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Superior cognitive goal maintenance in carriers of genetic markers linked to reduced striatal D2 receptor density (C957T and DRD2/ANKK1-TaqIA)

Maintaining goal representations is a critical component of cognitive control and is required for successful performance in many daily activities. This is particularly important when goal-relevant information needs to be maintained in working memory (WM), updated in response to changing task demands...

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Detalles Bibliográficos
Autores principales: Persson, Jonas, Stenfors, Cecilia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6101371/
https://www.ncbi.nlm.nih.gov/pubmed/30125286
http://dx.doi.org/10.1371/journal.pone.0201837
Descripción
Sumario:Maintaining goal representations is a critical component of cognitive control and is required for successful performance in many daily activities. This is particularly important when goal-relevant information needs to be maintained in working memory (WM), updated in response to changing task demands or internal goal states, and protected from interference by inhibiting counter-goal behaviors. Modulation of fronto-striatal dopamine is critical for updating and maintaining goals and representations. Here we test the hypothesis that a genetic predisposition (C957T T+ and DRD2/ANKK1-TaqIA A+) for reduced striatal D2 receptor availability would facilitate goal maintenance using the AX-continuous performance task (AX-CPT), on a sample of 196 adults (25–67 y). We demonstrate that carriers of two polymorphisms that have been linked to reduced striatal D2 receptor density show increased performance on context-dependent (BX) trials, and that the effect of these polymorphisms was only significant for long ISI trials where the demand for goal maintenance is high. The current results add further knowledge to the role of D2 receptor functioning in cognitive stability and flexibility, and could have implications for understanding cognitive deficits in patients characterized by altered dopamine functioning.