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(American Journal of Pathology. 1999;155:853-862.)
© 1999 American Society for Investigative Pathology

Regular Articles

Soluble Amyloid ß Peptide Concentration as a Predictor of Synaptic Change in Alzheimer's Disease

Lih-Fen Lue*, Yu-Min Kuo*, Alex E. Roher*, Libuse Brachova*, Yong Shen*, Lucia Sue*, Thomas Beach*, Janice H. Kurth{dagger}, Russel E. Rydel{ddagger} and Joseph Rogers*

From the Roberts Center,*
Haldeman Laboratory, and Civin Laboratory for Alzheimer's Research, Sun Health Research Institute, Sun City, Arizona; Phenogenex,{dagger}
La Jolla, California; and Elan Pharmaceuticals,{ddagger}
South San Francisco, California

We have characterized amyloid ß peptide (Aß) concentration, Aß deposition, paired helical filament formation, cerebrovascular amyloid angiopathy, apolipoprotein E (ApoE) allotype, and synaptophysin concentration in entorhinal cortex and superior frontal gyrus of normal elderly control (ND) patients, Alzheimer's disease (AD) patients, and high pathology control (HPC) patients who meet pathological criteria for AD but show no synapse loss or overt antemortem symptoms of dementia. The measures of Aß deposition, Aß-immunoreactive plaques with and without cores, thioflavin histofluorescent plaques, and concentrations of insoluble Aß, failed to distinguish HPC from AD patients and were poor correlates of synaptic change. By contrast, concentrations of soluble Aß clearly distinguished HPC from AD patients and were a strong inverse correlate of synapse loss. Further investigation revealed that Aß40, whether in soluble or insoluble form, was a particularly useful measure for classifying ND, HPC, and AD patients compared with Aß42. Aß40 is known to be elevated in cerebrovascular amyloid deposits, and Aß40 (but not Aß42) levels, cerebrovascular amyloid angiopathy, and ApoE4 allele frequency were all highly correlated with each other. Although paired helical filaments in the form of neurofibrillary tangles or a penumbra of neurites surrounding amyloid cores also distinguished HPC from AD patients, they were less robust predictors of synapse change compared with soluble Aß, particularly soluble Aß40. Previous experiments attempting to relate Aß deposition to the neurodegeneration that underlies AD dementia may have failed because they assayed the classical, visible forms of the molecule, insoluble neuropil plaques, rather than the soluble, unseen forms of the molecule.




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C. V. Zerbinatti, D. F. Wozniak, J. Cirrito, J. A. Cam, H. Osaka, K. R. Bales, M. Zhuo, S. M. Paul, D. M. Holtzman, and G. Bu
Increased soluble amyloid-{beta} peptide and memory deficits in amyloid model mice overexpressing the low-density lipoprotein receptor-related protein
PNAS, January 27, 2004; 101(4): 1075 - 1080.
[Abstract] [Full Text] [PDF]