Open Access Research article

Population studies of sporadic cerebral amyloid angiopathy and dementia: a systematic review

Hannah AD Keage1*, Roxanna O Carare2, Robert P Friedland3, Paul G Ince4, Seth Love5, James A Nicoll2, Stephen B Wharton4, Roy O Weller2 and Carol Brayne1

Author Affiliations

1 Department of Public Health and Primary Care, University of Cambridge, Cambridge, CB2 0SR, UK

2 Division of Clinical Neurosciences, School of Medicine, University of Southampton, Southampton, SO16 6YD, UK

3 School of Medicine, Case Western Reserve University, Cleveland, Ohio, 44106, USA

4 Academic Unit of Pathology, University of Sheffield, Sheffield, S10 2RX, UK

5 Bristol Neuroscience, University of Bristol, Bristol, BS8 1TD, UK

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BMC Neurology 2009, 9:3  doi:10.1186/1471-2377-9-3

Published: 13 January 2009

Abstract

Background

Deposition of amyloid-β (Aβ) in vessel walls of the brain as cerebral amyloid angiopathy (CAA) could be a major factor in the pathogenesis of dementia. Here we investigate the relationship between dementia and the prevalence of CAA in older populations. We searched the literature for prospective population-based epidemiological clinicopathological studies, free of the biases of other sampling techniques, which were used as a comparison.

Methods

To identify population-based studies assessing CAA and dementia, a previous systematic review of population-based clinicopathological studies of ageing and dementia was employed. To identify selected-sample studies, PsychInfo (1806–April Week 3 2008), OVID MEDLINE (1950–April Week 2 2008) and Pubmed (searched 21 April 2008) databases were searched using the term "amyloid angiopathy". These databases were also employed to search for any population-based studies not included in the previous systematic review. Studies were included if they reported the prevalence of CAA relative to a dementia classification (clinical or neuropathological).

Results

Four population-based studies were identified. They showed that on average 55–59% of those with dementia displayed CAA (of any severity) compared to 28–38% of the non-demented. 37–43% of the demented displayed severe CAA in contrast to 7–24% of the non-demented. There was no overlap in the range of these averages and they were less variable and lower than those reported in 38 selected sample studies (demented v non-demented: 32–100 v 0–77% regardless of severity; 0–50 v 0–11% for severe only).

Conclusion

CAA prevalence in populations is consistently higher in the demented as compared to the non-demented. This supports a significant role for CAA in the pathogenesis of dementia.