articleTop 1% cited

Secreted amyloid β–protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease

Nature Medicine · 1996 · Vol. 2(8) · pp. 864–870

Donalyn Scheuner✉(Case Western Reserve University)Christopher B. Eckman(Case Western Reserve University)M. Jensen(Karolinska Institutet)X.H. Song(Case Western Reserve University)Martin Citron(Brigham and Women's Hospital)Nobuhiro Suzuki(Takeda (Japan))Thomas D. Bird(University of Washington)John Hardy(University of South Florida)M. Hutton(University of South Florida)Walter A. Kukull(University of Washington)Eric B. Larson(University of Washington)Ephrat Levy‐Lahad(University of Puget Sound)Matti Viitanen(Karolinska Institutet)Elaine R. Peskind(Geriatric Research Education and Clinical Center)Parvoneh Poorkaj(University of Puget Sound)Gerald D. Schellenberg(University of Puget Sound)Rudolph E. Tanzi(Massachusetts General Hospital)Wilma Wasco(Harvard University)Lars Lannfelt(Karolinska Institutet)Dennis J. Selkoe(Brigham and Women's Hospital)Samuel Younkin(Mayo Clinic in Florida)

View via DOI Publisher page

Alzheimer's disease research and treatments Dementia and Cognitive Impairment Research Amyloidosis: Diagnosis, Treatment, OutcomesPresenilinSenile plaquesExtracellularAlzheimer's diseaseBETA (programming language)Amyloid (mycology)Amyloid betaAmyloid precursor proteinIn vivoMutation

MeSH terms

Alzheimer DiseaseCells, CulturedFemaleFibroblastsHumansMaleMembrane ProteinsMutationPeptide FragmentsAmyloid beta-PeptidesAmyloid beta-Protein PrecursorCulture Media, ConditionedPresenilin-1Presenilin-2

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The Amyloid Hypothesis of Alzheimer's Disease: Progress and Problems on the Road to Therapeutics