Assessment of Amyloid β Protein in Cerebrospinal Fluid as an Aid in the Diagnosis of Alzheimer's Disease
Article first published online: 19 NOV 2002
Journal of Neurochemistry
Volume 66, Issue 1, pages 259–265, January 1996
How to Cite
Southwick, P. C., Yamagata, S. K., Echols, C. L., Higson, G. J., Neynaber, S. A., Parson, R. E. and Munroe, W. A. (1996), Assessment of Amyloid β Protein in Cerebrospinal Fluid as an Aid in the Diagnosis of Alzheimer's Disease. Journal of Neurochemistry, 66: 259–265. doi: 10.1046/j.1471-4159.1996.66010259.x
- Issue published online: 19 NOV 2002
- Article first published online: 19 NOV 2002
- Received February 21, 1995; revised manuscript received June 27, 1995; accepted July 14, 1995.
- Alzheimer's disease;
- Amyloid β protein;
Abstract: The principal constituent of amyloid plaques found in the brains of individuals with Alzheimer's disease (AD) is a 39–42-amino-acid protein, amyloid β protein (Aβ). This study examined whether the measurement of Aβ levels in CSF has diagnostic value. There were 108 subjects enrolled in this prospective study: AD (n = 39), non-AD controls (dementing diseases/syndromes; n = 20), and other (n = 49). CSF was obtained by lumbar puncture, and Aβ concentrations were determined using a dual monoclonal antibody immunoradiometric sandwich assay. The mean Aβ value for the AD group (15.9 ± 6.8 ng/ml) was not significantly different from that for the non-AD control group (13.0 ± 7.1 ng/ml; p = 0.07), and substantial overlap in results were observed. Aβ values did not correlate with age (r = −0.05, p = 0.59), severity of cognitive impairment (r = 0.22, p = 0.21), or duration of AD symptoms (r = 0.14, p = 0.45). These findings are in conflict with other reports in the literature; discrepant results could be due to the instability of Aβ in CSF. Aβ immunoreactivity decays rapidly under certain conditions, particularly multiple freeze/thaw cycles. Use of a stabilizing sample treatment buffer at the time of lumbar puncture allows storage of CSF without loss of Aβ reactivity. In conclusion, the total CSF Aβ level is not a useful marker for current diagnosis of AD.