Amyloid burden correlates with cognitive decline in Alzheimer's disease presenting with aphasia
Version of Record online: 16 DEC 2013
© 2013 The Author(s) European Journal of Neurology © 2013 EAN
European Journal of Neurology
Volume 21, Issue 7, pages 1040–1043, July 2014
How to Cite
Jung, Y., Whitwell, J. L., Duffy, J. R., Strand, E. A., Machulda, M. M., Senjem, M. L., Lowe, V., Jack, C. R. and Josephs, K. A. (2014), Amyloid burden correlates with cognitive decline in Alzheimer's disease presenting with aphasia. European Journal of Neurology, 21: 1040–1043. doi: 10.1111/ene.12331
- Issue online: 12 JUN 2014
- Version of Record online: 16 DEC 2013
- Manuscript Accepted: 18 NOV 2013
- Manuscript Received: 2 AUG 2013
- NIH. Grant Number: R01-DC010367
- PET ;
Background and purpose
A subset of patients with Alzheimer's disease (AD) present with early and prominent language deficits. It is unclear whether the burden of underlying β-amyloid pathology is associated with language or general cognitive impairment in these subjects.
The relationship between cortical β-amyloid burden on [11C]Pittsburgh compound B (PiB) positron emission tomography (PET) and performance on the Montreal Cognitive Assessment (MoCA), the Wechsler Memory Scale − Third Edition (WMS-III), the Boston Naming Test (BNT) and the Western Aphasia Battery (WAB) was assessed using regression and correlation analyses in subjects presenting with aphasia who showed β-amyloid deposition on PiB PET.
The global PiB ratio was inversely correlated with MoCA (P = 0.02) and the WMS-III Visual Reproduction (VR) subtest (VR I, P = 0.02; VR II, P = 0.04). However, the correlations between PiB ratio, BNT (P = 0.13), WAB aphasia quotient (P = 0.11) and WAB repetition scores (P = 0.34) were not significant.
This study demonstrates that an increased cortical β-amyloid burden is associated with cognitive impairment, but not language deficits, in AD subjects presenting with aphasia. The results suggest that β-amyloid deposition could be partly contributing to impaired cognition in such patients whilst language dysfunction may be more influenced by other pathological mechanisms, perhaps downstream pathways of β-amyloid deposition.