Language, Social, and Executive Functions in High Functioning Autism: A Continuum of Performance

Landa, Rebecca; Goldberg, Melissa C.

doi:10.1007/s10803-005-0001-1

Cited by 220 publications

(211 citation statements)

References 72 publications

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“…The findings illustrate that WCST 2, 3, 4, 5, 6, 8, 11 and 13 were significantly affected by language ability and the group (1) with higher language skills was found to possess higher levels of executive functioning. This finding links/correlates with previous studies on executive functions and language problems (Marlowe, 2000;Singer & Bashir, 1999;Landa & Goldberg, 2005;Hooper et al, 2002). Hooper et al (2002) studied language skills and reported that impairments in language results in impairments in executive functions.…”

Section: R E T R a C T E Dsupporting

confidence: 89%

RETRACTED: Do Deaf Children Delay in Their Executive Functioning Due to Their Delayed Language Abilities?

Sipal¹,

Bayhan²

2011

PSYCH

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Section: R E T R a C T E Dsupporting

confidence: 89%

RETRACTED: Do Deaf Children Delay in Their Executive Functioning Due to Their Delayed Language Abilities?

Sipal¹,

Bayhan²

2011

PSYCH

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“…The behavioral deficits, brought about by impaired 5-HT tone during critical developmental periods in our mouse model, are akin to those described in humans with autism without mental retardation [47,52,70,109]. The lesioned mice had no obvious gross motor or locomotor deficits but males had a subtle indication of a fine motor control problem as is reported in autism [69,73,85,91,104,113,120].…”

Section: Discussionsupporting

confidence: 66%

Modeling early cortical serotonergic deficits in autism

Boylan

Blue

Höhmann

2007

Behavioural Brain Research

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Autism is a developmental brain disorder characterized by deficits in social interaction, language and behavior. Brain imaging studies demonstrate increased cerebral cortical volumes and micro-and macroscopic neuroanatomic changes in children with this disorder. Alterations in forebrain serotonergic function may underlie the neuroanatomic and behavioral features of autism. Serotonin is involved in neuronal growth and plasticity and these actions are likely mediated via serotonergic and glutamatergic receptors. Few animal models of autism have been described that replicate both etiology and pathophysiology. We report here on a selective serotonin (5-HT) depletion model of this disorder in neonatal mice that mimics neurochemical and structural changes in cortex and, in addition, displays a behavioral phenotype consistent with autism. Newborn male and female mice were depleted of forebrain 5-HT with injections of the serotonergic neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT), into the bilateral medial forebrain bundle (mfb). Behavioral testing of these animals as adults revealed alterations in social, sensory and stereotypic behaviors. Lesioned mice showed significantly increased cortical width. Serotonin immunocytochemistry showed a dramatic long-lasting depletion of 5-HT containing fibers in cerebral cortex until postnatal day (PND) 60. Autoradiographic binding to high affinity 5-HT transporters was significantly but transiently reduced in cerebral cortex of 5,7-DHT-depleted mice. AMPA glutamate receptor binding was decreased at PND 15. We hypothesize that increased cerebral cortical volume and sensorimotor, cognitive and social deficits observed in both 5-HT-depleted animals and in individuals with autism, may be the result of deficiencies in timely axonal pruning to key cerebral cortical areas.

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“…However, findings in the high-functioning end of the spectrum have been less consistent, with some authors reporting superior functioning on executive functioning tasks requiring an extradimensional conceptual shift (Landa & Goldberg, 2005), with a trend for individuals with ASD to have greater difficulty on intradimensional shifts, that is, a perceptual task. Studies of family members have also been conflicting with set-shifting deficits reported in fathers of ASD probands (Wong, Maybery, Bishop, Maley, & Hallmayer, 2006) but not in siblings (Wong et al, 2006).…”

Section: Set-shifting Deficitsmentioning

confidence: 99%

Anorexia nervosa and autism spectrum disorders: Guided investigation of social cognitive endophenotypes.

Zucker¹,

Losh²,

Bulik³

et al. 2007

Psychological Bulletin

255

211

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Death by suicide occurs in a disproportionate percentage of individuals with anorexia nervosa (AN), with a standardized mortality ratio indicating a 57-fold greater risk of death from suicide relative to an age-matched cohort. Longitudinal studies indicate impaired social functioning increases risk for fatal outcomes, while social impairment persists following recovery. Study of social cognition in AN may elucidate impaired processes that may influence therapeutic efficacy. Symptoms of autism spectrum disorders (ASD) are overrepresented in those who evidence a chronic course. Relative to that in AN, social information processing in ASD is well characterized and may inform systematic study in AN. This article (a) reviews impaired interpersonal processes in AN, (b) compares the phenotype of AN with that of ASD, (c) highlights deficits of social cognitive disturbance in ASD relative to AN, and (d) proposes a new framework to understand the interaction of individuals with AN with their social context.Keywords: anorexia nervosa, social cognition, autism, interpersonal functioning, eating disorders Individuals with anorexia nervosa (AN) have a nearly 12-fold greater risk of death from all causes and a 57-fold greater risk of death from suicide relative to their age-matched peers (Keel et al., 2003). Such troubling statistics speak to the incapacitating, perplexing, and isolating nature of AN, a severe psychiatric illness that negatively impacts the biological, emotional, and psychosocial functioning of both the affected individual and her or his family (Harris & Barraclough, 1998;Treasure, Whitaker, Whitney, & Schmidt, 2005). In fact, AN exacts a toll on the family reported to exceed that experienced by families with a child with a severe psychiatric disorder such as schizophrenia . Although guiding epidemiologic data are currently lacking, there has been increasing concern regarding several notable trends: (a) an upsurge of AN in both younger and older ages than has been previously reported Johnson, Cohen, Kasen, & Brook, 2006;Marcus & Kalarchian, 2003), (b) increased incidence in minority groups hitherto thought protected (Decaluwe, Braet, & Fairburn, 2003;Tanofsky-Kraff et al., 2003), and (c) recent published reports of extensive illness burden among family members Treasure, Whitaker, Whitney, & Schmidt, 2005;Whitney & Eisler, 2005). Such patterns highlight the broad impact of these illnesses and underscore the urgency of alternative approaches to illness management.While advances have been made in the treatment of adolescents with a relatively short duration of illness (Lock & le Grange, 2005), progress in the treatment of adults with AN remains limited, at best (W. S. Agras et al., 2004;Kaplan, 2002). Of note, a report issued by the National Institute of Mental Health (W. S. Agras et al., 2004) emphasized the absence of innovative treatment approaches over the past several decades. This conclusion was recently echoed in an evidence-based review calling for novel intervention strategies that target core biological...

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Language, Social, and Executive Functions in High Functioning Autism: A Continuum of Performance

Cited by 220 publications

References 72 publications

RETRACTED: Do Deaf Children Delay in Their Executive Functioning Due to Their Delayed Language Abilities?

RETRACTED: Do Deaf Children Delay in Their Executive Functioning Due to Their Delayed Language Abilities?

Modeling early cortical serotonergic deficits in autism

Anorexia nervosa and autism spectrum disorders: Guided investigation of social cognitive endophenotypes.

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