A Meta-Analysis of Working Memory Impairments in Children With Attention-Deficit/Hyperactivity Disorder

Martinussen, Rhonda; Hayden, Jill A.; Hogg‐Johnson, Sheilah; Tannock, Rosemary

doi:10.1097/01.chi.0000153228.72591.73

Cited by 1,068 publications

(963 citation statements)

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“…It is closely linked with the acquisition of complex cognitive skills (Cowan, 2013) such as reading (Cain, Oakhill, & Bryant, 2004), mathematics (Dumontheil & Klingberg, 2011), and other academic subjects (Clair‐Thompson & Gathercole, 2006; Gathercole, Pickering, Knight, & Stegmann, 2003). Deficits in working memory have been identified across a range of neurodevelopmental disorders, including attention deficit hyperactivity disorder (Holmes et al., 2014; Martinussen, Hayden, Hogg‐Johnson, & Tannock, 2005), dyslexia (Smith‐Spark & Fisk, 2007), dyscalculia (Rotzer et al., 2009; Szucs, Devine, Soltesz, Nobes, & Gabriel, 2013), and language disorders (Archibald & Gathercole, 2006; Gathercole & Baddeley, 1989; Montgomery, 2000; Weismer, Evans, & Hesketh, 1999). …”

Section: Introductionmentioning

confidence: 99%

Differences in brain morphology and working memory capacity across childhood

Bathelt

Gathercole

Johnson

et al. 2017

Developmental Science

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Working memory (WM) skills are closely associated with learning progress in key areas such as reading and mathematics across childhood. As yet, however, little is known about how the brain systems underpinning WM develop over this critical developmental period. The current study investigated whether and how structural brain correlates of components of the working memory system change over development. Verbal and visuospatial short‐term and working memory were assessed in 153 children between 5.58 and 15.92 years, and latent components of the working memory system were derived. Fractional anisotropy and cortical thickness maps were derived from T1‐weighted and diffusion‐weighted MRI and processed using eigenanatomy decomposition. There was a greater involvement of the corpus callosum and posterior temporal white matter in younger children for performance associated with the executive part of the working memory system. For older children, this was more closely linked with the thickness of the occipitotemporal cortex. These findings suggest that increasing specialization leads to shifts in the contribution of neural substrates over childhood, moving from an early dependence on a distributed system supported by long‐range connections to later reliance on specialized local circuitry. Our findings demonstrate that despite the component factor structure being stable across childhood, the underlying brain systems supporting working memory change. Taking the age of the child into account, and not just their overall score, is likely to be critical for understanding the nature of the limitations on their working memory capacity.

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Section: Introductionmentioning

confidence: 99%

Differences in brain morphology and working memory capacity across childhood

Bathelt

Gathercole

Johnson

et al. 2017

Developmental Science

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“…D1/D5 signalling mediates executive abilities including working memory , attention (Bayer et al, 2000;Granon et al, 2000), motor control (Dreher and Jackson, 1989;Meyer, 1993), and reward and reinforcement mechanisms (Beninger and Miller, 1998). Impairment of those functions is often observed in individuals with ADHD (Arnsten and Li, 2005b;Lijffijt et al, 2005;Luman et al, 2005;Martinussen et al, 2005;Willcutt et al, 2005). Moreover, a recent study in rodents suggested that D1 stimulation contributes to cognitive-enhancing effects of methylphenidate, a leading treatment for ADHD (Arnsten and Dudley, 2005a).…”

Section: Introductionmentioning

confidence: 99%

Investigation of the G protein subunit Gαolf gene (GNAL) in attention deficit/hyperactivity disorder

Laurin

Ickowicz

Pathare

et al. 2008

Journal of Psychiatric Research

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The dopamine system plays an important role in the regulation of attention and motor behavior, subsequently, several dopamine-related genes have been associated with Attention Deficit/ Hyperactivity Disorder (ADHD). Among them are the dopamine receptors D1 and D5 that mediate adenylyl cyclase activation through coupling with G s -like proteins. We thus hypothesized that the G s -like subunit Gα olf , expressed in D1-rich areas of the brain, contributes to the genetic susceptibility of ADHD. To evaluate the involvement of the Gα olf gene, GNAL, in ADHD, we examined the inheritance pattern of 12 GNAL polymorphisms in 258 nuclear families ascertained through a proband with ADHD (311 affected children) using the transmission/disequilibrium test (TDT). Categorical analysis of individual marker alleles demonstrated biased transmission of one polymorphism in GNAL intron 3 (rs2161961; P = 0.011). We also observed significant relationships between rs2161961 and dimensional symptoms of inattention and hyperactivity/ impulsivity (P = 0.003 and P = 0.008). In addition, because of recent evidence of imprinting at the GNAL locus, secondary analyses were split into maternal and paternal transmissions to assess a contribution of parental effects. We found evidence of strong maternal effect, with preferential transmission of maternal alleles for rs2161961A (P = 0.005) and rs8098539A (P = 0.035). These preliminary findings suggest a possible contribution of GNAL in the susceptibility to ADHD, with possible involvement of parent-of-origin effects.

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Section: Introductionmentioning

confidence: 99%

“…In this paper, we review research progress in the relevant fi elds, focusing on the potential relationship between prefrontal α 2A -adrenoceptors and ADHD in nonhuman primates [35][36][37][38][39] . including poor attention regulation [40] , limited working memory [41] , and inability to inhibit inappropriate motor activity [42] .Working memory is a fundamental higher-order function, underlies a wide range of executive functional processes [43,44] , and is primarily controlled by the PFC [45,46] .It has been shown that ADHD patients have altered architecture and less activation in the PFC [47][48][49] . Persistent working-memory problems are the main cognitive defi cit in ADHD [40,41,50,51] .…”

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confidence: 99%

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Prefrontal cortical α2A-adrenoceptors and a possible primate model of attention deficit and hyperactivity disorder

Sun

Luo

et al. 2015

Neurosci. Bull.

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Attention deficit and hyperactivity disorder (ADHD), a prevalent syndrome in children worldwide, is characterized by impulsivity, inappropriate inattention, and/or hyperactivity. It seriously afflicts cognitive development in childhood, and may lead to chronic under-achievement, academic failure, problematic peer relationships, and low self-esteem. There are at least three challenges for the treatment of ADHD. First, the neurobiological bases of its symptoms are still not clear. Second, the commonly prescribed medications, most showing short-term therapeutic efficacy but with a high risk of serious side-effects, are mainly based on a dopamine mechanism. Third, more novel and effi cient animal models, especially in nonhuman primates, are required to accelerate the development of new medications. In this article, we review research progress in the related fi elds, focusing on our previous studies showing that blockade of prefrontal cortical α 2A -adrenoceptors in monkeys produces almost all the typical behavioral symptoms of ADHD.Keywords: prefrontal cortex; α 2A -adrenoceptors; cognitive functions; attention defi cit and hyperactivity disorder; animal models ·Review· IntroductionAttention deficit and hyperactivity disorder (ADHD) is one of the most prevalent childhood neurodevelopmental conditions, affecting 3-5% of grade-school children worldwide [1] . It is characterized by i nappropriate levels of inattention, i mpulsivity, and/or hyperactivity [2][3][4] . These symptoms develop in childhood, and can persist into adolescence and adulthood [5] . ADHD seriously affects cognitive development [6][7][8] , and, without appropriate treatment, has consequences for the risk of anxiety, substance abuse, and depression in adulthood [ 2, 5, 9] .T he neurobiological bases o f ADHD symptoms are still not clear [10] . Clarifying them can help better understand the biological vulnerabilities that may underlie ADHD in a specifi c patient and how to modulate the responses to treatment, thereby contributing to better and more effective therapy.It has been suggested that the symptoms involve a dopaminergic mechanism in the prefrontal cortex (PFC) and striatum [11, 12] . Experimentally decreased dopamine (DA) release in the PFC results in ADHD-like symptoms [13, 14] .To date, DA dysregulation is thought to be central to the neurobiology of ADHD, and its pharmacological treatment, such as m ethylphenidate (MPH, i.e. Ritalin) [15][16][17] , levels the DA c oncentration in the synapse and extrasynaptic space in the PFC as a blocker of the DA transporter. MPH ameliorates inappropriate inattention [18][19][20] , decreases impulsivity [21] , and enhances inhibitory control [22] . However, as MPH is a prescription psychostimulant, there are strong concerns over drug dependence, paranoia, schizophrenia, and behavioral sensitization that might be caused by longterm therapy, similar to other stimulants [23][24][25].Converging evidence indicates that the pathophysiology of ADHD has multiple origins [26][27][28][29][30][31][32] ; for i...

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A Meta-Analysis of Working Memory Impairments in Children With Attention-Deficit/Hyperactivity Disorder

Cited by 1,068 publications

References 78 publications

Differences in brain morphology and working memory capacity across childhood

Differences in brain morphology and working memory capacity across childhood

Investigation of the G protein subunit Gαolf gene (GNAL) in attention deficit/hyperactivity disorder

Prefrontal cortical α2A-adrenoceptors and a possible primate model of attention deficit and hyperactivity disorder

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