Clinical and Subclinical Macrovascular Disease as Predictors of Cognitive Decline in Older Patients With Type 2 Diabetes

The Edinburgh Type 2 Diabetes Study

  1. On behalf of the Edinburgh Type 2 Diabetes Study (ET2DS) Investigators
  1. 1Centre for Population Health Sciences, University of Edinburgh, Edinburgh, Scotland, United Kingdom
  2. 2Metabolic Unit, Western General Hospital, Edinburgh, Scotland, United Kingdom
  3. 3Department of Radiology, Western General Hospital, Edinburgh, Scotland, United Kingdom
  4. 4Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, Scotland, United Kingdom
  5. 5Centre for Cardiovascular Sciences, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh, Scotland, United Kindgom
  6. 6Alzheimer Scotland Dementia Research Centre, University of Edinburgh, Edinburgh, Scotland, United Kingdom
  7. 7Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, Edinburgh, Scotland, United Kingdom
  8. 8Scottish Dementia Clinical Research Network, National Health Service, Edinburgh, Scotland, United Kingdom
  9. 9Psychology in the School of Philosophy, Psychology and Language Sciences, University of Edinburgh, Edinburgh, Scotland, United Kingdom
  1. Corresponding authors: Insa Feinkohl, I.Feinkohl{at}sms.ed.ac.uk, and Jackie Price, Jackie.Price{at}ed.ac.uk

Abstract

OBJECTIVE Macrovascular disease may contribute to increased risk of accelerated cognitive decline in patients with type 2 diabetes. We aimed to determine associations of measures of macrovascular disease with cognitive change in a cognitively healthy older population with type 2 diabetes.

RESEARCH DESIGN AND METHODS Eight-hundred thirty-one men and women (aged 60–75 years) attended two waves of the prospective Edinburgh Type 2 Diabetes Study (ET2DS). At baseline, clinical and subclinical macrovascular disease was measured, including cardiovascular event history, carotid intima-media thickness (cIMT), ankle brachial index (ABI), and serum N-terminal probrain natriuretic peptide (NT-proBNP). Seven neuropsychological tests were administered at baseline and after 4 years; scores were combined to a standardized general ability factor (g). Adjustment of follow-up g for baseline g assessed 4-year cognitive change. Adjustment for vocabulary (estimated premorbid ability) was used to estimate lifetime cognitive change.

RESULTS Measures of cognitive decline were significantly associated with stroke, NT-proBNP, ABI, and cIMT, but not with nonstroke vascular events. The association of stroke with increased estimated lifetime cognitive decline (standardized β, −0.12) and of subclinical markers with actual 4-year decline (standardized β, −0.12, 0.12, and −0.15 for NT-proBNP, ABI, and cIMT, respectively) reached the Bonferroni-adjusted level of statistical significance (P < 0.006). Results altered only slightly on adjustment for vascular risk factors.

CONCLUSIONS Stroke and subclinical markers of cardiac stress and generalized atherosclerosis are associated with cognitive decline in older patients with type 2 diabetes. Further investigation into the potential use of subclinical vascular disease markers in predicting cognitive decline is warranted.

  • Received October 31, 2012.
  • Accepted February 21, 2013.

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  1. Diabetes Care
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