Disease Modifying Therapies for Alzheimer's Disease Targeting Aβ Oligomers: Implications for Therapeutic Mechanisms. (25th August 2013)

• Record Type: Journal Article
• Authors: Matsubara, Etsuro; Takamura, Ayumi; Okamoto, Yasuhide; Oono, Hideto; Nakata, Takashi; Wakasaya, Yasuhito; Kawarabayashi, Takeshi; Shoji, Mikio
• Other Names: Kehoe Patrick Academic Editor.
• Is Part Of: BioMed research international. Volume 2013(2013)
• Publication Date: 2013-08-25
• Subjects: Medicine -- Periodicals; Biology -- Periodicals; Biotechnology -- Periodicals; Life sciences -- Periodicals; 610.5
• DOI: 10.1155/2013/984041
• Languages: English
• ISSNs: 2314-6133

Abstract

Abstract : Several lines of evidence indicate that amyloid β (A β ), particularly A β oligomers (A β Os), plays a causative role in Alzheimer's disease. However, the mechanisms underlying the action of an anti-A β O antibody to clarify the toxic action of A β Os remain elusive. Here, we showed that the anti-A β O antibody (monoclonal 72D9) can modify the A β aggregation pathway. We also found that 72D9 directly sequesters both extracellular and intraneuronal A β Os in a nontoxic state. Thus, therapeutic intervention targeting A β Os is a promising strategy for neuronal protection in Alzheimer's disease.