scholarly journals Electroacupuncture could balance the gut microbiota and improve the learning and memory abilities of Alzheimer’s disease animal model

PLoS ONE ◽  
2021 ◽  
Vol 16 (11) ◽  
pp. e0259530
Author(s):  
Jing Jiang ◽  
Hao Liu ◽  
Zidong Wang ◽  
Huiling Tian ◽  
Shun Wang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Model ◽  
Gut Microbiota ◽  
Learning And Memory ◽  
Amplicon Sequencing ◽  
Tnf Α ◽  
16S Rdna Amplicon Sequencing ◽  
Nerve System ◽  
Samp8 Mice

Alzheimer’s disease (AD), as one of most common dementia, mainly affects older people from the worldwide. In this study, we intended to explore the possible mechanism of improving cognitive function and protecting the neuron effect by electroacupuncture. Method: We applied senescence-accelerated mouse prone 8 (SAMP8) mice as AD animal model, used Morris water maze, HE staining, 16S rDNA amplicon sequencing of gut microbiota and ELISA to demonstrate our hypothesis. Results: electroacupuncture improved the learning and memory abilities in SAMP8 mice (P<0.05) and could protect the frontal lobe cortex and hippocampus of SAMP8 mice; electroacupuncture significantly decreased the expression of IL-1β (P<0.01), IL-6 (P<0.01) and TNF-α (P<0.01 in hippocampus, P<0.05 in serum) in serum and hippocampus; electroacupuncture balanced the quantity and composition of gut microbiome, especially of the relative abundance in Delta-proteobacteria (P<0.05) and Epsilon-proteobacteria (P<0.05). Conclusion: electroacupuncture treatment could inhibit the peripheral and central nerve system inflammatory response by balancing the gut microbiota.

Yishen Huazhuo Decoction Induces Autophagy to Promote the Clearance of Aβ1-42 in SAMP8 Mice: Mechanism Research of a Traditional Chinese Formula Against Alzheimer’s Disease

2020 ◽  
Vol 19 (4) ◽  
pp. 276-289
Author(s):  
Kai Wang ◽  
Weiming Sun ◽  
Jiachun Xu ◽  
Qijing Qin ◽  
Zhen Yu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Learning And Memory ◽  
Neuronal Loss ◽  
Tunel Staining ◽  
Initiation Increase ◽  
Apoptosis Index ◽  
Significant Difference ◽  
Related Proteins ◽  
Samp8 Mice

Background: Studies have found that autophagy could promote the clearance of Aβ. To promote and maintain the occurrence of autophagy in Alzheimer's disease (AD) might be a potential way to reduce neuronal loss and improve the learning and memory of AD. Objective: To investigate the possible mechanisms of Yishen Huazhuo Decoction (YHD) against AD model. Methods: Forty 7-month-old male SAMP8 mice were randomly divided into model (P8) group and YHD group, 20 in each group, with 20 SAMR1 mice as control (R1) group. All mice were intragastrically administered for 4 weeks, YHD at the dosage of 6.24g/kg for YHD group, and distilled water for P8 group and R1 group. Morris water maze (MWM) test, Nissl’s staining, TEM, TUNEL staining, immunofluorescence double staining, and western blot analysis were applied to learning and memory, structure and ultrastructure of neurons, autophagosome, apoptosis index, Aβ, LAMP1, and autophagy related proteins. Results: The escape latency time of YHD group was significantly shorter on the 4th and 5th day during MWM test than those in P8 group (P=0.011, 0.008<0.05), and the number of crossing platform in YHD group increased significantly (P=0.02<0.05). Nissl’s staining showed that the number of neurons in YHD group increased significantly (P<0.0001). TEM showed in YHD group, the nucleus of neurons was slightly irregular, with slightly reduced organelles, partially fused and blurred cristae and membrane of mitochondria. The apoptosis index of YHD group showed a decreasing trend, without statistically significant difference (P=0.093>0.05), while Caspase3 expression in YHD group was significantly lower (P=0.044<0.05). YHD could promote the clearance of Aβ1-42 protein, improve the expression of Beclin-1 and p-Bcl2 proteins, reduce mTOR and p62 proteins. Conclusions: YHD could induce autophagy initiation, increase the formation of autophagosomes and autolysosome, promote the degradation of autophagy substrates, thereby to regulate autophagy, thereby to promote the clearance of Aβ1-42 to improve memory impairment in SAMP8 mice.

Diphtheria toxoid nanoparticles improve learning and memory impairment in animal model of Alzheimer’s disease

2019 ◽  
Vol 72 (4) ◽  
pp. 814-826
Author(s):  
Samane Heydari ◽  
Mojtaba Hedayati Ch ◽  
Farshid Saadat ◽  
Mahmood Abedinzade ◽  
Iraj Nikokar ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Model ◽  
Learning And Memory ◽  
Memory Impairment ◽  
Diphtheria Toxoid ◽  
Model Of Alzheimer’S Disease

scholarly journals P2-021: METFORMIN AND TOPIRAMATE IMPROVE LEARNING AND MEMORY IN DIABETIC MICE AND SAMP8 MICE MODEL OF ALZHEIMER'S DISEASE

2014 ◽  
Vol 10 ◽  
pp. P477-P478 ◽  
Author(s):  
John Edward Morley ◽  
Michael L. Niehoff ◽  
Michael W. Bergin ◽  
Elizabeth C. Roesler ◽  
Gul N. Shah ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Learning And Memory ◽  
Diabetic Mice ◽  
Mice Model ◽  
Model Of Alzheimer’S Disease ◽  
Samp8 Mice

scholarly journals Inhibition of Stat3 Phosphorylation Attenuates Impairments in Learning and Memory in 5XFAD Mice, an Animal Model of Alzheimer’s Disease

2020 ◽  
Author(s):  
Moonseok Choi ◽  
Hyunju Kim ◽  
Eun-Jeong Yang ◽  
Hye-Sun Kim
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Model ◽  
Learning And Memory ◽  
Resting State ◽  
Reactive Astrocytes ◽  
Cultured Astrocytes ◽  
Stat3 Phosphorylation ◽  
5Xfad Mice ◽  
Primary Cultured Astrocytes

Abstract The novel functions of astrocytes under normal conditions have been extensively investigated in terms of synaptogenesis and memory formation. Meanwhile, the pathophysiological roles of astrocytes in the reactive state are thought to have important significance in the pathogenesis of neurodegenerative diseases, including Alzheimer’s disease (AD). However, the detailed mechanisms underlying the transition of astrocytes from the resting state to the reactive state during neurodegenerative disease largely remain to be defined. Here, we investigated the pathways involved in activating astrocytes from the resting state to the reactive state in primary cultured astrocytes treated with oligomeric Aβ and in the hippocampus of 5XFAD mice, an animal model of AD. Treatment with oligomeric Aβ induced an increase in reactive astrocytes, as assessed by the protein level of glial fibrillary acidic protein (GFAP), a marker of reactive astrocytes and this increase was caused by STAT3 phosphorylation in primary cultured astrocytes. The administration of Stattic, an inhibitor of STAT3, rescued the activation of astrocytes in primary cultured astrocytes and in the hippocampus of 6-month-old 5XFAD mice as well as impairments in learning and memory. Collectively, these results demonstrated that reactive astrocytes in the AD brain are induced via STAT3 phosphorylation and that the increase in reactive astrocytes and the impairments in learning and memory observed in 5XFAD mice are rescued by STAT3 inhibition, suggesting that the inhibition of STAT3 phosphorylation in astrocytes may be a novel therapeutic target for cognitive impairment in AD.

scholarly journals Electroacupuncture Could Influence the Expression of IL-1β and NLRP3 Inflammasome in Hippocampus of Alzheimer’s Disease Animal Model

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Jing Jiang ◽  
Ning Ding ◽  
Kang Wang ◽  
Zhigang Li
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Model ◽  
Nlrp3 Inflammasome ◽  
Day Treatment ◽  
Control Group ◽  
Acupuncture Points ◽  
Spatial Learning And Memory ◽  
Caspase 1 ◽  
Samp8 Mice

Background. Effective therapies for Alzheimer’s disease (AD) are still being explored. Electroacupuncture with traditional Chinese medicine theory may improve spatial learning and memory abilities and glucose metabolism rates in an animal model of AD. However, the mechanism of electroacupuncture in intervention of AD is still unclear. According to recent studies of AD mechanisms, the NLRP3 inflammasome regulated the expression of IL-1β in the brain which may mediate AD related processes. Therefore, in our study, we intend to explore the possible relation between electroacupuncture and the expression of NLRP 3 inflammasome in the hippocampus of an AD animal model. Method. In this study, 7.5-month-old male senescence-accelerated mouse prone 8 (SAMP8) mice were used as an AD animal model, which were randomly divided into two groups: Alzheimer’s disease model group (AD group) and electroacupuncture group (EA group). In the control paradigm, 7.5-month-old male SAMR1 mice were used as the normal control group (N group). DU20, DU26, and EX-HN3 were selected as the acupuncture points, and after a 15-day treatment of electroacupuncture, we used immunohistochemistry and Western blotting to examine the expression of IL-1β and NLRP3, ASC, and Caspase-1 in the hippocampus of the AD animal model. Results. Compared with N group, IL-1β, NLRP3, ASC, and Caspase-1 positive cells in AD group were increased, and the relative expression of all above proteins significantly increased (P < 0.01). Compared with AD group, the expression of IL-1β, NLRP3, ASC, and Caspase-1 in EA group was significantly decreased (P < 0.01). Conclusion. Electroacupuncture treatment could inhibit the inflammation reaction in the hippocampus of SAMP8 mice. What is more, the possible mechanism of electroacupuncture reduced the expression of IL-1β and NLRP3 inflammasome relative protein.

Paired helical filaments (PHF) in rats: An experimental animal model for Alzheimer's disease

1987 ◽  
Vol 45 ◽  
pp. 842-843
Author(s):  
V.J.A. Montpetit ◽  
S. Dancea ◽  
S.W. French ◽  
D.F. Clapin
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Model ◽  
Paired Helical Filaments ◽  
Ethanol Intoxication ◽  
Drg Neurons ◽  
Critical Difference ◽  
Suitable Animal Model ◽  
The Central Nervous System ◽  
Chronic Ethanol Intoxication

A continuing problem in Alzheimer research is the lack of a suitable animal model for the disease. The absence of neurofibrillary tangles of paired helical filaments is the most critical difference in the processes by which the central nervous system ages in most species other than man. However, restricting consideration to single phenomena, one may identify animal models for specific aspects of Alzheimer's disease. Abnormal fibers resembling PHF have been observed in dorsal root ganglia (DRG) neurons of rats in a study of chronic ethanol intoxication and spontaneously in aged rats. We present in this report evidence that PHF-like filaments occur in ethanol-treated rats of young age. In control animals lesions similar in some respects to our observations of cytoskeletal pathology in pyridoxine induced neurotoxicity were observed.Male Wistar BR rats (Charles River Labs) weighing 350 to 400 g, were implanted with a single gastrostomy cannula and infused with a liquid diet containing 30% of total calories as fat plus ethanol or isocaloric dextrose.

The Weak Combined Magnetic Fields Reduce the Brain β-Amyloid in an Animal Model of Sporadic Alzheimer's Disease

PIERS Online ◽  
2009 ◽  
Vol 5 (4) ◽  
pp. 311-315 ◽  
Author(s):  
Natalia V. Bobkova ◽  
Vadim V. Novikov ◽  
Natalia I. Medvinskaya ◽  
Irina Yu. Aleksandrova ◽  
Eugenii E. Fesenko
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Model ◽  
Magnetic Fields ◽  
Sporadic Alzheimer’S Disease ◽  
Combined Magnetic Fields ◽  
The Brain
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