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Dopamine and the development of executive dysfunction in autism spectrum disorders.

Kriete T, Noelle DC - PLoS ONE (2015)

Bottom Line: Indeed, this array of deficits is sufficiently prominent to have prompted a theory that executive dysfunction is at the heart of these disorders.A more detailed examination of these behaviors reveals, however, that some aspects of executive function remain developmentaly appropriate.By simulating the development of the prefrontal cortex, the computational model also offers a potential explanation for an observed lack of executive dysfunction early in life.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychology & Neuroscience, University of Colorado Boulder, Boulder, CO, USA.

ABSTRACT
Persons with autism regularly exhibit executive dysfunction (ED), including problems with deliberate goal-directed behavior, planning, and flexible responding in changing environments. Indeed, this array of deficits is sufficiently prominent to have prompted a theory that executive dysfunction is at the heart of these disorders. A more detailed examination of these behaviors reveals, however, that some aspects of executive function remain developmentaly appropriate. In particular, while people with autism often have difficulty with tasks requiring cognitive flexibility, their fundamental cognitive control capabilities, such as those involved in inhibiting an inappropriate but relatively automatic response, show no significant impairment on many tasks. In this article, an existing computational model of the prefrontal cortex and its role in executive control is shown to explain this dichotomous pattern of behavior by positing abnormalities in the dopamine-based modulation of frontal systems in individuals with autism. This model offers excellent qualitative and quantitative fits to performance on standard tests of cognitive control and cognitive flexibility in this clinical population. By simulating the development of the prefrontal cortex, the computational model also offers a potential explanation for an observed lack of executive dysfunction early in life.

No MeSH data available.


Related in: MedlinePlus

WCST Performance.XT Model & Human Data. Error bars represent standard error of the mean.
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pone.0121605.g002: WCST Performance.XT Model & Human Data. Error bars represent standard error of the mean.

Mentions: Our simulations of both healthy individuals (i.e., models with normal DA modulation) and persons with autism (i.e., models with reduced DA modulation) displayed a reliable difference between these groups, with the ASD models showing a reduction of cognitive flexibility as measured by an increase in perseverative errors. (See Table 1 for mean error results.) In particular, the number of perseverative errors was significantly higher in networks with reduced DA modulation, mirroring the behavior of people with ASD on this task, as reported in the literature [2,44–46]. Indeed, without performing any additional model fitting, the mean number of perseverative errors produced by the models provides a reasonable match to the human data of [46], as shown in Fig 2.


Dopamine and the development of executive dysfunction in autism spectrum disorders.

Kriete T, Noelle DC - PLoS ONE (2015)

WCST Performance.XT Model & Human Data. Error bars represent standard error of the mean.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4374973&req=5

pone.0121605.g002: WCST Performance.XT Model & Human Data. Error bars represent standard error of the mean.
Mentions: Our simulations of both healthy individuals (i.e., models with normal DA modulation) and persons with autism (i.e., models with reduced DA modulation) displayed a reliable difference between these groups, with the ASD models showing a reduction of cognitive flexibility as measured by an increase in perseverative errors. (See Table 1 for mean error results.) In particular, the number of perseverative errors was significantly higher in networks with reduced DA modulation, mirroring the behavior of people with ASD on this task, as reported in the literature [2,44–46]. Indeed, without performing any additional model fitting, the mean number of perseverative errors produced by the models provides a reasonable match to the human data of [46], as shown in Fig 2.

Bottom Line: Indeed, this array of deficits is sufficiently prominent to have prompted a theory that executive dysfunction is at the heart of these disorders.A more detailed examination of these behaviors reveals, however, that some aspects of executive function remain developmentaly appropriate.By simulating the development of the prefrontal cortex, the computational model also offers a potential explanation for an observed lack of executive dysfunction early in life.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychology & Neuroscience, University of Colorado Boulder, Boulder, CO, USA.

ABSTRACT
Persons with autism regularly exhibit executive dysfunction (ED), including problems with deliberate goal-directed behavior, planning, and flexible responding in changing environments. Indeed, this array of deficits is sufficiently prominent to have prompted a theory that executive dysfunction is at the heart of these disorders. A more detailed examination of these behaviors reveals, however, that some aspects of executive function remain developmentaly appropriate. In particular, while people with autism often have difficulty with tasks requiring cognitive flexibility, their fundamental cognitive control capabilities, such as those involved in inhibiting an inappropriate but relatively automatic response, show no significant impairment on many tasks. In this article, an existing computational model of the prefrontal cortex and its role in executive control is shown to explain this dichotomous pattern of behavior by positing abnormalities in the dopamine-based modulation of frontal systems in individuals with autism. This model offers excellent qualitative and quantitative fits to performance on standard tests of cognitive control and cognitive flexibility in this clinical population. By simulating the development of the prefrontal cortex, the computational model also offers a potential explanation for an observed lack of executive dysfunction early in life.

No MeSH data available.


Related in: MedlinePlus