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Tipping the scales towards routine APOE genotyping
  1. Ross Dunne1,
  2. Elizabeth Coulthard2
  1. 1 Geoffrey Jefferson Brain Research Centre, University of Manchester, Manchester, UK
  2. 2 Bristol Medical School, University of Bristol, Bristol, UK
  1. Correspondence to Dr Elizabeth Coulthard, Bristol Medical School, University of Bristol, Bristol, BS8 1QU, UK; elizabeth.coulthard{at}bristol.ac.uk

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Personalised Alzheimer’s disease prevention and treatment will rely on APOE genotyping but this well-validated predictor is rarely used in routine care

Preventing or delaying dementia due to Alzheimer’s disease (AD) requires personalised risk reduction plans.1 Obesity is a risk factor for dementia, but the ‘obesity paradox’ suggests that higher mid-life Body Mass Index (BMI) is a risk factor for later dementia, whereas higher BMI seems protective in later life. This is partially explained by the long AD prodrome itself causing weight loss,2 but heterogeneity between studies perhaps implies additional mechanisms.

Here, Shinohara et al 3 examine the role of APOE in the ‘obesity paradox’.2 They analyse the comprehensive National Alzheimer’s Coordinating Centre dataset to investigate the role of APOE and obesity in AD risk, building on their previous studies evaluating APOE and diabetes. This study generates testable hypotheses about …

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Footnotes

  • Twitter @sadneurons, @lizcoulthard

  • Correction notice Since first publication, the sentence 'lower BMI seems protective in later life' has been updated to 'higher BMI seems protective in later life'.

  • Contributors Both authors contributed to writing this work.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests EC has received payment from Novartis, Lilly, Eisai, Biogen and UCB for consultancy and/or delivering educational resources.

  • Provenance and peer review Not commissioned; internally peer reviewed.

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