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Dementia 2016
September 29-October 01, 2016
Volume 6 Issue 5(Suppl) J Alzheimers Dis Parkinsonism 2016
ISSN:2161-0460 JADP, an open access journal
conferenceseries .com
September 29-October 01, 2016 London, UK
5th International Conference on
Alzheimer’s Disease & Dementia
Gun Young Jung, J Alzheimers Dis Parkinsonism 2016, 6:5(Suppl)
RA improves cognitive function of Alzheimer’s disease mouse model through inhibition of BACE1
expression and neuroinflammation
Gun Young Jung
Sungkyunkwan University School of Pharmacy, Republic of Korea
Alzheimer’s disease (AD) is the most common dementing illness, and the peptide amyloid-β (Aβ) has a chief function in
the pathogenesis of AD. Sequential proteolysis of amyloid precursor protein (APP) by BACE1 and γ-secretase produces
Aβ which drives cerebral neuroinflammation. Recent findings have provided insight into a newly discovered inflammatory
mechanism that contributes to the pathogenesis of Alzheimer's disease mediated by multi-protein complexes called NLRP
inflammasomes. In the present study, we orally administered the brain penetrant, natural compound isolated from compound
RA to the transgenic APP/PS1 (bearingmutant humanAPP and presenilin-1 transgenes) and 3xTg-AD (bearingmutant human
APP, presenilin-1, and tau transgenes) mice models of Alzheimer’s disease. Oral treatment of natural compound reversed
transgene-associated behavioral deficits, but did not alter wild-type mouse behaviors. Furthermore, brain Aβ depositions as
well as abundance of various Aβ species were decreased in natural compound-treated AD mice. These effects occurred with
decreased cleavage of β-carboxy-terminal APP fragment, reduced BACE1 expression, attenuated neuroinflammation, and
reduced expression of NLRP inflammasome proteins. As in vitro validation, we treated neuronal and microglial cells with this
compound and found that the levels of NLRP inflammasome proteins, Aβ production, BACE1 expression, and oxidative stress
were significantly decreased. Collectively, our findings reveal this compound as a potential therapeutic modality for targeting
Aβ production and Aβ-induced NLRP inflammasomes.
Biography
Gun Young has completed his B.S. from Sungkyunkwan University School of Pharmacy in 2015. He is doing his master’s degree at Sungkyunkwan University
School of Pharmacy. His major expertise is molecular cell biology.