Cerebrospinal fluid of Alzheimer patients promotes beta-amyloid fibril formation in vitro.
Cerebral deposition of amyloid beta-peptide (Abeta) is an invariant feature of Alzheimer's disease (AD). To answer why soluble Abeta does not aggregate to beta-amyloid fibrils (fAbeta) in the brain of normal humans, we examined the influence of cerebrospinal fluid (CSF) obtained from AD and non-AD patients on the formation of fAbeta(1-40) and fAbeta(1-42) in vitro, by using fluorescence spectroscopy with thioflavin T and electron microscopy. Although the CSF obtained from both groups inhibited the formation of both fAbeta(1-40) and fAbeta(1-42), the CSF from non-AD patients inhibited the formation of fAbetas more strongly than that from AD patients. In AD patients, the final levels of fAbetas formation showed a significant negative correlation with the Abeta(1-42) level in CSF. These results indicate that fAbeta deposition in the brain of AD may be enhanced by the decrease of specific inhibitory factors and/or by the increase of specific accelerating factors in CSF.[1]References
- Cerebrospinal fluid of Alzheimer patients promotes beta-amyloid fibril formation in vitro. Ono, K., Noguchi, M., Matsumoto, Y., Yanase, D., Iwasa, K., Naiki, H., Yamada, M. Neurobiol. Dis. (2005) [Pubmed]
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