alexa Differential Appearance of Serum Aβ43 and Aβ4
ISSN: 2161-1025

Translational Medicine
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Research Article

Differential Appearance of Serum Aβ43 and Aβ42 in the Patients with Alzheimer¬ís Disease

Kun Zou1*, Shuyu Liu1, Junjun Liu1, Chiaki Tanabe1, Tomoji Maeda1, Yasuo Terayama2, Satoshi Takahashi2 and Hiroto Komano1

1Department of Neuroscience, School of Pharmacy, Iwate Medical University, Yahaba, Iwate 028-3694, Japan

2Department of Internal Medicine, Division of Neurology and Gerontology, School of Medicine, Iwate Medical University, Morioka, Iwate 020-8505, Japan

*Corresponding Author:
Kun Zou
Department of Neuroscience, School of Pharmacy
Iwate Medical University, 2-1-1 Nishitokuta
Yahaba, Iwate 028-3694, Japan
Tel: 81-19-698-1820
Fax: 81-19-698-1864
E-mail: [email protected]

Received Date: November 01, 2011; Accepted Date: December 02, 2011; Published Date: December 04, 2011

Citation: Zou K, Liu S, Liu J, Tanabe C, Maeda T, et al. (2011) Differential Appearance of Serum Aβ43 and Aβ42 in the Patients with Alzheimer’s Disease. Translational Medic 1:103. doi:10.4172/2161-1025.1000103

Copyright: © 2011 Zou K, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



A longer amyloid-β protein (Aβ), Aβ43, deposits in amyloid plaques more frequently than Aβ40 in both sporadic and familial Alzheimer’s disease (AD) brains, which shares a similar feature of Aβ42 [1,2]. A recent study reported that Aβ43 is more amyloidogenic and neurotoxic than Aβ42 in vitro and is abundant in the brain of patients with Alzheimer’s disease [3]. These studies indicate that Aβ43 could be another key molecule for AD etiology other than Aβ42. Reduced Aβ42 levels and Aβ42/Aβ40 ratio in plasma and cerebrospinal fluid (CSF) were related with cognitive decline and AD [4,5]. However, Aβ43 levels in biological fluid and their relationship with Aβ42 and Aβ40 in living patients with AD remain unclear. Here we examined Aβ43, Aβ42 and Aβ40 levels in the serum of patients with AD and normal controls, and we found differential appearance of serum Aβ43 and Aβ42 in AD patients.

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