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Neurobiol Aging. 2015 Aug;36(8):2340-7. doi: 10.1016/j.neurobiolaging.2015.04.011. Epub 2015 Apr 25.

Cerebrospinal fluid biomarkers and cerebral atrophy in distinct clinical variants of probable Alzheimer's disease.

Author information

1
Department of Neurology, Memory and Aging Center, University of California San Francisco, San Francisco, CA, USA; Helen Wills Neuroscience Institute, University of California Berkeley, Berkeley, CA, USA; Department of Neurology & Alzheimer Center, VU University Medical Center, Amsterdam, The Netherlands; Department of Radiology & Nuclear Medicine, VU University Medical Center, Amsterdam, The Netherlands. Electronic address: r.ossenkoppele@vumc.nl.
2
Department of Veterans Affairs Medical Center, Center for Imaging of Neurodegenerative diseases, San Francisco, CA, USA; Institute of Neuroscience and Physiology, Laboratory of Clinical Neurochemistry, University of Gothenburg, Gothenburg, Sweden.
3
Department of Clinical Chemistry, VU University Medical Center, Amsterdam, The Netherlands.
4
Department of Radiology & Nuclear Medicine, VU University Medical Center, Amsterdam, The Netherlands.
5
Department of Neurology & Alzheimer Center, VU University Medical Center, Amsterdam, The Netherlands.
6
Department of Neurology & Alzheimer Center, VU University Medical Center, Amsterdam, The Netherlands; Department of Epidemiology and Biostatistics, VU University Medical Center, Amsterdam, The Netherlands.
7
Department of Neurology, Memory and Aging Center, University of California San Francisco, San Francisco, CA, USA; Helen Wills Neuroscience Institute, University of California Berkeley, Berkeley, CA, USA.

Abstract

Different clinical variants of probable Alzheimer's disease (AD) share underlying plaques and tangles but show distinct atrophy patterns. We included 52 posterior cortical atrophy, 29 logopenic variant primary progressive aphasia, 53 early-onset and 42 late-onset AD patients, selected for abnormal cerebrospinal fluid (CSF)-amyloid-beta42, with CSF and magnetic resonance imaging data available. Bootstrapping revealed no differences in the prevalence of abnormal CSF total-tau and phosphorylated-tau between probable AD variants (range total-tau: 84.9%-92.3%, phosphorylated-tau: 79.2%-93.1%, p > 0.05). Voxelwise linear regressions showed various relationships between lower CSF-Aβ42 and syndrome-specific atrophy, involving precuneus, posterior cingulate, and medial temporal lobe in early-onset AD, occipital cortex and middle temporal gyrus in posterior cortical atrophy; anterior cingulate, insular cortex and precentral gyrus (left > right) in logopenic variant primary progressive aphasia; and medial temporal lobe, thalamus, and temporal pole in late-onset AD (all at p < 0.001 uncorrected). In contrast, CSF-tau was not related to gray matter atrophy in any group. Our findings suggest that lower CSF-amyloid-beta42 - and not increased total-tau and phosphorylated-tau - relates to reduced gray matter volumes, mostly in regions that are typically atrophied in distinct clinical variants of probable AD.

KEYWORDS:

Alzheimer's disease; Amyloid; Atrophy; Cerebrospinal fluid; Magnetic resonance imaging; Tau

[Indexed for MEDLINE]
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