LW-AFC, a new formula derived from Liuwei Dihuang decoction, ameliorates behavioral and pathological deterioration via modulating the neuroendocrine-immune system in PrP-hAβPPswe/PS1ΔE9 transgenic mice

Wang, Jianhui; Xi, Lei; Cheng, Xiaorui; Zhang, Xiaorui; Liu, Gang; Cheng, Jin; Xu, Yang; Ju, Zeng; Zhou, Wen; Zhang, Yongxiang

doi:10.1186/s13195-016-0226-6

Cited by 38 publications

(24 citation statements)

References 106 publications

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“…A number of drugs targeting Aβ clearance (such as Aβ antibodies) or production (such as Aβ secretase inhibitors) have proceeded to clinical trials, but most of them failed to improve the cognitive functions in patients, which are mainly attributed to the signal targets, side effects, or the neuroinflammatory responses of these drugs ( 9 , 10 ). By contrast, many traditional medicines and natural products have shown great progress toward AD prevention and treatment ( 11 , 12 ). These studies also shed new light on the discovery and development of useful agents from established traditional medicines and safe natural products to halt the progression of neurodegenerative disease.…”

Section: Introductionmentioning

confidence: 99%

Sodium rutin ameliorates Alzheimer’s disease–like pathology by enhancing microglial amyloid-β clearance

et al. 2019

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The accumulation of aggregated amyloid-β (Aβ) in the brain is the first critical step in the pathogenesis of Alzheimer’s disease (AD), which also includes synaptic impairment, neuroinflammation, neuronal loss, and eventual cognitive defects. Emerging evidence suggests that impairment of Aβ phagocytosis and clearance is a common phenotype in late-onset AD. Rutin (quercetin-3-rutinoside) has long been investigated as a natural flavonoid with different biological functions in some pathological circumstances. Sodium rutin (NaR), could promote Aβ clearance by increasing microglial by increasing the expression levels of phagocytosis-related receptors in microglia. Moreover, NaR promotes a metabolic switch from anaerobic glycolysis to mitochondrial OXPHOS (oxidative phosphorylation), which could provide microglia with sufficient energy (ATP) for Aβ clearance. Thus, NaR administration could attenuate neuroinflammation and enhance mitochondrial OXPHOS and microglia-mediated Aβ clearance, ameliorating synaptic plasticity impairment and eventually reversing spatial learning and memory deficits. Our findings suggest that NaR is a potential therapeutic agent for AD.

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Section: Introductionmentioning

confidence: 99%

Sodium rutin ameliorates Alzheimer’s disease–like pathology by enhancing microglial amyloid-β clearance

et al. 2019

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“…Exploration of innate immune-mediated mechanisms and the use of immunomodulation as a disease-modification strategy have been promising in the preclinical research of AD [11]. Animal studies have shown that targeting the innate immune molecules or their respective signaling pathways may substantially ameliorate AD-related pathology [11][12][13][14].…”

Section: Introductionmentioning

confidence: 99%

The role of interleukin-33 in patients with mild cognitive impairment and Alzheimer’s disease

Liang

Tsai

et al. 2020

Alz Res Therapy

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Background: The neuroprotective role of interleukin (IL)-33 is supported by numerous preclinical studies, but it remains uninvestigated in clinical studies of Alzheimer's disease (AD). We aimed to examine the association between human blood levels of IL-33 and cognitive preservation in amnestic mild cognitive impairment (aMCI) and AD. Methods: A total of 100 participants (26 controls, 35 aMCI patients, and 39 AD patients) completed two Mini-Mental State Examinations (MMSEs) over a 1-year interval. In all 100 participants at the second MMSE, we examined the plasma levels of IL-33, IL-β, IL-1 receptor agonist (IL-1RA), beta amyloid (Aβ), and tau and apolipoprotein E (ApoE) genotyping; we also performed Hopkins Verbal Learning Test, Trail Making Test, forward and backward digit span, and Clinical Dementia Rating. Results: IL-33 expression showed a positive trend among controls (1/26 = 3.8%), aMCI (9/35 = 25.7%), and AD (17/39 = 43.6%) (trend analysis: P < 0.001). Patients expressing IL-33 preserved their cognitive function compared with IL-33 nonexpressing patients (1-year ΔMMSE, 0.16 ± 1.6 vs − 1.5 ± 2.6; P = 0.006). The cognitive preservation was not associated with the lower levels of Aβ, tau, and ApoE ε4, while higher levels of ApoE ε4 and phosphorylated tau were indeed associated with cognitive decline. The aMCI patients with AD conversion during study period had higher proportion of IL-33(−) than non-AD converters (90.9% vs 53.3%, P = 0.04). Conclusions: IL-33 or its associated signaling pathways may represent a new treatment paradigm for aMCI and AD.

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“…Exploration of innate immune-mediated mechanisms and the use of immunomodulation as a disease-modi cation strategy have been promising in the preclinical research of AD [11]. Animal studies have shown that targeting the innate immune molecules or their respective signaling pathways may substantially ameliorate AD-related pathology [11][12][13][14].…”

Section: Introductionmentioning

confidence: 99%

The role of Interleukin-33 in patients with mild cognitive impairment and Alzheimer’s disease

Liang

Su²,

Tsai

et al. 2020

Preprint

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Background: The neuroprotective role of interleukin (IL)-33 is supported by numerous pre-clinical studies, but it remains uninvestigated in clinical studies of Alzheimer’s disease (AD). We aimed to examine the association between human blood levels of IL-33 and cognitive preservation in amnestic mild cognitive impairment (aMCI) and AD.Methods: A total of 100 participants (26 controls, 35 aMCI patients, and 39 AD patients) completed two Mini Mental State Examination (MMSE) over a 1-year interval. In all 100 participants at the second MMSE, we examined the plasma levels of IL-33, IL-β, IL-1 receptor agonist (IL-1RA), beta amyloid (Aβ), and tau and apolipoprotein E (ApoE) genotyping; we also performed Hopkins Verbal Learning Test, Trail Making Test, forward and backward digit span, and Clinical Dementia Rating. Results: IL-33 expression showed a positive trend among controls (1/26 = 3.8%), aMCI (9/35 = 25.7%), and AD (17/39 = 43.6%) (trend analysis: P < 0.001). Patients expressing IL-33 preserved their cognitive function compared with IL-33 non-expressing patients (1-year ΔMMSE: 0.16 ± 1.6 vs -1.5 ± 2.6; P = 0.006). The cognitive preservation was not associated with the lower levels of Aβ, tau, and ApoE ε4, while higher levels of ApoE ε4 and phosphorylated tau were indeed associated with cognitive decline. The aMCI patients with AD conversion during study period had higher proportion of IL-33(-) than non-AD converters (90.9% vs 53.3%, P = 0.04).Conclusions: IL-33 or its associated signaling pathways may represent a new treatment paradigm for aMCI and AD.

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LW-AFC, a new formula derived from Liuwei Dihuang decoction, ameliorates behavioral and pathological deterioration via modulating the neuroendocrine-immune system in PrP-hAβPPswe/PS1ΔE9 transgenic mice

Cited by 38 publications

References 106 publications

Sodium rutin ameliorates Alzheimer’s disease–like pathology by enhancing microglial amyloid-β clearance

Sodium rutin ameliorates Alzheimer’s disease–like pathology by enhancing microglial amyloid-β clearance

The role of interleukin-33 in patients with mild cognitive impairment and Alzheimer’s disease

The role of Interleukin-33 in patients with mild cognitive impairment and Alzheimer’s disease

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