Low cerebrospinal-fluid concentrations of soluble amyloid β-protein precursor in hereditary Alzheimer's disease

Martin Farlow, Bernardino Ghetti, Merrill Benson, W. E. van Nostrand, J. S. Farrow, S. L. Wagner

Research output: Contribution to journalArticle

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Abstract

In Alzheimer's disease, deposits of amyloid β-protein are apparently derived from intracellular processing of a large precursor protein. We have measured concentrations of this precursor in cerebrospinal fluid (CSF) from six members of a family affected by presenile Alzheimer's disease associated with a point mutation of the precursor gene. One gene carrier with clinical signs of the disorder had low CSF concentrations of the precursor, similar to those of three patients with sporadic Alzheimer's disease subsequently confirmed at necropsy. Two symptom-free gene carriers had CSF precursor concentrations similar to those of non-demented controls, though the value was lower in one, who had deficits revealed on neuropsychological testing, than in the other. These findings suggest that low concentrations of soluble amyloid precursor proteins in the CSF reflect the process that results in amyloid plaque formation and vascular deposition in Alzheimer's disease.

Original languageEnglish (US)
Pages (from-to)453-454
Number of pages2
JournalThe Lancet
Volume340
Issue number8817
DOIs
StatePublished - Aug 22 1992

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Inborn Genetic Diseases
Amyloid beta-Protein Precursor
Cerebrospinal Fluid
Alzheimer Disease
Genes
Amyloidogenic Proteins
Protein Precursors
Amyloid Plaques
Point Mutation
Blood Vessels

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Low cerebrospinal-fluid concentrations of soluble amyloid β-protein precursor in hereditary Alzheimer's disease. / Farlow, Martin; Ghetti, Bernardino; Benson, Merrill; van Nostrand, W. E.; Farrow, J. S.; Wagner, S. L.

In: The Lancet, Vol. 340, No. 8817, 22.08.1992, p. 453-454.

Research output: Contribution to journalArticle

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