Non-fibrillar amyloid-{beta} peptide reduces NMDA-induced neurotoxicity, but not AMPA-induced neurotoxicity

Journal Article · Fri Sep 04 00:00:00 EDT 2009 · Biochemical and Biophysical Research Communications

DOI:https://doi.org/10.1016/J.BBRC.2009.06.130· OSTI ID:22199786

Niidome, Tetsuhiro ^[1]; Goto, Yasuaki; Kato, Masaru; Wang, Pi-Lin ^[1]; Goh, Saori; Tanaka, Naoki ^[2]; Akaike, Akinori ^[3]; Kihara, Takeshi; Sugimoto, Hachiro ^[1]

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1. Department of Neuroscience for Drug Discovery, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto 606-8501 (Japan)
2. Department of Biomolecular Engineering, Kyoto Institute of Technology, Kyoto 606-8585 (Japan)
3. Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto 606-8501 (Japan)

Amyloid-{beta} peptide (A{beta}) is thought to be linked to the pathogenesis of Alzheimer's disease. Recent studies suggest that A{beta} has important physiological roles in addition to its pathological roles. We recently demonstrated that A{beta}42 protects hippocampal neurons from glutamate-induced neurotoxicity, but the relationship between A{beta}42 assemblies and their neuroprotective effects remains largely unknown. In this study, we prepared non-fibrillar and fibrillar A{beta}42 based on the results of the thioflavin T assay, Western blot analysis, and atomic force microscopy, and examined the effects of non-fibrillar and fibrillar A{beta}42 on glutamate-induced neurotoxicity. Non-fibrillar A{beta}42, but not fibrillar A{beta}42, protected hippocampal neurons from glutamate-induced neurotoxicity. Furthermore, non-fibrillar A{beta}42 decreased both neurotoxicity and increases in the intracellular Ca{sup 2+} concentration induced by N-methyl-D-aspartate (NMDA), but not by {alpha}-amino-3-hydrozy-5-methyl-4-isoxazole propionic acid (AMPA). Our results suggest that non-fibrillar A{beta}42 protects hippocampal neurons from glutamate-induced neurotoxicity through regulation of the NMDA receptor.

• OSTI ID: 22199786
• Journal Information: Biochemical and Biophysical Research Communications, Vol. 386, Issue 4; Other Information: Copyright (c) 2009 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
APOPTOSIS
ATOMIC FORCE MICROSCOPY
CALCIUM IONS
CONCENTRATION RATIO
GENE REGULATION
HIPPOCAMPUS
NERVE CELLS
NERVOUS SYSTEM DISEASES
PATHOGENESIS
PEPTIDES
PROPIONIC ACID
RECEPTORS