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Amyloid‐β associated cortical thinning in clinically normal elderly
Author(s) -
Becker J. Alex,
Hedden Trey,
Carmasin Jeremy,
Maye Jacqueline,
Rentz Dorene M.,
Putcha Deepti,
Fischl Bruce,
Greve Douglas N.,
Marshall Gad A.,
Salloway Stephen,
Marks Donald,
Buckner Randy L.,
Sperling Reisa A.,
Johnson Keith A.
Publication year - 2011
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.22333
Subject(s) - precuneus , pittsburgh compound b , posterior cingulate , magnetic resonance imaging , atrophy , hippocampal formation , alzheimer's disease , neuroimaging , pathology , medicine , hippocampus , psychology , neuroscience , cardiology , cortex (anatomy) , disease , radiology , cognition
Abstract Objective: Both amyloid‐β (Aβ) deposition and brain atrophy are associated with Alzheimer's disease (AD) and the disease process likely begins many years before symptoms appear. We sought to determine whether clinically normal (CN) older individuals with Aβ deposition revealed by positron emission tomography (PET) imaging using Pittsburgh Compound B (PiB) also have evidence of both cortical thickness and hippocampal volume reductions in a pattern similar to that seen in AD. Methods: A total of 119 older individuals (87 CN subjects and 32 patients with mild AD) underwent PiB PET and high‐resolution structural magnetic resonance imaging (MRI). Regression models were used to relate PiB retention to cortical thickness and hippocampal volume. Results: We found that PiB retention in CN subjects was (1) age‐related and (2) associated with cortical thickness reductions, particularly in parietal and posterior cingulate regions extending into the precuneus, in a pattern similar to that observed in mild AD. Hippocampal volume reduction was variably related to Aβ deposition. Interpretation: We conclude that Aβ deposition is associated with a pattern of cortical thickness reduction consistent with AD prior to the development of cognitive impairment. ANN NEUROL 2010;