RP1, a RAGE antagonist peptide, can improve memory impairment and reduce Aβ plaque load in the APP/PS1 mouse model of Alzheimer's disease

Huang, Yiyun; Fang, Nian; Luo, Huiru; Zou, Yao; Zhou, Lili; Zeng, Quan; Fang, Shisong; Xiao, Fei; Zheng, Qi

doi:10.1016/j.neuropharm.2020.108304

Cited by 23 publications

(19 citation statements)

References 80 publications

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“…Receptor for advanced glycation end-products binds a broad repertoire of molecules, including AGEs, Aβs, S100 calcium-binding protein B (S100B), macrophage-1 antigen (Mac-1), high-mobility group box 1 (HMGB1), products of non-enzymatic glycoxidation, and amphoterin ( Saleh et al, 2013 ; Huang Y.Y. et al, 2020 ).…”

Section: Amyloid-β Deposition Due To Blood–brain Barrier Dysfunctionmentioning

confidence: 99%

“…In AD, evidence shows that the combination of RAGE and Aβ lead to a series of reactions, including oxidative stress, reduced cerebral blood flow, and vascular dysfunction ( Huang Y.Y. et al, 2020 ).…”

Section: Amyloid-β Deposition Due To Blood–brain Barrier Dysfunctionmentioning

confidence: 99%

“…In addition, Aβ–RAGE engagement results in sustained nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, which in turn increases RAGE expression and forms a positive-feedback loop causing inflammatory damage. A transient proinflammatory response is transformed into a chronic pathophysiological condition in the CNS, and the positive-feedback loop also damages endothelial cells and the BBB, exacerbating AD pathology ( Batkulwar et al, 2018 ; Fang et al, 2018 ; Huang Y.Y. et al, 2020 ).…”

Section: Amyloid-β Deposition Due To Blood–brain Barrier Dysfunctionmentioning

confidence: 99%

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Relationship Between Amyloid-β Deposition and Blood–Brain Barrier Dysfunction in Alzheimer’s Disease

Wang

Chen²,

Han

et al. 2021

Front. Cell. Neurosci.

108

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Amyloid-β (Aβ) is the predominant pathologic protein in Alzheimer’s disease (AD). The production and deposition of Aβ are important factors affecting AD progression and prognosis. The deposition of neurotoxic Aβ contributes to damage of the blood–brain barrier. However, the BBB is also crucial in maintaining the normal metabolism of Aβ, and dysfunction of the BBB aggravates Aβ deposition. This review characterizes Aβ deposition and BBB damage in AD, summarizes their interactions, and details their respective mechanisms.

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Section: Amyloid-β Deposition Due To Blood–brain Barrier Dysfunctionmentioning

confidence: 99%

Section: Amyloid-β Deposition Due To Blood–brain Barrier Dysfunctionmentioning

confidence: 99%

Section: Amyloid-β Deposition Due To Blood–brain Barrier Dysfunctionmentioning

confidence: 99%

See 1 more Smart Citation

Relationship Between Amyloid-β Deposition and Blood–Brain Barrier Dysfunction in Alzheimer’s Disease

Wang

Chen²,

Han

et al. 2021

Front. Cell. Neurosci.

108

View full text Add to dashboard Cite

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“…RAGE inhibitor/modulator PF-0449470052, which failed in phase II studies, and TTP4000, which finished its phase I trial in February 2013, are the only clinical candidates (NCT01548430). The trial's findings are still secret [54,37].…”

Section: Transit Modulation Between Cns and Peripheral Circulationmentioning

confidence: 99%

The Role of Polyphenols in the Treatment of Alzheimer's Disease: Narrative Review

Alattiya

Tarish

Hashim

et al. 2021

Al-Rafidain J Med Sci

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Many epidemiological studies have suggested that consuming a diet rich in polyphenols can help prevent Alzheimer's disease (AD). Based on well-known in vitro and in vivo models of cerebral Aβ amyloidosis, we examined the data on the effects of various natural polyphenols on the aggregation of amyloid-protein (Aβ). These polyphenols effectively prevent oligomerization and fibril formation of Aβ through differential binding patterns, lowering Aβ oligomer-induced synaptic and neuronal toxicity, according to in vitro investigations. Furthermore, in a transgenic mouse model fed orally with such polyphenolic compounds, soluble Aβ oligomers as well as insoluble Aβ deposits in the brain were significantly reduced. Natural polyphenols exhibit anti-amyloidogenic effects on Aβ, in addition to well-known anti-oxidative and anti-inflammatory activities, according to an updated assessment of the literature, implying their potential as therapeutic and/or preventive agents for AD treatment. To prove polyphenols' efficacy as disease-modifying agents, well-designed clinical trials or preventive treatments using various polyphenols are required.

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“…From a pathological perspective, amyloid-β (Aβ) deposition in the hippocampus of the brain can cause inflammation and oxidative stress, which may lead to neurodegenerative changes in the brain, a key pathological factor contributing to the development of AD (Chiang et al, 2021). Some researchers have found that reducing or preventing the accumulation of Aβ in the brain could effectively improve memory and cognitive function in AD model mice (Huang et al, 2020;Luo et al, 2020). Therefore, depolymerization or elimination of toxic Aβ aggregates in patients is very important for delaying the progression of neurodegenerative changes associated with AD (Le & Cho, 2021).…”

mentioning

confidence: 99%

Improvement of electroacupuncture on APP/PS1 transgenic mice in behavioral probably due to reducing deposition of Aβ in hippocampus

Sun

Wang

Zhao

et al. 2021

The Anatomical Record

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Alzheimer's disease (AD) is a fatal neurodegenerative disease for which currently no cure is available. Electroacupuncture (EA) has been widely used in China as an alternative therapeutic approach for neurological diseases. The cognitive decline in patients with AD has been reported to be closely related to the deposition of amyloid-β (Aβ) in the hippocampus of the brain, and the Morris water maze (MWM) test is a widely used method for assessing the behavior of animal models. In this study, the MWM test was performed to evaluate the effects of EA treatment on cognitive function and memory, and the micro-positron emission tomography scan was used to assess the hippocampal Aβ deposition. The results showed that the cognitive function of APP/PS1 mice was significantly improved and the rate of [18F]AV-45 uptake was reduced in the EA group, compared with the AD group. Our study suggested that EA can exert a therapeutic effect in AD by improving spatial learning and memory and inhibiting the hippocampal Aβ deposition. 电针对APP/PS1转基因小鼠行为学的改善可能与减少海马Aβ沉积有关摘要:老年痴呆症疾病(AD)是一种致命的神经退行性疾病，目前没有治愈方Run-Quan Sun, Zi-Dong Wang, and Jun Zhao are co-first authors.

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RP1, a RAGE antagonist peptide, can improve memory impairment and reduce Aβ plaque load in the APP/PS1 mouse model of Alzheimer's disease

Cited by 23 publications

References 80 publications

Relationship Between Amyloid-β Deposition and Blood–Brain Barrier Dysfunction in Alzheimer’s Disease

Relationship Between Amyloid-β Deposition and Blood–Brain Barrier Dysfunction in Alzheimer’s Disease

The Role of Polyphenols in the Treatment of Alzheimer's Disease: Narrative Review

Improvement of electroacupuncture on APP/PS1 transgenic mice in behavioral probably due to reducing deposition of Aβ in hippocampus

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