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Articles by A Rumley
Total Records ( 3 ) for A Rumley
  S Rafnsson , I. J Deary , M. C Whiteman , A Rumley , G. D. O Lowe and F. G. R. Fowkes

Introduction: vascular risk factors and diseases can negatively impact cognitive function. Determinants of blood flow are implicated in thrombogenesis and ischaemic events, yet little is known about their relationship with cognition.

Methods: blood rheology data were collected in 1987/88, and cognitive testing was performed in 1998/99 when the mean (±standard deviation) age of the study sample was 73.1 years (±5.0). Follow-up assessment was performed 4 years later. Information was collected on verbal declarative memory, non-verbal reasoning, verbal fluency, information processing speed and a general cognitive factor representing the variance common to the individual test scores.

Results: after controlling for age, sex and cognitive performance in 1998/99, blood viscosity (BV) (P < 0.05) and fibrinogen (P < 0.05) predicted decline in non-verbal reasoning over 4 years. When estimated from pre-morbid level, decline in general cognition (P < 0.05), non-verbal reasoning (P < 0.05) and information processing speed (P < 0.01) was associated with BV levels. Haematocrit (HCT) had similar effects (P < 0.01 to P < 0.001). All associations persisted after control for multiple confounders. When examined together, HCT but not BV independently predicted cognitive decline.

Conclusions: blood rheology is independently related to cognitive decline in older people. The value of strategies aimed at preserving cognition through influencing blood rheology needs investigation.

  R. E Marioni , I. J Deary , M. W Strachan , G. D Lowe , A Rumley , G. D Murray and J. F. Price

Background: the association between the rheological factors haematocrit and plasma viscosity and cognitive ability has not been extensively studied. It is possible that blood viscosity affects cerebral blood flow and cognitive function. This study tested the contemporaneous associations between these two markers of rheology and cognitive ability and estimated lifetime cognitive change in an elderly population with type 2 diabetes.

Methods: a cross-sectional cohort of 1,066 men and women with type 2 diabetes (Edinburgh Type 2 Diabetes Study) was used for the analysis. Plasma viscosity and haematocrit were measured in venous blood samples at baseline. Contemporaneously, a battery of seven cognitive tests was administered to all participants. These data were used to derive a general intelligence factor, g. A vocabulary-based test was also administered as an estimate of prior intelligence, and adjustment for scores on this test was used to estimate lifetime cognitive decline.

Results: increased plasma viscosity was associated with poorer age- and sex-adjusted scores on the cognitive domains of processing speed, mental flexibility and general intelligence, g, with standardised regression coefficients –0.092 (P < 0.01), –0.077 (P < 0.05) and –0.093 (P < 0.01), respectively. After adjusting for vocabulary, education level, cardiovascular dysfunction, duration of diabetes and glycaemic control, the associations remained significant for the measure of processing speed and g, with standardised regression coefficients –0.059 (P < 0.05) and –0.051 (P < 0.05). Increased haematocrit was significantly associated with better age- and sex-adjusted cognitive scores on the majority of the tests and with g. However, significant associations were not retained after adjustments for additional covariates.

Conclusions: increased plasma viscosity is associated with decreased cognitive ability and increased estimated lifetime cognitive decline. The relationship between haematocrit and cognitive ability requires further study.

  N. L Smith , M. H Chen , A Dehghan , D. P Strachan , S Basu , N Soranzo , C Hayward , I Rudan , M Sabater Lleal , J. C Bis , M. P. M de Maat , A Rumley , X Kong , Q Yang , F. M. K Williams , V Vitart , H Campbell , A Malarstig , K. L Wiggins , C. M Van Duijn , W. L McArdle , J. S Pankow , A. D Johnson , A Silveira , B McKnight , A. G Uitterlinden , Aleksic Wellcome Trust Case Control Consortium; , J. B Meigs , A Peters , W Koenig , M Cushman , S Kathiresan , J. I Rotter , E. G Bovill , A Hofman , E Boerwinkle , G. H Tofler , J. F Peden , B. M Psaty , F Leebeek , A. R Folsom , M. G Larson , T. D Spector , A. F Wright , J. F Wilson , A Hamsten , T Lumley , J. C. M Witteman , W Tang and C. J. O'Donnell

Background— Plasma levels of coagulation factors VII (FVII), VIII (FVIII), and von Willebrand factor (vWF) influence risk of hemorrhage and thrombosis. We conducted genome-wide association studies to identify new loci associated with plasma levels.

Methods and Results— The setting of the study included 5 community-based studies for discovery comprising 23 608 European-ancestry participants: Atherosclerosis Risk In Communities Study, Cardiovascular Health Study, British 1958 Birth Cohort, Framingham Heart Study, and Rotterdam Study. All subjects had genome-wide single-nucleotide polymorphism (SNP) scans and at least 1 phenotype measured: FVII activity/antigen, FVIII activity, and vWF antigen. Each study used its genotype data to impute to HapMap SNPs and independently conducted association analyses of hemostasis measures using an additive genetic model. Study findings were combined by meta-analysis. Replication was conducted in 7604 participants not in the discovery cohort. For FVII, 305 SNPs exceeded the genome-wide significance threshold of 5.0x10–8 and comprised 5 loci on 5 chromosomes: 2p23 (smallest P value 6.2x10–24), 4q25 (3.6x10–12), 11q12 (2.0x10–10), 13q34 (9.0x10–259), and 20q11.2 (5.7x10–37). Loci were within or near genes, including 4 new candidate genes and F7 (13q34). For vWF, 400 SNPs exceeded the threshold and marked 8 loci on 6 chromosomes: 6q24 (1.2x10–22), 8p21 (1.3x10–16), 9q34 (<5.0x10–324), 12p13 (1.7x10–32), 12q23 (7.3x10–10), 12q24.3 (3.8x10–11), 14q32 (2.3x10–10), and 19p13.2 (1.3x10–9). All loci were within genes, including 6 new candidate genes, as well as ABO (9q34) and VWF (12p13). For FVIII, 5 loci were identified and overlapped vWF findings. Nine of the 10 new findings were replicated.

Conclusions— New genetic associations were discovered outside previously known biological pathways and may point to novel prevention and treatment targets of hemostasis disorders.

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