Articles

  • the Korean Society for Brain and Neural Sciences

Article

Original Article

Exp Neurobiol 2013; 22(1): 31-37

Published online March 30, 2013

https://doi.org/10.5607/en.2013.22.1.31

© The Korean Society for Brain and Neural Sciences

AAD-2004 Attenuates Progressive Neuronal Loss in the Brain of Tg-betaCTF99/B6 Mouse Model of Alzheimer Disease

In-Sun Baek1, Tae-Kyung Kim2,3, Ji-Seon Seo2, Kang-Woo Lee1,3, Young Ae Lee4, Jaeyoung Cho4, Byoung Joo Gwag4,5 and Pyung-Lim Han1,2,3*

Departments of 1Chemistry and Nano Science, 2Brain and Cognitive Sciences, and 3Brain Disease Research Institute, Ewha Womans University, Seoul 120-750, 4GNT Pharma Co. Ltd., Yongin 446-901, 5Department of Neuroscience, Ajou University School of Medicine, Suwon 443-749, Korea

Correspondence to: *To whom correspondence should be addressed.
TEL: 82-2-3277-4130, FAX: 82-2-3277-3419
e-mail: plhan@ewha.ac.kr

Abstract

Alzheimer's disease (AD) is a neurodegenerative disease that proceeds with the age-dependent neuronal loss, an irreversible event which causes severe cognitive and psychiatric devastations. In the present study, we investigated whether the compound, AAD-2004 [2-hydroxy-5-[2-(4-trifluoromethylphenyl)-ethylaminobenzoic acid] which has anti-oxidant and anti-inflammatory properties, is beneficial for the brain of Tg-betaCTF99/B6 mice, a murine AD model that was recently developed to display age-dependent neuronal loss and neuritic atrophy in the brain. Administration of AAD-2004 in Tg-betaCTF99/B6 mice from 10 months to 18 months of age completely repressed the accumulation of lipid peroxidation in the brain. AAD-2004 markedly suppressed neuronal loss and neuritic atrophy, and partially reversed depleted expression of calbindin in the brain of Tg-beta-CTF99/B6. These results suggest that AAD-2004 affords neurodegeneration in the brain of AD mouse model.

Keywords: Alzheimer's disease, neuronal loss, neuritic atrophy, neuroprotection, small molecule