HY2109 ameliorates brain inflammation and improves memory impairments in Alzheimer’s disease mice model

International Congress on Neuroimmunology and Therapeutics

DoubleTree by Hilton Hotel San Francisco Airport, San Francisco, CA, USA

Jung Ah Cho

Posters-Accepted Abstracts: J Neurol Disord

Abstract :

Alzheimerâ??s disease (AD) is the most common cause of dementia. Neuro-inflammation and neuronal apoptosis due to progressive deposition of amyloid beta (Aβ) in the brain incur defects in cognition and memory. In this study, we showed that HY2109 could improve memory deficits in AD mice model (5XFAD). As a vehicle group, the 5XFAD mice were given with PBS. HY2109 significantly reduced the time to find platform, increased platform crosses and quadrant occupancy in water maze test, suggesting improvement in learning and memory of 5XFAD mice after treatment with HY2109 compared with control group. Furthermore HY2109 treatment significantly decreased the number of amyloid plaque, the number of astrocyte and microglia in the frontal cortex. The number of astrocyte was also decreased by HY2109 treatment in hippocampus. iNOS expression of astrocyte in the frontal cortex was drastically reduced by HY2109 treatment. TUNEL (+) apoptotic cells in the frontal cortex were significantly lower in HY2109-group of mice. Interestingly, CD11b+Gr1-F4/80+ myeloid cells were significantly increased in the spleen and brain of 5XFAD mice that were treated with HY2109. Blood CCL3 was significantly lower in HY2109 group of mice. These findings suggest that HY2109 might be a new molecular entity that can control pathogenesis of Alzheimer disease.