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P2–370: An integrated framework for computational neuroanatomy: Comparing cortical thickness against manual tracing of the hippocampus
Author(s) -
Zijdenbos Alex P.,
Lerch Jason P.,
Evans Alan C.,
Schuff Norbert,
Weiner Michael W.
Publication year - 2006
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2006.05.1210
Subject(s) - entorhinal cortex , atrophy , hippocampal formation , hippocampus , neuroimaging , neuroscience , neuroanatomy , brain size , cortex (anatomy) , medicine , magnetic resonance imaging , nuclear medicine , psychology , radiology
immunohistochemistry, and adjacent frozen tissue for A 1-40 and A 1-42 ELISA. Results: In every AD case, 6-CN staining labeled A plaques, but not other amyloid pathology (e.g. NFT, DN, NT). Pretreatment of tissue with formic acid completely abolished 6-CN staining. 6-CN was most readily detected in compact plaques containing A 1-40, but also detected A 1-42 plaques. Diffuse A plaques were lightly labeled with 6-CN. 6-CN-labeled plaque load did not correlate with A 1-40 or A 1-42 ELISA levels assessed separately. However, there was a significant positive correlation of 6-CN plaque load with total insoluble A ELISA levels (r 0.85, p 0.05) and a trend for a positive correlation with total A plaque load determined by quantitative immunohistochemistry. Conclusions: These data suggest that the extent of 6-CN labeling of plaques in AD brains reflects levels of total insoluble A , rather than either A 1-40 or A 1-42 peptides preferentially. Thus, 6-CN labeling (and by inference, PIB retention in vivo) should reflect the extent of abnormal folding of all A peptides into insoluble aggregates, and can prove useful for evaluation of anti-A therapies and facilitation of AD diagnosis.