Blood-borne factors inhibit Alzheimer's β-amyloid fibril formation in vitro

• Published in: Experimental neurology Vol. 202; no. 1; pp. 125 - 132
• Main Authors: Ono, Kenjiro, Noguchi-Shinohara, Moeko, Samuraki, Miharu, Matsumoto, Yasuko, Yanase, Daisuke, Iwasa, Kazuo, Naiki, Hironobu, Yamada, Masahito
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier Inc 01.11.2006; Elsevier
• Subjects: Aged; Aged, 80 and over; Alzheimer Disease - blood; Alzheimer Disease - cerebrospinal fluid; Alzheimer Disease - physiopathology; Alzheimer's disease; Amyloid beta-Peptides - chemistry; Amyloid beta-Peptides - metabolism; Amyloid beta-Peptides - ultrastructure; Biological and medical sciences; Brain Chemistry - physiology; Cerebrospinal Fluid - chemistry; Cerebrospinal Fluid - metabolism; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Electron microscopy; Enzyme-Linked Immunosorbent Assay - methods; Female; Fundamental and applied biological sciences. Psychology; Humans; In Vitro Techniques; Isolated neuron and nerve. Neuroglia; Male; Medical sciences; Microscopy, Electron, Transmission - methods; Middle Aged; Neurology; Peptide Fragments; Plaque, Amyloid - chemistry; Plaque, Amyloid - metabolism; Plaque, Amyloid - ultrastructure; Plasma; Plasma - chemistry; Plasma - metabolism; Retrospective Studies; Spectrometry, Fluorescence - methods; Thioflavin T; Time Factors; Vertebrates: nervous system and sense organs; β-amyloid fibrils; Plasma; Thioflavin T; β-amyloid fibrils; Electron microscopy; Alzheimer's disease; Human; Nervous system diseases; Healthy subject; Alzheimer disease; Cytotoxicity; Cerebrospinal fluid; Cerebral disorder; β Amyloid protein; Central nervous system disease; T-Lymphocyte; Environment; Degenerative disease; Amyloid; Aggregate; Cytotoxic T lymphocyte
• ISSN: 0014-4886; 1090-2430
• DOI: 10.1016/j.expneurol.2006.05.019

Soluble amyloid β-protein (Aβ) does not aggregate to β-amyloid fibrils (fAβ) in the brain of normal humans. We recently found that the cerebrospinal fluid (CSF) from non-Alzheimer's disease (AD) subjects inhibited the formation of fAβ(1–40) and fAβ(1–42) more strongly than that from AD subjects, although the CSF obtained from both groups inhibited the fAβs formation in vitro. Here, we examined the influence of plasma obtained from AD, non-AD and healthy control (CTL) subjects on the formation of fAβ(1–40) and fAβ(1–42) in vitro. Although the plasma obtained from all groups inhibited the formation of fAβ(1–40) and fAβ(1–42), the plasma from non-AD and CTL subjects inhibited the formation of fAβs more strongly than that from AD subjects. These results indicate that the plasma as well as CSF in AD would provide a molecular environment favorable for fAβ formation, suggesting a decrease of specific inhibitory factors and/or increase of specific accelerating factors.