High levels of amyloid-β Protein from S182 (Glu246) familial alzheimer’s cells

Ralph N. Martins, Brian A. Turner, Richard T. Carroll, David Sweeney, K. S. Kim, Henryk M. Wisniewski, John P. Blass, Gary E. Gibson, Sam Gandy*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

53 Citations (Scopus)

Abstract

Most early-onset familial Alzheimer disease is associated with missense mutations in S182, a membrane protein on chromosome 14. We investigated amyloid-β protein (Aβ) precursor (AβPP) metabolism in skin fibroblasts from S182 (Glu246)-affected individuals and unaffected family members. Steady-state AβPP levels were similar among all lines as was the degree of increase in soluble AβPP released upon stimulation of cells with either phorbol ester or serum. Among all lines studied, Ali levels were consistently detectable only in the medium of a single line of S182 (Glu246) cells, consistent with the conclusion that some S182 mutant lines may accumulate Aβ in their conditioned media. Studies of cells from additional individuals and under other conditions will be required to establish this association of elevated Aβ levels with S182 mutations.

Original languageEnglish
Pages (from-to)217-220
Number of pages4
JournalNeuroReport
Volume7
Issue number1
Publication statusPublished - 29 Dec 1995
Externally publishedYes

Keywords

  • Alzheimer’s disease
  • Amyloid-β protein
  • Glu<sup>246</sup>
  • Precursor
  • S182

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