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Amyloid burden correlates with cognitive decline in A lzheimer's disease presenting with aphasia
Author(s) -
Jung Y.,
Whitwell J. L.,
Duffy J. R.,
Strand E. A.,
Machulda M. M.,
Senjem M. L.,
Lowe V.,
Jack C. R.,
Josephs K. A.
Publication year - 2014
Publication title -
european journal of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 124
eISSN - 1468-1331
pISSN - 1351-5101
DOI - 10.1111/ene.12331
Subject(s) - aphasia , pittsburgh compound b , medicine , cognition , episodic memory , audiology , cognitive decline , dementia , alzheimer's disease , amyloid (mycology) , disease , psychology , neuroscience , pathology , psychiatry
Background and purpose A subset of patients with A lzheimer'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. Methods The relationship between cortical β‐amyloid burden on [ 11 C ] P ittsburgh compound B ( P i B ) positron emission tomography ( PET ) and performance on the M ontreal C ognitive A ssessment ( M o CA ), the W echsler M emory S cale − T hird E dition ( WMS ‐III), the B oston N aming T est ( BNT ) and the W estern A phasia B attery ( WAB ) was assessed using regression and correlation analyses in subjects presenting with aphasia who showed β‐amyloid deposition on P i B PET . Results The global P i B ratio was inversely correlated with M o CA ( P = 0.02) and the WMS ‐III V isual R eproduction ( VR ) subtest ( VR I, P = 0.02; VR II, P = 0.04). However, the correlations between P i B ratio, BNT ( P = 0.13), WAB aphasia quotient ( P = 0.11) and WAB repetition scores ( P = 0.34) were not significant. Conclusion 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.