Differentiation of cognitive abilities across the life span.

Tucker‐Drob, Elliot M.

doi:10.1037/a0015864

Cited by 278 publications

(363 citation statements)

References 84 publications

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“…A trend identified from the figures is that cognitive impairment associated with IUGR appeared to increase as children age. This may reflect the increased differentiation of neurodevelopmental domains throughout childhood, 39 and that outcome measures at older ages are better able to identify task-specific impairments. A further explanation may be that subtle delays in early childhood may impair the development of executive function, broadly defined as top-down monitoring and control processes that regulate thoughts and behaviour.…”

Section: Discussionmentioning

confidence: 99%

Differential effect of intrauterine growth restriction on childhood neurodevelopment: a systematic review

Murray

Fernandes

Fazel

et al. 2015

BJOG

235

149

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Background Neurodevelopmental disorders are increasingly believed to originate from intrauterine growth restriction (IUGR). Current reviews exploring the neurodevelopmental effects of IUGR, however, are mostly based on birthweight, an inadequate proxy. Objective We aimed to examine the association between IUGR documented in utero, and neurodevelopmental outcomes during childhood. Search strategy Medline, CINAHL, PsycInfo and Scopus were searched for relevant studies published after 1970. Selection criteria The analysis included studies that identified IUGR in utero, with follow‐up assessments between 1 month and 12 years of age. Data collection and analysis Data was extracted for cognitive, behavioural, language, motor, hearing, vision or sleep outcomes. Studies were summarised separately for children born at <35 and ≥35 weeks gestation. Main results Of 28 876 titles identified, 38 were suitable for inclusion. IUGR children born ≥35 weeks gestation scored on average 0.5 SD lower than non‐IUGR children across all neurodevelopmental assessments. IUGR children born <35 weeks of gestation scored approximately 0.7 SD lower than non‐IUGR children across all neurodevelopmental assessments. IUGR children with evidence of fetal circulatory redistribution (preferential perfusion of the brain) had more severe neurodevelopmental impairments than those born IUGR alone. Conclusions IUGR increases the risk of neurodevelopmental impairment during childhood differentially across domains. IUGR children born preterm or with evidence of fetal circulatory redistribution are more severely affected. Tweetable abstract IUGR is associated with an overall risk for neurodevelopmental delay in a range of neurodevelopmental domains.

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Section: Discussionmentioning

confidence: 99%

Differential effect of intrauterine growth restriction on childhood neurodevelopment: a systematic review

Murray

Fernandes

Fazel

et al. 2015

BJOG

235

149

View full text Add to dashboard Cite

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“…Several important cognitive abilities decline with age, even in the absence of dementia or other pathologies [Hedden and Gabrieli, 2004; Tucker‐Drob, 2009]. Given modern demographic shifts [Harper, 2014], cognitive ageing has pressing and increasing economic and social implications for Western societies.…”

Section: Introductionmentioning

confidence: 99%

Brain volumetric changes and cognitive ageing during the eighth decade of life

Ritchie

Dickie

Cox

et al. 2015

Human Brain Mapping

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Later‐life changes in brain tissue volumes—decreases in the volume of healthy grey and white matter and increases in the volume of white matter hyperintensities (WMH)—are strong candidates to explain some of the variation in ageing‐related cognitive decline. We assessed fluid intelligence, memory, processing speed, and brain volumes (from structural MRI) at mean age 73 years, and at mean age 76 in a narrow‐age sample of older individuals (n = 657 with brain volumetric data at the initial wave, n = 465 at follow‐up). We used latent variable modeling to extract error‐free cognitive levels and slopes. Initial levels of cognitive ability were predictive of subsequent brain tissue volume changes. Initial brain volumes were not predictive of subsequent cognitive changes. Brain volume changes, especially increases in WMH, were associated with declines in each of the cognitive abilities. All statistically significant results were modest in size (absolute r‐values ranged from 0.114 to 0.334). These results build a comprehensive picture of macrostructural brain volume changes and declines in important cognitive faculties during the eighth decade of life. Hum Brain Mapp 36:4910–4925, 2015. © 2015 The Authors. Human Brain Mapping Published by Wiley Periodicals, Inc

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“…Although the computerbased version was based upon standard administration protocols, the current absence of such data necessitates that these results be interpreted with appropriate caution. The measure of fluid cognitive function provided by UK Biobank (which we have called VNR) showed a relatively modest age-related trajectory, in contrast to the steeper and well-replicated age-related decline that would be expected for this construct 66,67 (Supplementary Figure 4). This may partly explain the relatively modest correlation of VNR with TMT performance, when compared to those previously reported 9 and may have also had a bearing on our analyses of genetic overlap within UK Biobank.…”

Section: Discussionmentioning

confidence: 98%

Genetic contributions to Trail Making Test performance in UK Biobank

et al. 2017

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The Trail Making Test (TMT) is a widely used test of executive function and has been thought to be strongly associated with general cognitive function. We examined the genetic architecture of the TMT and its shared genetic aetiology with other tests of cognitive function in 23 821 participants from UK Biobank. The single-nucleotide polymorphism-based heritability estimates for trail-making measures were 7.9% (part A), 22.4% (part B) and 17.6% (part B − part A). Significant genetic correlations were identified between trail-making measures and verbal-numerical reasoning (r g 40.6), general cognitive function (r g 40.6), processing speed (r g 40.7) and memory (r g 40.3). Polygenic profile analysis indicated considerable shared genetic aetiology between trail making, general cognitive function, processing speed and memory (standardized β between 0.03 and 0.08). These results suggest that trail making is both phenotypically and genetically strongly associated with general cognitive function and processing speed.Molecular Psychiatry advance online publication, 19 September 2017; doi:10.1038/mp.2017.189 INTRODUCTIONThe Trail Making Test (TMT) is widely used in both research and clinical settings as a test of some aspects of executive function. [1][2][3] The TMT is usually given as two parts, from which three measures are derived. In TMT Part A (TMT A), participants are required to connect an array of numbers in ascending order, by drawing a continuous line (trail) between them as quickly and accurately as possible. TMT Part B (TMT B) requires participants to connect an array of both numbers and letters in alternating ascending order (1, A, 2, B, 3, C and so on) with the same emphasis on speed and accuracy (Supplementary Figure 1). Subtracting TMT A completion time from that of TMT B (TMT B − A) is thought to allow the relative contributions of visual search and psychomotor speed to be parsed from the more complex executive functions (such as cognitive flexibility) required to alternate between numbers and letters. [4][5][6][7][8] TMT performance has been ascribed to a number of cognitive processes, 'including attention, visual search and scanning, sequencing and shifting, psychomotor speed, abstraction, flexibility, ability to execute and modify a plan of action, and ability to maintain two trains of thought simultaneously '. 9 It is considered a useful tool in research and clinical practice due to the sensitivity of the task (particularly TMT B and B − A) to frontal lobe damage (in some, but not other studies 10 ) and dementia. [11][12][13] There are declines in both TMT A and B performance in ageing. 10,[14][15][16][17][18][19][20] There is also evidence for performance deficits on TMT B in mood disorders 21 and in patients with schizophrenia and their relatives 18,[22][23][24][25][26][27] Family-based and twin-based studies have provided evidence for a genetic contribution to individual differences in trail making, estimating the heritability for trail making part A between 0.23 and 0.38, and between 0.39 and 0.65...

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Differentiation of cognitive abilities across the life span.

Cited by 278 publications

References 84 publications

Differential effect of intrauterine growth restriction on childhood neurodevelopment: a systematic review

Differential effect of intrauterine growth restriction on childhood neurodevelopment: a systematic review

Brain volumetric changes and cognitive ageing during the eighth decade of life

Genetic contributions to Trail Making Test performance in UK Biobank

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