@article{Henry2019,
title = {The relationship between sleep duration, cognition and dementia: a Mendelian randomization study},
author = {Albert Henry and Michail Katsoulis and Stefano Masi and Ghazaleh Fatemifar and Spiros Denaxas and Dionisio Acosta and Victoria Garfield and Caroline E Dale },
url = {https://academic.oup.com/ije/advance-article/doi/10.1093/ije/dyz071/5486060},
year = {2019},
date = {2019-05-07},
journal = {International Journal of Epidemiology},
abstract = {Short and long sleep duration have been linked with poorer cognitive outcomes, but it remains unclear whether these associations are causal.

Methods
We conducted the first Mendelian randomization (MR) study with 77 single-nucleotide polymorphisms (SNPs) for sleep duration using individual-participant data from the UK Biobank cohort (N = 395 803) and summary statistics from the International Genomics of Alzheimer’s Project (N cases/controls = 17 008/37 154) to investigate the potential impact of sleep duration on cognitive outcomes.

Results
Linear MR suggested that each additional hour/day of sleep was associated with 1% [95% confidence interval (CI) = 0–2%; P = 0.008] slower reaction time and 3% more errors in visual-memory test (95% CI = 0–6%; P = 0.05). There was little evidence to support associations of increased sleep duration with decline in visual memory [odds ratio (OR) per additional hour/day of sleep = 1.10 (95% CI = 0.76–1.57); P = 0.62], decline in reaction time [OR = 1.28 (95% CI = 0.49–3.35); P = 0.61], all-cause dementia [OR = 1.19 (95% CI = 0.65–2.19); P = 0.57] or Alzheimer’s disease risk [OR = 0.89 (95% CI = 0.67–1.18); P = 0.41]. Non-linear MR suggested that both short and long sleep duration were associated with poorer visual memory (P for non-linearity = 3.44e–9) and reaction time (P for non-linearity = 6.66e–16).

Conclusions
Linear increase in sleep duration has a small negative effect on reaction time and visual memory, but the true association might be non-linear, with evidence of associations for both short and long sleep duration. These findings suggest that sleep duration may represent a potential causal pathway for cognition.},
keywords = {13017, cognition, dementia, sleep},
pubstate = {published},
tppubtype = {article}
}

@article{Frangou2019,
title = {Insulin resistance: Genetic associations with depression and cognition in population based cohorts},
author = {S Frangou and M Shirali and MJ Adams and DM Howard and J Gibson and LS Hall and BH Smith and S Padmanabhan and AD Murray and DJ Porteous and CS Haley and IJ Deary and TK Clarke and AM McIntosh},
url = {https://www.ncbi.nlm.nih.gov/pubmed/30965038},
year = {2019},
date = {2019-04-06},
journal = {Experimental Neurology},
abstract = {Insulin resistance, broadly defined as the reduced ability of insulin to exert its biological action, has been associated with depression and cognitive dysfunction in observational studies. However, it is unclear whether these associations are causal and whether they might be underpinned by other shared factors. To address this knowledge gap, we capitalized on the stability of genetic biomarkers through the lifetime, and on their unidirectional relationship with depression and cognition. Specifically, we determined the association between quantitative measures of cognitive function and depression and genetic instruments of insulin resistance traits in two large-scale population samples, the Generation Scotland: Scottish Family Health Study (GS: SFHS; N = 19,994) and in the UK Biobank (N = 331,374). In the GS:SFHS, the polygenic risk score (PRS) for fasting insulin was associated with verbal intelligence and depression while the PRS for the homeostasis model assessment of insulin resistance was associated with verbal intelligence. Despite this overlap in genetic architecture, Mendelian randomization analyses in the GS:SFHS and in the UK Biobank samples did not yield evidence for causal associations from insulin resistance traits to either depression or cognition. These findings may be due to weak genetic instruments, limited cognitive measures and insufficient power but they may also indicate the need to identify other biological mechanisms that may mediate the relationship from insulin resistance to depression and cognition.},
keywords = {4844, cognition, depression, featured, genetics, insulin},
pubstate = {published},
tppubtype = {article}
}

@article{Olivo2019,
title = {Low neuroticism and cognitive performance are differently associated to overweight and obesity: A cross-sectional and longitudinal UK Biobank study},
author = {Gaia Olivo and Shaili Gour and Helgi B.Schiöth},
url = {https://www.sciencedirect.com/science/article/pii/S0306453018310114?dgcid=rss_sd_all},
year = {2019},
date = {2019-03-01},
journal = {Psychoneuroendocrinology},
abstract = {Background

A growing body of research has linked personality traits to cognitive performance. This relationship might play a role in the predisposition toward obesity. Neuroticism and executive function seem to be particularly involved, and reduced executive function has been proposed to underlie the association of neuroticism with sedentary behaviors and fatty food consumption. Despite the link between neuroticism, cognitive functions and obesity has been largely reported, conflicting evidence exists. Moreover, information regarding other cognitive domains, and studies on overweight individuals, are still scarce.

Methods

We examined cross-sectional associations of neuroticism and cognitive function with overweight and obesity in a sample of 170 310 individuals from the UK Biobank cohort, adjusted for sociodemographic and life-style factors. Measures on fluid intelligence (FI) (reasoning ability), trail making test (TMT) (executive function), numeric memory test and pairs matching (PM) task (short-term memory) were extracted from the database. Correlations between neuroticism and cognitive performance were explored. Moreover, we investigated whether neuroticism and executive function could predict BMI variability over time.

Results

Reduced FI and short-term memory were associated with overweight and obesity, while reduced executive function was associated with obesity but not with overweight. Low neuroticism was associated with being overweight rather than lean or obese independently of gender and life-style. Furthermore, baseline neuroticism scores could predict BMI variations over 5–10 years follow-up, and high neuroticism correlated with lower cognitive performance.

Conclusions

Lower cognitive performance is associated with both overweight and obesity, except for executive function, which was only related to obesity. Neuroticism correlated with performance on most of the cognitive domains tested, supporting the link between personality and cognition. Our findings also support the role of neuroticism in leading to greater weight variability over time, rather than to overweight/obesity itself.},
keywords = {23482, BMI, cognition, neuroticism},
pubstate = {published},
tppubtype = {article}
}

@article{Cullen2018,
title = {Cross-sectional and longitudinal analyses of outdoor air pollution exposure and cognitive function in UK Biobank},
author = {B Cullen and D Newby and D Lee and DM Lyall and AJ Nevado-Holgado and JJ Evans and JP Pell and S Lovestone and J Cavanagh},
url = {https://www.ncbi.nlm.nih.gov/pubmed/30108252},
year = {2018},
date = {2018-08-14},
journal = {Scientific Reports},
abstract = {Observational studies have shown consistently increased likelihood of dementia or mild cognitive impairment diagnoses in people with higher air pollution exposure history, but evidence has been less consistent for associations with cognitive test performance. We estimated the association between baseline neighbourhood-level exposure to airborne pollutants (particulate matter and nitrogen oxides) and (1) cognitive test performance at baseline and (2) cognitive score change between baseline and 2.8-year follow-up, in 86,759 middle- to older-aged adults from the UK Biobank general population cohort. Unadjusted regression analyses indicated small but consistent negative associations between air pollutant exposure and baseline cognitive performance. Following adjustment for a range of key confounders, associations were inconsistent in direction and of very small magnitude. The largest of these indicated that 1 interquartile range higher air pollutant exposure was associated on average with 0.35% slower reaction time (95% CI: 0.13, 0.57), a 2.92% higher error rate on a visuospatial memory test (95% CI: 1.24, 4.62), and numeric memory scores that were 0.58 points lower (95% CI: -0.96, -0.19). Follow-up analyses of cognitive change scores did not show evidence of associations. The findings indicate that in this sample, which is five-fold larger than any previous cross-sectional study, the association between air pollution exposure and cognitive performance was weak. Ongoing follow-up of the UK Biobank cohort will allow investigation of longer-term associations into old age, including longitudinal tracking of cognitive performance and incident dementia outcomes.},
keywords = {11332, air pollution, cognition},
pubstate = {published},
tppubtype = {article}
}

@article{Firth2018bb,
title = {Association Between Muscular Strength and Cognition in People With Major Depression or Bipolar Disorder and Healthy Controls},
author = {J Firth and JA Firth and B Stubbs and D Vancampfort and FB Schuch M Hallgren and N Veronese and AR Yung and J Sarris},
url = {https://www.ncbi.nlm.nih.gov/pubmed/29710135},
year = {2018},
date = {2018-04-18},
journal = {JAMA Psychiatry},
abstract = {Importance:

Objective physical fitness measures, such as handgrip strength, are associated with physical, mental, and cognitive outcomes in the general population. Although people with mental illness experience reduced physical fitness and cognitive impairment, the association between muscular strength and cognition has not been examined to date.

Objective:

To determine associations between maximal handgrip strength and cognitive performance in people with major depression or bipolar disorder and in healthy controls.

Design, Setting, and Participants:

In a multicenter, population-based study conducted between February 13, 2005, and October 1, 2010, in the United Kingdom, cross-sectional analysis was conducted of baseline data from 110 067 participants in the UK Biobank. Data analysis was performed between August 3 and August 18, 2017. Invitations were mailed to approximately 9.2 million UK homes, recruiting 502 664 adults, all aged 37 to 73 years. Clinically validated measures were used to identify individuals with major recurrent depression (moderate or severe) or bipolar disorder (type I or type II) and healthy controls (those with no indication of present or previous mood disorders).

Main Outcomes and Measures:

Handgrip dynamometry was used to measure muscular function. Cognitive functioning was assessed using computerized tasks of reaction time, visual memory, number memory, reasoning, and prospective memory. Generalized linear mixed models assessed the association between handgrip strength and cognitive performance, controlling for age, educational level, sex, body weight, and geographic region.

Results:
Of the 110 067 participants, analyses included 22 699 individuals with major depression (mean [95% range] age, 55.5 [41-68] years; 7936 [35.0%] men), 1475 with bipolar disorder (age, 54.4 [41-68] years; 748 [50.7%] men), and 85 893 healthy controls (age, 53.7 [41-69] years; 43 000 [50.0%] men). In those with major depression, significant positive associations (P < .001) between maximal handgrip strength and improved performance on all 5 cognitive tasks were found, including visual memory (coefficient, -0.146; SE, 0.014), reaction time (coefficient, -0.036; SE, 0.002), reasoning (coefficient, 0.213; SE, 0.02), number memory (coefficient, 0.160; SE, 0.023), and prospective memory (coefficient, 0.341; SE, 0.024). Similar results were found in healthy controls. Among participants with bipolar disorder, handgrip strength was positively associated with improved visual memory (coefficient, -0.129; SE, 0.052; P = .01), reaction time (coefficient, -0.047; SE, 0.007; P < .001), prospective memory (coefficient, 0.262; SE, 0.088; P = .003), and reasoning (coefficient, 0.354; SE, 0.08; P < .001).

Conclusions and Relevance:

Grip strength may provide a useful indicator of cognitive impairment in people with major depression and bipolar disorder. Future research should investigate causality, assess the functional implications of handgrip strength in psychiatric populations, and examine how interventions to improve muscular fitness affect neurocognitive status and socio-occupational functioning},
keywords = {22125, bipolar, cognition, depression, muscle strength},
pubstate = {published},
tppubtype = {article}
}

@article{Kievit2018,
title = {The neural determinants of age-related changes in fluid intelligence: a pre-registered, longitudinal analysis in UK Biobank},
author = {RA Kievit and D Fuhrmann and GS Borgeest and IL Simpson-Kent and RNA Henson},
url = {https://www.ncbi.nlm.nih.gov/pubmed/29707655},
year = {2018},
date = {2018-04-05},
journal = {Wellcome Open Research},
abstract = {Background: Fluid intelligence declines with advancing age, starting in early adulthood. Within-subject declines in fluid intelligence are highly correlated with contemporaneous declines in the ability to live and function independently. To support healthy aging, the mechanisms underlying these declines need to be better understood. Methods: In this pre-registered analysis, we applied latent growth curve modelling to investigate the neural determinants of longitudinal changes in fluid intelligence across three time points in 185,317 individuals (N=9,719 two waves},
keywords = {ageing, cognition, fliud intelligence},
pubstate = {published},
tppubtype = {article}
}

@article{Piumatti2018,
title = {The relationship between alcohol use and long-term cognitive decline in middle and late life: a longitudinal analysis using UK Biobank.},
author = {G Piumatti and SC Moore and DM Berridge and C Sarkar and J Gallacher},
url = {https://www.ncbi.nlm.nih.gov/pubmed/29325150},
year = {2018},
date = {2018-01-09},
journal = {Journal of public health},
abstract = {Background:

Using UK Biobank data, this study sought to explain the causal relationship between alcohol intake and cognitive decline in middle and older aged populations.

Methods:

Data from 13 342 men and women, aged between 40 and 73 years were used in regression analysis that tested the functional relationship and impact of alcohol on cognitive performance. Performance was measured using mean reaction time (RT) and intra-individual variation (IIV) in RT, collected in response to a perceptual matching task. Covariates included body mass index, physical activity, tobacco use, socioeconomic status, education and baseline cognitive function.

Results:
A restricted cubic spline regression with three knots showed how the linear (β1 = -0.048, 95% CI: -0.105 to -0.030) and non-linear effects (β2 = 0.035, 95% CI: 0.007-0.059) of alcohol use on mean RT and IIV in RT (β1 = -0.055, 95% CI: -0.125 to -0.034; β2 = 0.034, 95% CI: 0.002-0.064) were significant adjusting for covariates. Cognitive function declined as alcohol use increased beyond 10 g/day. Decline was more apparent as age increased.

Conclusions:

The relationship between alcohol use and cognitive function is non-linear. Consuming more than one UK standard unit of alcohol per day is detrimental to cognitive performance and is more pronounced in older populations.},
keywords = {14935, alcohol, cognition},
pubstate = {published},
tppubtype = {article}
}

@article{Hagenaars2017bb,
title = {Cognitive ability and physical health: a Mendelian randomization study},
author = {Ian Deary & Sarah Harris J E Saskia P. Hagenaars Catharine R. Gale},
url = {https://www.nature.com/articles/s41598-017-02837-3},
year = {2017},
date = {2017-06-01},
journal = {Scientific Reports},
abstract = {Causes of the association between cognitive ability and health remain unknown, but may reflect a shared genetic aetiology. This study examines the causal genetic associations between cognitive ability and physical health. We carried out two-sample Mendelian randomization analyses using the inverse-variance weighted method to test for causality between later life cognitive ability, educational attainment (as a proxy for cognitive ability in youth), BMI, height, systolic blood pressure, coronary artery disease, and type 2 diabetes using data from six independent GWAS consortia and the UK Biobank sample (N = 112 151). BMI, systolic blood pressure, coronary artery disease and type 2 diabetes showed negative associations with cognitive ability; height was positively associated with cognitive ability. The analyses provided no evidence for casual associations from health to cognitive ability. In the other direction, higher educational attainment predicted lower BMI, systolic blood pressure, coronary artery disease, type 2 diabetes, and taller stature. The analyses indicated no causal association from educational attainment to physical health. The lack of evidence for causal associations between cognitive ability, educational attainment, and physical health could be explained by weak instrumental variables, poorly measured outcomes, or the small number of disease cases.},
keywords = {10279, cognition, genetics, physical activity},
pubstate = {published},
tppubtype = {article}
}

@article{Kyle2017,
title = {Sleep and cognitive performance: cross-sectional associations from the UK Biobank (N=477,966)},
author = {Feige Rutter Spiegelhalder B M K SD Kyle C Sexton},
url = {https://academic.oup.com/sleep/article-abstract/40/suppl_1/A119/3781566},
year = {2017},
date = {2017-04-28},
journal = {Sleep},
abstract = {Abstract
Introduction:

The relationship between insomnia symptoms and cognitive performance is unclear, particularly at the population level. We conducted the largest examination of this association to date through analysis of the UK Biobank, a large population-based sample of adults aged 40–69 yrs. We also sought to determine associations between cognitive performance and self-reported chronotype, sleep medication use, and sleep duration.
Methods:

This cross-sectional, population-based study involved 477,966 participants, comprising 133,582 with frequent insomnia symptoms (age: 57.4 ± 7.7 yrs; 62.1% female) and 344,384 controls without (age: 56.1 ± 8.2 yrs; 51.9% female). Cognitive performance was assessed through a touchscreen test battery probing reasoning, basic reaction time, numeric memory, visual memory and prospective memory. Adjusted linear and logistic regression models included relevant demographic (age, gender, socioeconomic status), clinical (depressive symptoms, psychiatric medication use, BMI) and sleep variables.
Results:

Insomnia symptoms were associated with cognitive impairment in unadjusted models, however these effects were reversed after full adjustment, leaving those with frequent insomnia symptoms showing statistically better cognitive performance over those without (for reasoning, reaction time, visual memory and prospective memory). Relative to intermediate chronotype, evening chronotype was associated with superior task performance, while morning chronotype was associated with the poorest performance. Sleep medication use and both long (>9hrs) and short (<7hrs) sleep duration were associated with impaired performance.
Conclusion:

Our results suggest that frequent insomnia symptoms are not reliably associated with cognitive impairment at the population level after adjustment for relevant confounding variables. Further work is required to examine mechanistic underpinnings of an apparent evening chronotype advantage in cognitive performance, as well as impairment associated with morning chronotype, sleep medication use, and sleep duration extremes.},
keywords = {6818, cognition, featured, sleep},
pubstate = {published},
tppubtype = {article}
}

@article{DonaldLyall2016,
title = {Associations between single and multiple cardiometabolic diseases and cognitive abilities in 474 129 UK Biobank participants},
author = {Jana Anderson Jason Gill Daniel Mackay Andrew McIntosh Daniel Smith Ian Deary Naveed Sattar Jill Pell M R F M J J P Donald M. Lyall Carlos A. Celis-Morales},
url = {http://eurheartj.oxfordjournals.org/content/early/2016/11/13/eurheartj.ehw528.full?ijkey=zzUsMxeRlw9KDj6&amp;keytype=ref},
year = {2016},
date = {2016-11-16},
journal = {European Heart Journal},
abstract = {Cardiometabolic diseases (hypertension, coronary artery disease [CAD] and diabetes are known to associate with poorer cognitive ability but there are limited data on whether having more than one of these conditions is associated with additive effects. We aimed to quantify the magnitude of their associations with non-demented cognitive abilities and determine the extent to which these associations were additive.},
keywords = {7155, cardiometabolic, cognition, featured},
pubstate = {published},
tppubtype = {article}
}

@article{Kendall2016,
title = {Cognitive performance among carriers of pathogenic copy number variants: Analysis of 152,000 UK Biobank subjects},
author = {Valentina Escott-Price Mark Einona Rhys Thomas Jonathan Hewitt Michael O’Donovan Michael Owen James Walters George Kirov C J Kimberley M. Kendall Elliott Rees},
url = {http://www.sciencedirect.com/science/article/pii/S0006322316327111},
year = {2016},
date = {2016-08-18},
journal = {Biological Psychiatry},
abstract = {Background

The UK Biobank is a unique resource for biomedical research, with extensive phenotypic and genetic data on half a million adultsfrom the general population. We aimed to examine the effect of neurodevelopmental copy number variants (CNVs) on the cognitive performance of participants.
Methods
We used Affymetrix Power Tools and PennCNV-Affy software to analyse Affymetrix microarraysof the first 152,728genotypedindividuals. We annotated a list of 93 CNVs and compared their frequencies with control datasets. Weanalysed the performance on seven cognitive tests of carriers of 12 CNVs associated with schizophrenia (N = 1,087) and of carriers of another 41neurodevelopmental CNVs (N = 484).
Results

The frequencies of the 93 CNVs in the Biobank subjects were remarkably similar to those among 26,628 controls from other datasets. Carriersof schizophrenia-associated CNVs and of the group of 41 other neurodevelopmental CNVs had impaired performance on the cognitive tests, with nine of 14 comparisons remaining statistically significant aftercorrection for multiple testing.They also had lower educational and occupational attainment (p-values between 10-7and 10-18).Thedeficits in cognitive performance were modest (z score reductions between 0.01 and 0.51), compared to individuals with schizophrenia in the Biobank (z score reductions between 0.35 and 0.90).
Conclusions

This is the largest study on the cognitive phenotypes of CNVs to date. Adult carriers of neurodevelopmentalCNVs from the general population have significant cognitivedeficits. The UK Biobank will allow unprecedented opportunities for analysis of furtherphenotypic consequences of CNVs.},
keywords = {14421, CNVs, cognition, genetics},
pubstate = {published},
tppubtype = {article}
}

@article{Lyall2016c,
title = {Cognitive Test Scores in UK Biobank: Data Reduction in 480,416 Participants and Longitudinal Stability in 20,346 Participants},
author = {Mike Allerhand Daniel Smith Daniel Mackay Jonathan Evans Jana Anderson Chloe Fawns-Ritchie Andrew McIntosh Ian Deary Jill Pell J M J P Donald M. Lyall Breda Cullen},
url = {http://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0154222},
year = {2016},
date = {2016-04-25},
journal = {Plos One},
abstract = {UK Biobank includes 502,649 middle- and older-aged adults from the general population who have undergone detailed phenotypic assessment. The majority of participants completed tests of cognitive functioning, and on average four years later a sub-group of N = 20,346 participants repeated most of the assessment. These measures will be used in a range of future studies of health outcomes in this cohort. The format and content of the cognitive tasks were partly novel. The aim of the present study was to validate and characterize the cognitive data: to describe the inter-correlational structure of the cognitive variables at baseline assessment, and the degree of stability in scores across longitudinal assessment. Baseline cognitive data were used to examine the inter-correlational/factor-structure, using principal components analysis (PCA). We also assessed the degree of stability in cognitive scores in the subsample of participants with repeat data. The different tests of cognitive ability showed significant raw inter-correlations in the expected directions. PCA suggested a one-factor solution (eigenvalue = 1.60), which accounted for around 40% of the variance. Scores showed varying levels of stability across time-points (intraclass correlation range = 0.16 to 0.65). UK Biobank cognitive data has the potential to be a significant resource for researchers looking to investigate predictors and modifiers of cognitive abilities and associated health outcomes in the general population.},
keywords = {7155/744, cognition},
pubstate = {published},
tppubtype = {article}
}

@article{Lyall2016c,
title = {Alzheimer disease genetic risk factor APOE e4 and cognitive abilities in 111,739 UK Biobank participants},
author = {Stuart Ritchie Davies Gail Breda Cullen Carlos Celis Mark Bailey Jana Anderson Jon Evans Daniel Mckay Andrew Mcintosh Naveed Sattar Daniel Smith Ian Deary J E S F M J J Donald M. Lyall Joey Ward and Jill P Pell},
url = {https://www.ncbi.nlm.nih.gov/pubmed/27103599},
year = {2016},
date = {2016-04-21},
journal = {Age and ageing},
abstract = {Background: the apolipoprotein (APOE) e4 locus is a genetic risk factor for dementia. Carriers of the e4 allele may be more vulnerable to conditions that are independent risk factors for cognitive decline, such as cardiometabolic diseases.

Objective: we tested whether any association with APOE e4 status on cognitive ability was larger in older ages or in those with cardiometabolic diseases.

Subjects: UK Biobank includes over 500,000 middle- and older aged adults who have undergone detailed medical and cognitive phenotypic assessment. Around 150,000 currently have genetic data. We examined 111,739 participants with complete genetic and cognitive data.

Methods: baseline cognitive data relating to information processing speed, memory and reasoning were used. We tested for interactions with age and with the presence versus absence of type 2 diabetes (T2D), coronary artery disease (CAD) and hypertension.

Results: in several instances, APOE e4 dosage interacted with older age and disease presence to affect cognitive scores. When adjusted for potentially confounding variables, there was no APOE e4 effect on the outcome variables.

Conclusions: future research in large independent cohorts should continue to investigate this important question, which has potential implications for aetiology related to dementia and cognitive impairment.},
keywords = {7155, ageing, alzheimers, cognition, genetics},
pubstate = {published},
tppubtype = {article}
}

@article{Davies2016,
title = {Genome-wide association study of cognitive functions and educational attainment in UK Biobank (N=112 151)},
author = {Liewald Hill Hagenaars Harris Ritchie Luciano Fawns-Ritchie Lyall Cullen Cox Hayward Porteous Evans McIntosh Gallacher Craddock Pell Smith Gale D C W D S P S E S J M C D B S R C D J J A M J N J P D J C R G Davies R E Marioni and I J Deary},
url = {http://www.nature.com/mp/journal/vaop/ncurrent/full/mp201645a.html},
year = {2016},
date = {2016-04-05},
journal = {Molecular Psychiatry},
abstract = {People’s differences in cognitive functions are partly heritable and are associated with important life outcomes. Previous genome-wide association (GWA) studies of cognitive functions have found evidence for polygenic effects yet, to date, there are few replicated genetic associations. Here we use data from the UK Biobank sample to investigate the genetic contributions to variation in tests of three cognitive functions and in educational attainment. GWA analyses were performed for verbal–numerical reasoning (N=36 035), memory (N=112 067), reaction time (N=111 483) and for the attainment of a college or a university degree (N=111 114). We report genome-wide significant single-nucleotide polymorphism (SNP)-based associations in 20 genomic regions, and significant gene-based findings in 46 regions. These include findings in the ATXN2, CYP2DG, APBA1 and CADM2 genes. We report replication of these hits in published GWA studies of cognitive function, educational attainment and childhood intelligence. There is also replication, in UK Biobank, of SNP hits reported previously in GWA studies of educational attainment and cognitive function. GCTA-GREML analyses, using common SNPs (minor allele frequency>0.01), indicated significant SNP-based heritabilities of 31% (s.e.m.=1.8%) for verbal–numerical reasoning, 5% (s.e.m.=0.6%) for memory, 11% (s.e.m.=0.6%) for reaction time and 21% (s.e.m.=0.6%) for educational attainment. Polygenic score analyses indicate that up to 5% of the variance in cognitive test scores can be predicted in an independent cohort. The genomic regions identified include several novel loci, some of which have been associated with intracranial volume, neurodegeneration, Alzheimer’s disease and schizophrenia.},
keywords = {10279, cognition, education},
pubstate = {published},
tppubtype = {article}
}

@article{Hagenaars2016b,
title = {Shared genetic aetiology between cognitive functions and physical and mental health in UK Biobank (N=112 151) and 24 GWAS consortia},
author = {Davies Hill Liewald Ritchie Marioni Fawns-Ritchie Cullen Malik METASTROKE Consortium International Worrall Sudlow Wardlaw Gallacher Pell McIntosh Smith Gale Deary G W D D C M S J R E C B R B B C L M J M J J A M D J C R J S P Hagenaars S E Harris},
url = {http://www.nature.com/mp/journal/vaop/ncurrent/full/mp2015225a.html},
year = {2016},
date = {2016-01-26},
journal = {Molecular Psychiatry - Nature},
abstract = {Causes of the well-documented association between low levels of cognitive functioning and many adverse neuropsychiatric outcomes, poorer physical health and earlier death remain unknown. We used linkage disequilibrium regression and polygenic profile scoring to test for shared genetic aetiology between cognitive functions and neuropsychiatric disorders and physical health. Using information provided by many published genome-wide association study consortia, we created polygenic profile scores for 24 vascular–metabolic, neuropsychiatric, physiological–anthropometric and cognitive traits in the participants of UK Biobank, a very large population-based sample (N=112 151). Pleiotropy between cognitive and health traits was quantified by deriving genetic correlations using summary genome-wide association study statistics and to the method of linkage disequilibrium score regression. Substantial and significant genetic correlations were observed between cognitive test scores in the UK Biobank sample and many of the mental and physical health-related traits and disorders assessed here. In addition, highly significant associations were observed between the cognitive test scores in the UK Biobank sample and many polygenic profile scores, including coronary artery disease, stroke, Alzheimer’s disease, schizophrenia, autism, major depressive disorder, body mass index, intracranial volume, infant head circumference and childhood cognitive ability. Where disease diagnosis was available for UK Biobank participants, we were able to show that these results were not confounded by those who had the relevant disease. These findings indicate that a substantial level of pleiotropy exists between cognitive abilities and many human mental and physical health disorders and traits and that it can be used to predict phenotypic variance across samples.},
keywords = {10279, cognition, disease, genetics},
pubstate = {published},
tppubtype = {article}
}

@article{Dawes2015b,
title = {Hearing Loss and Cognition: The Role of Hearing Aids, Social Isolation and Depression},
author = {Piers Dawes and Richard Emsley and Karen J Cruickshanks and David R Moore and Heather Fortnum and Mark Edmondson-Jones and Abby McCormack and Kevin J Munro},
url = {http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0119616},
year = {2015},
date = {2015-03-11},
journal = {PLOS ONE},
keywords = {11516, cognition, depression, Hearing loss},
pubstate = {published},
tppubtype = {article}
}