HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

Plasma amyloid beta-peptide 1-42 and incipient Alzheimer's disease.

Abstract
Mutations in the amyloid precursor protein and presenilin 1 and 2 genes result in elevated plasma levels of the amyloid beta-peptide species terminating at amino acid residue 42 (A beta1-42). In a longitudinal study of unrelated elderly individuals, those who subsequently developed Alzheimer's disease had higher plasma levels of A beta1-42 at entry than did those who remained free of dementia. The results indicate that elevated plasma levels of the released A beta peptide A beta1-42 may be detected several years before the onset of symptoms, supporting that extracellular A beta1-42 plays an important role in the pathogenesis of late-onset Alzheimer's disease.
AuthorsR Mayeux, M X Tang, D M Jacobs, J Manly, K Bell, C Merchant, S A Small, Y Stern, H M Wisniewski, P D Mehta
JournalAnnals of neurology (Ann Neurol) Vol. 46 Issue 3 Pg. 412-6 (Sep 1999) ISSN: 0364-5134 [Print] United States
PMID10482274 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • Amyloid beta-Peptides
  • Peptide Fragments
  • amyloid beta-protein (1-43)
Topics
  • Age of Onset
  • Aged
  • Aged, 80 and over
  • Alzheimer Disease (blood)
  • Amyloid beta-Peptides (blood)
  • Female
  • Humans
  • Male
  • Odds Ratio
  • Peptide Fragments (blood)

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: