title: Regional β-amyloid burden does not correlate with cognitive or language deficits in Alzheimer's disease presenting as aphasia.
abstract: OBJECTIVE
  A subset of patients with Alzheimer's disease (AD) present with early and prominent language impairment (aphasic AD). Our previous study demonstrated an association between global β-amyloid burden measured on [(11)C] Pittsburgh compound B (PiB) positron emission tomography and general cognitive impairment, but not with aphasia, in such subjects. As a follow-up, whether there is any association between regional β-amyloid burden, atrophy on magnetic resonance imaging (MRI) and global cognitive impairment, aphasia or other cognitive and functional impairment in aphasic AD is assessed.
  
  
  METHODS
  Forty-four aphasic AD subjects who underwent PiB scanning and volumetric MRI and were determined to be positive for β-amyloid deposition were analyzed. All had completed detailed neurological, neuropsychological and language batteries. Spearman's rank-order correlation was utilized to assess for associations.
  
  
  RESULTS
  Greater visuospatial impairment was associated with increased β-amyloid burden in the primary visual cortex (P = 0.001). Although there were many trends for associations between neurocognitive and language deficits and regional β-amyloid burden, there were no strong associations that survived correction for multiple comparisons. However, neurocognitive and language impairment in these subjects strongly correlated with the degree of left lateral temporal and inferior parietal atrophy (P < 0.004).
  
  
  CONCLUSIONS
  The findings from this study suggest a close relation between the severity of regional atrophy and cognitive and language impairment, but argue against a strong association between regional β-amyloid burden and such deficits in aphasic AD subjects. Hence, other pathological factors may be driving the previously identified association between global β-amyloid deposition and general cognitive impairment in aphasic AD.
authors.affiliation: Department of Neurology, Mayo Clinic, Rochester, MN, USA.
authors.forename: Y
authors.initials: Y
authors.lastname: Jung
authors.affiliation: Department of Radiology, Mayo Clinic, Rochester, MN, USA.
authors.forename: J L
authors.initials: JL
authors.lastname: Whitwell
authors.affiliation: Department of Neurology, Mayo Clinic, Rochester, MN, USA.
authors.forename: J R
authors.initials: JR
authors.lastname: Duffy
authors.affiliation: Department of Neurology, Mayo Clinic, Rochester, MN, USA.
authors.forename: E A
authors.initials: EA
authors.lastname: Strand
authors.affiliation: Department of Psychiatry and Psychology (Neuropsychology), Mayo Clinic, Rochester, MN, USA.
authors.forename: M M
authors.initials: MM
authors.lastname: Machulda
authors.affiliation: Department of Information Technology, Mayo Clinic, Rochester, MN, USA.
authors.forename: M L
authors.initials: ML
authors.lastname: Senjem
authors.affiliation: Department of Radiology, Mayo Clinic, Rochester, MN, USA.
authors.forename: C R
authors.initials: CR
authors.lastname: Jack
authors.affiliation: Department of Nuclear Medicine, Mayo Clinic, Rochester, MN, USA.
authors.forename: V J
authors.initials: VJ
authors.lastname: Lowe
authors.affiliation: Department of Neurology, Mayo Clinic, Rochester, MN, USA.
authors.forename: K A
authors.initials: KA
authors.lastname: Josephs
mesh_terms: D000368:Aged; D000544:Alzheimer Disease / Q000150:complications / Q000378:metabolism / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D001037:Aphasia / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D003072:Cognition Disorders / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged
chemical_list: D016229:Amyloid beta-Peptides
keywords: PET; PiB; aphasia; beta-amyloid; dementia