Premium
A novel extract of Nerium oleander ameliorates neuroinflammation and amyloid plaques in the transgenic mouse model of Alzheimer’s disease
Author(s) -
Lee Hyounggon
Publication year - 2020
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.047641
Subject(s) - neuroinflammation , oxidative stress , genetically modified mouse , microglia , apoptosis , transgene , inflammation , oleanolic acid , immunohistochemistry , medicine , amyloid (mycology) , pharmacology , pathology , biology , immunology , biochemistry , gene , alternative medicine
Background There have been numerous efforts for the development of the therapy for Alzheimer’s disease (AD) although effective treatment is not still available. Previous studies demonstrated the protective effect of PBI‐05204, a novel botanical extract of Nerium oleander , on oxidative damage and neuronal cell death. Both oleanolic acid and triterpenoids, the main constituent of both extracts, have been shown to modulate multiple cellular pathways including oxidative stress, inflammation, proliferation and apoptosis. Give that these neurotoxic mechanisms are pathologically linked with AD, the treatment of PBI‐05204 may be an effective therapy for AD. Thus, in this study, we examined its therapeutic effect on AD‐related pathological changes in the transgenic mouse model of AD to evaluate the therapeutic effect of PBI‐05204 on the pathological changes linked to AD. Method We treated the APP/PSEN1dE9 transgenic mice with PBI‐05204 for four months (4‐8 months of age) and examined neuropathological changes such as Aβ accumulation and neuroinflammation using immunohistochemistry and immunoblot assay. Result In our analysis, we found that Aβ plaques were significantly reduced by the treatment of PBI‐05204 compared to the control group. Furthermore, the treatment with PBI‐05204 significantly reduced neuroinflammation, which is evidenced by the reduced activation of microglia and astrocytes. Conclusion Collectively, our data clearly indicate that the treatment of PBI‐05204 reduces Aβ pathology and neuroinflammation in APP/PSEN1dE9 transgenic mouse model, suggesting the therapeutic potential of PBI‐05204 for the treatment of AD.