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Letter
Cerebrovascular risk factors in early-onset dementia
  1. Emily R Atkins1,
  2. Max K Bulsara2,
  3. Peter K Panegyres1
  1. 1Neurodegenerative Disorders Research, Subiaco, Western Australia, Australia
  2. 2Institute for Health and Rehabilitation Research, University of Notre Dame, Fremantle, Western Australia, Australia
  1. Correspondence to Dr P K Panegyres, Neurodegenerative Disorders Research Pty Ltd, 185 York Street, Subiaco, Western Australia 6008, Australia; publications{at}panegyres.com.au

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Introduction

Alzheimer's disease (AD) is the leading cause of dementia. Research into environmental factors is currently focused on cerebrovascular risk factors.1 Treatment of vascular risk factors has been associated with slower cognitive decline and reduced risk of AD in older populations.2 Genetics are important in rare genetically determined autosomal dominant familial patients with AD or frontotemporal dementia (FTD).3 Apolipoprotein E (APOE) is a risk factor for familial late-onset sporadic AD, but its role as a risk factor in younger populations is unclear. The role of APOE as a risk factor for FTD is controversial.

Early-onset dementia is dementia that develops in individuals prior to the age of 65 years, and some studies suggest it is associated with a higher mortality. AD and FTD are the most common causes of dementia in this population.4 The onset of FTD may be characterised by behavioural change and speech disturbance, whereas AD is usually characterised by defective episodic memory. It is hypothesised that cerebrovascular risk factors, such as hypertension and diabetes, are associated with the development of early-onset Alzheimer's disease (EOAD) but not early-onset FTD. We set out to investigate this hypothesis in a cohort of early-onset AD and FTD patients.

The participants in this study are a cohort of 123 consecutive prospectively analysed early-onset dementia patients with clinically …

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Footnotes

  • Funding York Neuroscience Discovery.

  • Competing interests None.

  • Ethics approval Ethics approval was provided by the governing body of Neurodegenerative Disorders Research.

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