This study aimed to estimate the magnitude of geographical variation in dementia rates and suggest explanations for this variation. Small-area studies are scarce, and none has adequately investigated the relative contribution of genetic and environmental factors to the distribution of dementia.
We present 2 complementary small-area hierarchical Bayesian disease-mapping studies using the comprehensive Swedish Twin Registry (n = 27,680) and the 1932 Scottish Mental Survey cohort (n = 37,597). The twin study allowed us to examine the effect of unshared environmental factors. The Scottish Mental Survey study allowed us to examine various epochs in the life course—approximately age 11 years and adulthood.
We found a 2- to 3-fold geographical variation in dementia odds in Sweden, after twin random effects—likely to capture genetic and shared environmental variance—were removed. In Scotland, we found no variation in dementia odds in childhood but substantial variation, following a broadly similar pattern to Sweden, by adulthood.
There is geographical variation in dementia rates. Most of this variation is likely to result from unshared environmental factors that have their effect in adolescence or later. Further work is required to confirm these findings and identify any potentially modifiable socioenvironmental risk factors for dementia responsible for this geographical variation in risk. However, if these factors do exist and could be optimized in the whole population, our results suggest that dementia rates could be halved.
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From the aAlzheimer Scotland Dementia Research Centre, University of Edinburgh, Edinburgh, United Kingdom; bScottish Dementia Clinical Research Network, NHS Scotland, Edinburgh, United Kingdom; cCentre for Cognitive Ageing & Cognitive Epidemiology, University of Edinburgh, Edinburgh, United Kingdom; dDivision of Psychiatry, University of Edinburgh, Edinburgh, United Kingdom; eDepartment of Psychology, University of Southern California, Los Angeles, CA; fDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; gGreater Glasgow & Clyde Nursing Homes Medical Practice, NHS Greater Glasgow & Clyde, Glasgow, United Kingdom; hPublic Health and Intelligence, NHS National Services Scotland, Edinburgh, United Kingdom; and iDepartment of Epidemiology and Public Health, UCL, London, United Kingdom.
Submitted 29 June 2014; accepted 18 September 2014; posted 9 January 2015.
Supplemental digital content is available through direct URL citations in the HTML and PDF versions of this article (www.epidem.com). This content is not peer-reviewed or copy-edited; it is the sole responsibility of the author.
Currently employed by the University of Edinburgh and NHS Lothian; from 2009 to 2013, TCR was supported by Alzheimer Scotland. TCR, GDB, IJD, and JMS are members of both the Alzheimer Scotland Dementia Research Centre and the University of Edinburgh Centre for Cognitive Ageing and Cognitive Epidemiology, part of the cross council Lifelong Health and Wellbeing Initiative (G0700704/84698). Funding from the BBSRC, EPSRC, ESRC, and MRC is gratefully acknowledged for the latter. Collection of Swedish dementia data was supported by NIH Grant No. R01 AG08724. All researchers are independent from the funders.
The authors report no conflicts of interest.
Correspondence: Tom Russ, Kennedy Tower, Royal Edinburgh Hospital, Morningside Terrace, Edinburgh EH10 5HF, United Kingdom. E-mail: firstname.lastname@example.org.