Exp Neurobiol.  2013 Mar;22(1):31-37. 10.5607/en.2013.22.1.31.

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

• Baek IS
• Kim TK
• Seo JS
• Lee KW
• Lee YA
• Cho J
• Gwag BJ
• Han PL

• KMID: 2165439
• DOI: http://doi.org/10.5607/en.2013.22.1.31

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.

Keyword

Alzheimer's disease; neuronal loss; neuritic atrophy; neuroprotection; small molecule

MeSH Terms

Alzheimer Disease
Animals
Aspirin
Atrophy
Brain
Calcium-Binding Protein, Vitamin D-Dependent
Lipid Peroxidation
Mice
Neurodegenerative Diseases
Neurons
Aspirin
Calcium-Binding Protein, Vitamin D-Dependent