Alzheimer's Disease Research Today is a free monthly online journal that collates and summarizes the latest research about Alzheimer's Disease, including details on diagnosis, memory loss, heredity, treatment, medication.

Transferrin neutralization of amyloid beta 25-35 cytotoxicity.

Giunta S, Galeazzi R, Valli MB, Corder EH, Galeazzi L

Laboratorio Analisi Chimico-Cliniche, Microbiologiche e Diagnostica Molecolare, Ospedale Geriatrico INRCA (IRCCS), via della Montagnola 81, 60100 Ancona, Italy. s.giunta@incra.it

BACKGROUND: Fibrillar aggregates of amyloid beta 25-35 (Abeta(25-35)) form rapidly in vitro able to lyse human red blood cells (RBCs). Human sera, albumin, and apolipoprotein E (ApoE) each limit fibrillation and cytotoxicity. Potentially, these substances protect neurons from Abeta(1-40/42) aggregates. Transferrin (TF) is investigated in this study. METHODS: The Mattson red blood cells model was employed to determine whether co-incubation of transferrin and Abeta(25-35) prevented lysis. The formation of fibrillar Abeta(25-35) in the presence of transferrin was investigated using Congo red staining and spectrophotometric studies. RESULTS: We found that incubation of 20 muM Abeta(25-35) with physiologic levels of transferrin prevented red blood cells lysis and the formation of macro-aggregates. CONCLUSIONS: These in vitro results suggest that transferrin may limit fibrillar beta amyloid formation in vivo and cytotoxicity.

Published 8 November 2004 in Clin Chim Acta, 350(1): 129-36.
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