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NNALS a the Social Brain Network and Autism

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NNALS a the Social Brain Network and Autism ANNALS 69 MINI REVIEW The Social Brain Network and Autism Vivek Misra The Institute of Neurological Sciences, VHS Multispecialty Hospital and Research Institute, RG Salai, Taramani Chennai – 600113 Tamil Nadu, India ABSTRACT Available research data in Autism suggests the role of a network of brain areas, often known as the ‘social brain’. Recent studies highlight the role of genetic mutations as underlying patho-mechanism in Autism. This mini review, discusses the basic concepts behind social brain networks, theory of mind and genetic factors associated with Autism. It critically evaluates and explores the relationship between the behavioral outcomes and genetic factors providing a conceptual framework for understanding of autism. KEYWORDS: Autism, Behavioral Genetics, Brain Networks Corresponding Author: Vivek Misra, The Institute of Neurological Sciences, VHS Multispecialty Hospital and Research Institute, RG Salai, Taramani Chennai – 600113 Tamil Nadu, India Tel.: +91-44-22541349, E-mail: [email protected] doi : 10.5214/ans.0972.7531.210208 Introduction the cerebellum.2 The corpus callosum and worlds. They can master complex technical major inter-hemispheric connection tracts operations but cannot learn from verbal in- It is hypothesized that the deficits in social are smaller than non-autistic, age- and structions and environmental clues, act on cognition and related cognitive functions gender-matched individuals. hints or understand humor or irony. in Autism results from reduced synchro- nization between these key brain regions Social brain network in autism ToM deficits in autism have been linked to during different social and emotional abnormal patterns of hypo activation in tasks: recent research suggests autism to Neuropsychiatric and neuropsychological superior temporal gyrus, superior tempo- be a ‘neural connectivity disorder’. evaluations in Autism have revealed selec- ral sulcus, and basal temporal areas and tive dysfunction of ‘social cognition’, with hyper activation in Brodmann’s area 9/10, These interconnected neural systems can sparing of motor, perceptual and basic compared to healthy subjects who perfor- be understood through the relationship cognitive skills. Social cognition includes a med well on ToM tasks. Furthermore, it has between functionally relevant anatomic range of skills and functions required for been demonstrated that the amygdala and areas and neurochemical pathways, the successful interpersonal interaction, medi- left medial prefrontal cortex, which are core programming of which is genetically mod- ated by a ‘Social Brain Network’, consist- regions in healthy subjects were not invol- ulated during neurodevelopment and me- ing brain regions that are dysfunctional ved at all in autistic subjects.7 While re- diated through a range of neuropeptides in autism: Fusiform face area (perception duced amygdala and medial PFC function and interacting neurotransmitter systems. of personal identity), inferior frontal gyrus has also been associated with difficulty in It has been suggested that autism emerges (facial expression imitation), posterior su- attributing emotional states to others.8 from a developmental cascade in which a perior temporal sulcus (perception of facial fundamental deficit in attention to social expressions and eye gaze tasks), superior Mirror neuron system in autism stimuli beginning as early as infancy leads frontal gyrus (theory of mind, i.e., taking The Mirror Neuron System, which is pos- to impaired interactions with primary care- another person’s perspective) and the tulated to underlie the ability to mimic, givers. This results in abnormal develop- 3-5 amygdala (emotion processing). learn and understand the actions of oth- ment of social cognition, which in turn ers 9 has also been implicated in autism.10 adversely affects later behavioral and func- Theory of mind in autism Mirror neurons are those in the ventral tional domains such as language develop- One theory of autism proposes that the motor regions that fire when subjects ob- ment which are dependent on these early core deficit is an inability to metalize and serve actions performed by con-specifics, processes. infer the state of mind of another per- particularly when the subject has to mimic A common neuroanatomical theme in au- son, or “Theory of Mind” (TOM).6 Autis- or learn that action. Although mirror neu- tism is over-connectivity in closely related tic individuals perform poorly on typical ron dysfunction has been proposed in au- areas and decreased connectivity in lon- ToM tasks, which involve guessing what a tism behavioral paradigms, but has not ger circuitry needing large scale integra- character is thinking based on a vignette revealed differences between autistic and tion. Disordered development of grey and presented in words or pictorially. Difficul- non-autistic children in imitating and un- white matter in autistic individuals has ty in metalizing leads to being unable to derstanding hand gestures.11 It has been been demonstrated in the frontal and tem- share or express emotions as they cannot proposed that lack of empathy, or the dif- poral cortices, where selective increase in anticipate thoughts and actions of others ficulty to ‘feel what you feel’ is linked to late developing white matter and narrow or even understand that others have their mirror neuron system dysfunction, but the mini columns in frontal and temporal cor- own intentions, feelings and points of view evidence is sparse. tex has been associated with early acceler- is been inferred from the study. Commu- Genetic factors in autism ated postnatal head growth.1Studies have nication is a way of influencing others to found fewer, abnormally small and densely construct a picture of the world similar The programming of various brain net- packed neurons especially in lateral nucle- to ones own, but in autism, individuals works is genetically modulated dur- us of the thalamus and the Purkinje cells of cannot conceive that others have inner ing neurodevelopment and mediated www.annalsofneurosciences.org ANNALS OF NEUROSCIENCES VOLUME 21 NUMBER 2 APRIL 2014 ANNALS MINI REVIEW 70 through a range of neuropeptides and • Autism plus phenotype consisting of tion, but result in varying clinical pheno- interacting neurotransmitter systems. Autism Spectrum Disorders (ASD) caused types when they cross a certain thresh- Studies have reported that there are ap- by rare, single-gene mutations; for e.g., old through complex gene-gene and proximately 103 disease genes, 44 ge- fragile X in 5-10% in Autism Plus. gene-environment interactions. nomic loci are associated with autism.12 • Broad autism phenotype caused by • A severe and specific phenotype caused A recent review of genetic studies of genetic variations in single or multiple by ‘de-novo’ mutations in the patient autism identified three basic phenotype/ genes. These variations are common or transmitted through asymptomatic genotype combinations:13 and are present in the general popula- carriers of such mutation. Table I. Disease genes and genetic disorders reported in individual with ASD Gene Locus Mutations/ Encoded protein/gene function Clinical features References CNVs NTNG1 1p13.3 mutations Protein acting as axon guidance cues Schizophrenia, ASDs (14) during nervous system development CLCN6 1p36.22 mutations Member of voltage-dependent chloride ASDs (15) channel in the nervous system NRXN1 2p16.3 mutations, Cell adhesion molecule and a receptor ASDs, schizophrenia, epilepsy, (16-20) CNVs in the nervous system, formation and ADHD, ID, speech delay, hyperactivity, maintenance of synaptic junctions depression, learning difficulties TBR1 2q24.2 mutations Transcription factor required for normal Schizophrenia, ASDs (21) brain development SCN2A 2q24.3 mutations Sodium channel, voltage-gated, type II, ASDs epilepsy (22, 23) alpha subunit SCN1A 2q24.3 mutations Sodium channel, voltage-gated, type I, ASDs epilepsy (12, 24) alpha subunit CNTN4 3p32.2 mutations Axonal-associated cell adhesion molecule ASDs (25) FOXP1 3p13 mutations Transcription factor ID, ASDs (12, 24) TBL1XR1 3q26.32 mutations Transcription activation ASDs (21) CDH10 5p14.2 mutations Neuronal cell-adhesion molecule ASDs (26) CDH9 5p14.1 mutations Neuronal cell-adhesion molecule ASDs (26) SLIT3 5q34q35.1 mutations Axonal guidance regulator Depression, schizophrenia, ASDs (21) SYNGAP1 6p21.32 mutations, Development of cognition and ID, ASDs (27) CNVs proper synapse function AHI1 6q23.3 mutations Cerebellar and cortical development Joubert syndrome (12, 25) in humans HOXA1 7p15.3 mutations Transcription factor ASDs (12) RELN 7q22.1 deletions Cell positioning and neuronal migration ASDs (28) during brain development CNTNAP2 7q36.1 mutations, Cell adhesion molecule and receptor in Focal cortical dysplasia, ASDs, ID, epi- (12) CNVs the nervous system lepsy, schizophrenia, bipolar disorder DLGAP2 8p23.3 CNVs Molecular organization of synapses and ASDs (27) neuronal cell signaling CHD7 8q12.2 mutations, Chromatin remodeling CHARGE syndrome, ASDs (12) deletions RIPK2 8q21.3 mutations Interacts with p38 kinase ASDs (15) UNC13B 9p13.3 mutations Synaptic vesicle maturation in a subset of ASDs (15) excitatory/glutamatergic synapses ABCA1 9q31.1 mutations Neuronal structure and function Bipolar disorder, schizophrenia, ASDs (15) LAMC3 9q34.12 mutations Laminin, plays a role in forming the con- ASDs, ID (24) volution of the cerebral cortex TSC1 9q34.13 mutations Regulation of protein synthesis in a wide Tuberous sclerosis, ASDs (29) range of cell
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