AAD-2004 Attenuates Progressive Neuronal Loss in the Brain of Tg-betaCTF99/B6 Mouse Model of Alzheimer Disease.
- Author:
In Sun BAEK
1
;
Tae Kyung KIM
;
Ji Seon SEO
;
Kang Woo LEE
;
Young Ae LEE
;
Jaeyoung CHO
;
Byoung Joo GWAG
;
Pyung Lim HAN
Author Information
- Publication Type:Original Article
- Keywords: Alzheimer's disease; neuronal loss; neuritic atrophy; neuroprotection; small molecule
- MeSH: Alzheimer Disease; Animals; Aspirin; Atrophy; Brain; Calcium-Binding Protein, Vitamin D-Dependent; Lipid Peroxidation; Mice; Neurodegenerative Diseases; Neurons
- From:Experimental Neurobiology 2013;22(1):31-37
- CountryRepublic of Korea
- Language:English
- 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.
