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April 1, 1992Proceedings of the National Academy of SciencesOpen Access

Decreased levels of soluble amyloid beta-protein precursor in cerebrospinal fluid of live Alzheimer disease patients.

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Authors

WNWilliam E. Van NostrandUniversity of Rhode IslandSWSteven L. WagnerUniversity of California, San DiegoWSWilliam R. ShankleThe Memory Clinic

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Cite This Study

Nostrand et al. (1992) studied this question.

synapsesocial.com/papers/6a1be1545b8f4ede65a93052https://doi.org/10.1073/pnas.89.7.2551
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Also Consider

Synapse has enriched 3 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Evidence that β-Amyloid Protein in Alzheimer's Disease Is Not Derived by Normal Processing1990 · 896 citations
  2. 2The Alzheimer amyloid precursor protein. Identification of a stable intermediate in the biosynthetic/degradative pathway.1990 · 282 citations
  3. 3Amyloid fibrils in hereditary cerebral hemorrhage with amyloidosis of Icelandic type is a variant of gamma-trace basic protein (cystatin C).1986 · 335 citations