygdala. We hypothesize an 'aversive world' syndrome that could, even if not a primary cause of the disorder itself, underlie some core symptoms in autism, such as impairments in social interactions and resistance to rehabilitation.

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“…Also, structural MRI studies suggest abnormalities in the development of the amygdala in ASD. Initial reports were contradictory, showing evidence for smaller [217], larger [218,219] and equivalent [220] amygdala volumes in subjects with ASD compared to controls. However, more recent data suggest an unusual developmental time course for the amydala in ASD, in which the amydala is larger in children with ASD (ages 7.5 to 12.5 years old) compared to several control groups, whereas no differences are detectable between adolescents with ASD versus controls [221].…”

Section: Impairments Of Facial Expression Recognition In Asdmentioning

confidence: 97%

Autism and the development of face processing

Golarai

Grill-Spector

Reiss

2006

Clinical Neuroscience Research

158

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Autism is a pervasive developmental condition, characterized by impairments in non-verbal communication, social relationships and stereotypical patterns of behavior. A large body of evidence suggests that several aspects of face processing are impaired in autism, including anomalies in gaze processing, memory for facial identity and recognition of facial expressions of emotion. In search of neural markers of anomalous face processing in autism, much interest has focused on a network of brain regions that are implicated in social cognition and face processing. In this review, we will focus on three such regions, namely the STS for its role in processing gaze and facial movements, the FFA in face detection and identification and the amygdala in processing facial expressions of emotion. Much evidence suggests that a better understanding of the normal development of these specialized regions is essential for discovering the neural bases of face processing anomalies in autism. Thus, we will also examine the available literature on the normal development of face processing. Key unknowns in this research area are the neuro-developmental processes, the role of experience and the interactions among components of the face processing system in shaping each of the specialized regions for processing faces during normal development and in autism. Published by Elsevier B.V. on behalf of Association for Research in Nervous and Mental Disease.

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Brain structural abnormalities in young children with autism spectrum disorder

Abstract: These structural findings suggest abnormal brain developmental processes early in the clinical course of autism. Research currently is underway to better elucidate mechanisms underlying these structural abnormalities and their longitudinal progression.

Cited by 840 publications

References 39 publications

The ups and downs of Wnt signaling in prevalent neurological disorders

The ups and downs of Wnt signaling in prevalent neurological disorders

Abnormal Fear Conditioning and Amygdala Processing in an Animal Model of Autism

Autism and the development of face processing

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