Reduction of amyloid beta by Aβ3-10-KLH vaccine also decreases tau pathology in 3×Tg-AD mice

Zhang, Huiyi; Zhu, Kun; Meng, Yuan; Ding, Li; Wang, Jinchun; Yin, Wen-Chao; Yan, Yi; Cao, Yunpeng

doi:10.1016/j.brainresbull.2018.07.019

Cited by 13 publications

(10 citation statements)

References 44 publications

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“…Compared to the two transgenic mice, the 3xTg-AD mice model containing three transgenic genes has a single genetic background avoiding biological differences. As the animal model closest to the family-type AD, it has the main neuropathological features of AD-SP and NFT, and important pathological changes in AD such as neuronal death and synaptic loss in the brain 29 . The emergence of cognitive impairment and early pathogenesis of 3xTg-AD mice make the research process more economical and rapid.…”

Section: Discussionmentioning

confidence: 99%

High-throughput metabolomics and ingenuity pathway approach reveals the pharmacological effect and targets of Ginsenoside Rg1 in Alzheimer’s disease mice

Zhang

Geng

et al. 2019

Sci Rep

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Ginsenoside Rg1, a natural triterpenoid saponins compound isolated from the Panax species, has been found to possess neuroprotective properties in neurodegenerative diseases such as Alzheimer’s disease (AD). However, its pharmacological mechanism on AD has not been studied. In this study, an ultra-performance liquid chromatography combined with quadrupole time of-flight mass spectrometry (UPLC-Q/TOF-MS) based non-targeted metabolomics strategy was performed to explore the mechanism of Ginsenoside Rg1 protecting against AD mice by characterizing metabolic biomarkers and regulation pathways changes. A total of nineteen potential metabolites in serum were discovered and identified to manifest the difference between wild-type mice and triple transgenic mice in control and model group, respectively. Fourteen potential metabolites involved in ten metabolic pathways such as linoleic acid metabolism, arachidonic acid metabolism, tryptophan metabolism and sphingolipid metabolism were affected by Rg1. From the ingenuity pathway analysis (IPA) platform, the relationship between gene, protein, metabolites alteration and protective activity of ginsenoside Rg1 in AD mice are deeply resolved, which refers to increased level of albumin, amino acid metabolism and molecular transport. In addition, quantitative analysis of key enzymes in the disturbed pathways by proteomics parallel reaction was employed to verify changed metabolic pathway under Ginsenoside Rg1. The UPLC-Q/TOF-MS based serum metabolomics method brings about new insights into the pharmacodynamic studies of Ginsenoside Rg1 on AD mice.

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Section: Discussionmentioning

confidence: 99%

High-throughput metabolomics and ingenuity pathway approach reveals the pharmacological effect and targets of Ginsenoside Rg1 in Alzheimer’s disease mice

Zhang

Geng

et al. 2019

Sci Rep

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“…Humoral immune response was detected by enzyme-linked immunoabsorbent assay(ELISA) [15]. In brief, we use 96-microwell plates coated with GST-Aβ proteins to detect the Aβ peptide in serum samples diluted with PBS at 1:1,000.…”

Section: Immunoreactivity Of Antisera and Response To Aβ Polymersmentioning

confidence: 99%

DNA Vaccination Target on Amyloid Oligomer also Reduce tau Pathology and Improve Synaptic Function in Aged 3xTg-AD Mice

Sha

Xing

Wang

et al. 2020

Preprint

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Background: Active immunotherapy has been widely used as a potential therapeutic method for both treatment and prevention of Alzheimer’s disease (AD). Amyloid deposition and tau hyperphosphorylation are main pathological hallmarks of AD. Reduction in both is required to regulate synaptic proteins neurotransmission which can finally protect cognitive function. Growing evidence suggests that the most toxic β-Amyloid peptide (Aβ) oligomers can be detected from the very beginning of AD development, so it is wise for us to develop effective therapy method focus on Aβ oligomers rather than monomers. Methods: The 3×Tg-AD mice were randomly divided into two groups immunized with p(Aβ3–10)10-MT and PBS respectively. The PBS group was used for positive group while C57/B6 mice was used for negative group. ELISA was used to detect the antibody titers and Morris Water Maze was to analysis the cognitive function. The Aβ ,Tau hyperphosphorylation, Neuron and synaptic protein were detected through immunohistochemistry and western blot. Results: Mice immunized with p(Aβ3–10)10-MT can not only reduce the levels of Aβ oligomers and plaque deposits but also protect neuron as well as synaptic function, finally prevent the decline spatial memory in transgenic mice. Conclusions: Our novel DNA genetic vaccine is highly safe and effective, thus providing strong evidence for the treatment and prevention of early AD.

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Section: Role Of Peripheral Inflammation In Admentioning

confidence: 99%

“…In an attempt to cure AD, active immunization against Aβ was performed in mice and humans [50,51]. Studies reported that immunization had a therapeutic effect on mouse models of AD [50][51][52]. Unfortunately, clinical Aβ vaccination trials have been interrupted due to the development of meningoencephalitis in 6% of the patients, likely involving the appearance of pro-inflammatory macrophages, CD4+ and CD8+ T cells [50].…”

Section: Role Of Peripheral Inflammation In Admentioning

confidence: 99%

The Role of Inflammation in Amyloid Diseases

Foguel¹

2019

Amyloid Diseases

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Amyloid diseases are characterized by the abnormal accumulation of proteinaceous aggregates (amyloid fibrils or plaques) in tissues and organs. This class of diseases is also characterized by the presence of inflammation. Amyloid fibrils arise from the partial denaturing and unfolding of native proteins. The accumulation of amyloid fibrils causes tissue damage and elicits local and nonlocal immune cell infiltration into tissue and proinflammatory cytokine production. Moreover, these conditions fuel a vicious cycle that can increase amyloid production and create an environment of chronic inflammation. A chronically inflamed tissue rapidly deteriorates and loses its function. In this chapter, we will discuss important data gathered over the years describing the role of inflammation in amyloid diseases. We will describe how inflammation begins and how it affects disease progression for major amyloid diseases, such as Alzheimer's disease (AD) and hereditary TTR amyloidosis (hATTR). Lastly, we will discuss the recent advancements in treatments for amyloid diseases and how they address inflammation in affected patients.

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Reduction of amyloid beta by Aβ3-10-KLH vaccine also decreases tau pathology in 3×Tg-AD mice

Cited by 13 publications

References 44 publications

High-throughput metabolomics and ingenuity pathway approach reveals the pharmacological effect and targets of Ginsenoside Rg1 in Alzheimer’s disease mice

High-throughput metabolomics and ingenuity pathway approach reveals the pharmacological effect and targets of Ginsenoside Rg1 in Alzheimer’s disease mice

DNA Vaccination Target on Amyloid Oligomer also Reduce tau Pathology and Improve Synaptic Function in Aged 3xTg-AD Mice

The Role of Inflammation in Amyloid Diseases

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