Alzheimer's disease and hereditary cerebral hemorrhage with amyloidosis–dutch type share a decrease in cerebrospinal fluid levels of amyloid β-protein precursor
✍ Scribed by Dr. William E. van Nostrand; Steven L. Wagner; Joost Haan; Egbert Bakker; Raymund A. C. Roos
- Publisher
- John Wiley and Sons
- Year
- 1992
- Tongue
- English
- Weight
- 419 KB
- Volume
- 32
- Category
- Article
- ISSN
- 0364-5134
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✦ Synopsis
Abstract
The amyloid β‐protein is a 39‐42 amino acid peptide that is deposited in senile plaques and in cerebral vessel walls in individuals with Alzheimer's disease, Down's syndrome, hereditary cerebral hemorrhage with amyloidosis–Dutch type (HCHW A‐D), and, to a much lesser extent, normal aging. It is derived from abnormal proteolytic processing of its parent protein, the amyloid β ‐protein precursor. Here we show that individuals with the HCHWA‐D mutation and clinically manifesting the disease have markedly decreased cerebrospinal fluid levels of soluble amyloid β‐protein precursor (0.7 ± 0.4 μg/ml) compared with age‐matched normal subjects (3.0 ± 0.2 μg/ml) as determined by quantitative immunoblotting and enzyme‐linked immunosorbent assays. Similarly, age‐matched patients diagnosed with probable Alzheimer's disease also have decreased cerebrospinal fluid levels of soluble amyloid β‐protein precursor (1.0 ± 0.3 μg/ml). These parallel findings suggest a common biochemical marker for these two diseases and further establish the pathogenic relatedness of HCHWA‐D and Alzheimer's disease.