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Neurobiol Aging. 2012 May;33(5):1006.e25-36. doi: 10.1016/j.neurobiolaging.2011.10.001. Epub 2011 Nov 1.

Cerebrovascular disease, β-amyloid, and cognition in aging.

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1
Helen Wills Neuroscience Institute, University of California, Berkeley, CA 94720, USA. nlmarchant@gmail.com

Abstract

The present study evaluated cerebrovascular disease (CVD), β-amyloid (Aβ), and cognition in clinically normal elderly adults. Fifty-four participants underwent magnetic resonance imaging (MRI), Pittsburgh compound B (PIB)-positron emission tomography (PET) imaging, and neuropsychological evaluation. High white matter hyperintensity burden and/or presence of infarct defined CVD status (CVD-: n = 27; CVD+: n = 27). PIB-positron emission tomography ratios of Aβ deposition were extracted using Logan plotting (cerebellar reference). Presence of high levels of Aβ in prespecified regions determined PIB status (PIB-: n = 33; PIB+: n = 21). Executive functioning and episodic memory were measured using composite scales. CVD and Aβ, defined as dichotomous or continuous variables, were unrelated to one another. CVD+ participants showed lower executive functioning (p = 0.001) when compared with CVD- individuals. Neither PIB status nor amount of Aβ affected cognition (ps ≥ 0.45), and there was no statistical interaction between CVD and PIB on either cognitive measure. Within this spectrum of normal aging CVD and Aβ aggregation appear to be independent processes with CVD primarily affecting cognition.

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