Autism spectrum disorders (ASD) represent a formidable challenge for
psychiatry and neuroscience because of their high prevalence, life-long nature,
complexity and substantial heterogeneity. Facing these obstacles requires
large-scale multidisciplinary efforts. While the field of genetics has pioneered
data sharing for these reasons, neuroimaging had not kept pace. In response, we
introduce the Autism Brain Imaging Data Exchange (ABIDE) – a grassroots
consortium aggregating and openly sharing 1112 existing resting-state functional
magnetic resonance imaging (R-fMRI) datasets with corresponding structural MRI
and phenotypic information from 539 individuals with ASD and 573 age-matched
typical controls (TC; 7–64 years) (http://fcon_1000.projects.nitrc.org/indi/abide/). Here, we
present this resource and demonstrate its suitability for advancing knowledge of
ASD neurobiology based on analyses of 360 males with ASD and 403 male
age-matched TC. We focused on whole-brain intrinsic functional connectivity and
also survey a range of voxel-wise measures of intrinsic functional brain
architecture. Whole-brain analyses reconciled seemingly disparate themes of both
hypo and hyperconnectivity in the ASD literature; both were detected, though
hypoconnectivity dominated, particularly for cortico-cortical and
interhemispheric functional connectivity. Exploratory analyses using an array of
regional metrics of intrinsic brain function converged on common loci of
dysfunction in ASD (mid and posterior insula, posterior cingulate cortex), and
highlighted less commonly explored regions such as thalamus. The survey of the
ABIDE R-fMRI datasets provides unprecedented demonstrations of both replication
and novel discovery. By pooling multiple international datasets, ABIDE is
expected to accelerate the pace of discovery setting the stage for the next
generation of ASD studies.
Background-The ε4 allele of the apolipoprotein E gene (APOE) is the chief known genetic risk factor for Alzheimer's disease, the most common cause of dementia late in life. To determine the relation between brain responses to tasks requiring memory and the genetic risk of Alzheimer's disease, we performed APOE genotyping and functional magnetic resonance imaging (MRI) of the brain in older persons with intact cognition.
Until recently, our understanding of how language is organized in the brain depended on analysis of behavioral deficits in patients with fortuitously placed lesions. The availability of functional magnetic resonance imaging (fMRI) for in vivo analysis of the normal brain has revolutionized the study of language. This review discusses three lines of fMRI research into how the semantic system is organized in the adult brain. These are (a) the role of the left inferior frontal lobe in semantic processing and dissociations from other frontal lobe language functions, (b) the organization of categories of objects and concepts in the temporal lobe, and (c) the role of the right hemisphere in comprehending contextual and figurative meaning. Together, these lines of research broaden our understanding of how the brain stores, retrieves, and makes sense of semantic information, and they challenge some commonly held notions of functional modularity in the language system.
To examine mirror neuron abnormalities in autism, high-functioning children with autism and matched controls underwent fMRI while imitating and observing emotional expressions. Although both groups performed the tasks equally well, children with autism showed no mirror neuron activity in the inferior frontal gyrus (pars opercularis). Notably, activity in this area was inversely related to symptom severity in the social domain, suggesting that a dysfunctional 'mirror neuron system' may underlie the social deficits observed in autism.
Under typical conditions, medial prefrontal cortex (mPFC) connections with the amygdala are immature during childhood and become adult-like during adolescence. Rodent models show that maternal deprivation accelerates this development, prompting examination of human amygdala-mPFC phenotypes following maternal deprivation. Previously institutionalized youths, who experienced early maternal deprivation, exhibited atypical amygdalamPFC connectivity. Specifically, unlike the immature connectivity (positive amygdala-mPFC coupling) of comparison children, children with a history of early adversity evidenced mature connectivity (negative amygdala-mPFC coupling) and thus, resembled the adolescent phenotype. This connectivity pattern was mediated by the hormone cortisol, suggesting that stress-induced modifications of the hypothalamic-pituitary-adrenal axis shape amygdala-mPFC circuitry. Despite being age-atypical, negative amygdala-mPFC coupling conferred some degree of reduced anxiety, although anxiety was still significantly higher in the previously institutionalized group. These findings suggest that accelerated amygdala-mPFC development is an ontogenetic adaptation in response to early adversity.fMRI | emotion regulation | stress | neurodevelopment
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