Genes, brain, and behavior: Bridging disciplines

Fossella, John; Casey, B. J.

doi:10.3758/cabn.6.1.1

Cited by 18 publications

(14 citation statements)

References 28 publications

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“…As more evidence accumulates from the use of these tasks in rodents and humans, we will be able to better understand which behavioral mechanisms have been conserved across species and which tasks are best able to probe conserved mechanisms in the context of disease. This offers exciting new prospects for understanding diseases, such as NF1, through an integration of cognitive, clinical, and basic neuroscience approaches (Chadman et al 2009, Fossella & Casey 2006). …”

Section: Tasks Used To Assess Behavior In Animal Models Of Nf1mentioning

confidence: 99%

“…Tasks are also being developed for use in humans to parallel key features of commonly used rodent tasks (Demeter et al 2008). The use of these tasks to obtain convergent evidence from multiple approaches offers exciting new prospects for understanding disease through the integration of the cognitive, clinical, and basic neurosciences (Chadman et al 2009, Fossella & Casey 2006). …”

Section: Tasks Used To Assess Behavior In Animal Models Of Nf1mentioning

confidence: 99%

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Molecular and Cellular Mechanisms of Learning Disabilities: A Focus on NF1

Shilyansky

Lee

Silva

2010

Annu. Rev. Neurosci.

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Neurofibromatosis Type I (NF1) is a single-gene disorder characterized by a high incidence of complex cognitive symptoms, including learning disabilities, attention deficit disorder, executive function deficits, and motor coordination problems. Since the underlying genetic cause of this disorder is known, study of NF1 from a molecular, cellular, and systems perspective has provided mechanistic insights into the etiology of higher-order cognitive symptoms associated with the disease. In particular, studies of animal models of NF1 indicated that disruption of Ras regulation of inhibitory networks is critical to the etiology of cognitive deficits associated with NF1. Animal models of Nf1 identified mechanisms and pathways that are required for cognition, and represent an important complement to the complex neuropsychological literature on learning disabilities associated with this condition. Here, we review findings from NF1 animal models and human populations affected by NF1, highlighting areas of potential translation and discussing the implications and limitations of generalizing findings from this single-gene disease to idiopathic learning disabilities.

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Section: Tasks Used To Assess Behavior In Animal Models Of Nf1mentioning

confidence: 99%

Section: Tasks Used To Assess Behavior In Animal Models Of Nf1mentioning

confidence: 99%

Molecular and Cellular Mechanisms of Learning Disabilities: A Focus on NF1

Shilyansky

Lee

Silva

2010

Annu. Rev. Neurosci.

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“…Pharmacological and genetic methods offer another avenue for examining these questions (Posner, Rothbart, & Sheese, 2007; Fossella & Casey, 2006; Parasuraman & Greenwood, 2004; Sarter & Bruno, 2004; Greenwood & Parasuraman, 2003; Everitt & Robbins, 1997). However, the specific neurotransmission systems involved in the influence of attention on working memory stores are not known.…”

Section: Introductionmentioning

confidence: 99%

Both a Nicotinic Single Nucleotide Polymorphism (SNP) and a Noradrenergic SNP Modulate Working Memory Performance when Attention is Manipulated

Greenwood

Sundararajan

Lin

et al. 2009

Journal of Cognitive Neuroscience

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We investigated the relation between the two systems of visuospatial attention and working memory by examining the effect of normal variation in cholinergic and noradrenergic genes on working memory performance under attentional manipulation. We previously reported that working memory for location was impaired following large location precues, indicating the scale of visuospatial attention has a role in forming the mental representation of the target. In one of the first studies to compare effects of two single nucleotide polymorphisms (SNPs) on the same cognitive task, we investigated the neurotransmission systems underlying interactions between attention and memory. Based on our previous report that the CHRNA4 rs#1044396 C/T nicotinic receptor SNP affected visuospatial attention, but not working memory, and the DBH rs#1108580 G/A noradrenergic enzyme SNP affected working memory, but not attention, we predicted that both SNPs would modulate performance when the two systems interacted and working memory was manipulated by attention. We found the scale of visuospatial attention deployed around a target affected memory for location of that target. Memory performance was modulated by the two SNPs. CHRNA4 C/C homozygotes and DBH G allele carriers showed the best memory performance but also the greatest benefit of visuospatial attention on memory. Overall, however, the CHRNA4 SNP exerted a stronger effect than the DBH SNP on memory performance when visuospatial attention was manipulated. This evidence of an integrated cholinergic influence on working memory performance under attentional manipulation is consistent with the view that working memory and visuospatial attention are separate systems which can interact.

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“…In turn, these processes inevitably will become the targets for interventions that aim to restore normal developmental process or to initiate compensatory processes that return a patient to a functional neurodevelopmental trajectory. [9,36,37,44,45] Emphasizing the importance of developmental neuroscience to understanding the fundamental biology of mental illness, the 2008 NAMHC Workgroup report entitled Transformative Neurodevelopmental Research In Mental Illness recommended that the NIMH refocus its discovery and translational neuroscience portfolio on identifying and translating testable developmental targets into new preemption and treatment efforts. [5] As shown by increased funding for both developmental cellular and molecular and cognitive and affective neuroscience, a brief review of the NIHM portfolio, program announcements, and RFAs along with the strategic plan highlights the importance NIMH places on this undertaking.…”

Section: Transformational Developmental Neurosciencementioning

confidence: 99%

Looking to the future of research in pediatric anxiety disorders

March

2010

Depress. Anxiety

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Dramatic advances in science and changes in the structure of medicine will condition the future of clinical research across every therapeutic area in medicine. For the field of pediatric anxiety disorders to thrive it will be important to embrace and actively participate in this revolution so that anxious youth are viewed as a key target population and, consequently, preemptive, preventive, and curative interventions will be developed for children by first intent.

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Genes, brain, and behavior: Bridging disciplines

Cited by 18 publications

References 28 publications

Molecular and Cellular Mechanisms of Learning Disabilities: A Focus on NF1

Molecular and Cellular Mechanisms of Learning Disabilities: A Focus on NF1

Both a Nicotinic Single Nucleotide Polymorphism (SNP) and a Noradrenergic SNP Modulate Working Memory Performance when Attention is Manipulated

Looking to the future of research in pediatric anxiety disorders

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