SNM Annual Meeting Abstracts
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     



J Nucl Med. 2008; 49 (Supplement 1):215P
This Article
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Google Scholar
Right arrow Articles by Becker, J. A.
Right arrow Articles by Johnson, K.
PubMed
Right arrow Articles by Becker, J. A.
Right arrow Articles by Johnson, K.

Neurosciences: Neurology

Neurology Posters

Amyloid deposition and cortical thickness in aging and Alzheimer’s disease

J. Alex Becker1, Jeremy Carmasin1, Bruce Fischl1, Doug Greve1, Amy DeLuca1, Pete LaViolette1, Alan Fischman1, Dorene Rentz2, Reisa Sperling2 and Keith Johnson1

1 Massachusetts General Hospital, Boston, Massachusetts; 2 Brigham and Women's Hospital, Boston, Massachusetts

926

Objectives: A clear relationship between amyloid plaque burden and neuronal loss or regional atrophy has not been demonstrated in autopsy studies. To examine this relationship, we tested the hypothesis that regional fibrillar amyloid burden, as measured by 11C Pittsburgh Compound B (PiB), is associated with reduced cortical thickness.

Methods: C11-PIB PET data and 3T MRI-MPRAGE were acquired in 48 subjects who were CDR0, CDR0.5 or CDR1 and processed with Freesurfer.

Results: Amyloid deposition and cortical thinning were significantly greater in the CDR0.5/1 group compared to the CDR0 group in superior temporal, lateral parietal, precuneus, posterior cingulate, and medial frontal areas. When PiB and thickness data were regressed locally, i.e., at each vertex, greater amyloid was significantly related to cortical thinning in posterior cingulate/precuneus and temporal areas (p<0.001).

Conclusions: Amyloid deposition is associated locally with cortical thinning, predominantly in posterior cingulate/precuneus and temporal cortices, areas where both dysfunction and atrophy are commonly observed in AD. Our findings suggest that damage to neuronal populations, whether due to soluble or insoluble amyloid or other factors, occurs at sites of amyloid deposition.

Research Support: NIH/NIA, Massachusetts ADRC, Alzheimer Association





This Article
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Google Scholar
Right arrow Articles by Becker, J. A.
Right arrow Articles by Johnson, K.
PubMed
Right arrow Articles by Becker, J. A.
Right arrow Articles by Johnson, K.