scholarly journals Herbal Mixture of Carthamus tinctorius L. Seed and Taraxacum coreanum Attenuates Amyloid Beta-Induced Cognitive Dysfunction In Vivo

Foods ◽  
2022 ◽  
Vol 11 (2) ◽  
pp. 142
Author(s):  
Meitong He ◽  
Jihyun Kim ◽  
Chanhum Park ◽  
Eunju Cho
Keyword(s):  
Learning And Memory ◽  
Cognitive Dysfunction ◽  
Amyloid Beta ◽  
Carthamus Tinctorius ◽  
Aging Brain ◽  
Pathological Feature ◽  
Cognitive Improvement ◽  
Taraxacum Coreanum ◽  
Related Proteins

Deposition of amyloid-beta (Aβ) in the aging brain has been often observed and is thought to be a pathological feature of Alzheimer’s disease. The use of natural products for disease prevention and treatment is gaining attention worldwide. Carthamus tinctorius L. seed and Taraxacum coreanum have been used as traditional medicines in Asian countries, where they have been reported to exert anti-inflammatory and anti-oxidative effects. It has been demonstrated that the combination of C. tinctorius L. seed and T. coreanum has an effect on cognitive enhancement, indicating a ratio of 5:5 synergistically enhancing learning and memory abilities in comparison with a single treatment. Here, we aimed to investigate the protective effect of C. tinctorius L. seed and T. coreanum mixture (CT) at different concentrations on cognition in Aβ25-35-infused mice. CT-administered mice showed significant cognitive improvement in the T-maze, novel object recognition, and Morris water maze tests. Moreover, amyloidogenesis-related proteins, such as β-secretase and γ-secretase, were detected and their protein levels decreased after treatment with CT. Our study shows that CT attenuates cognitive dysfunction by improving learning and memory capability and regulating Aβ-related proteins in Aβ25-35-injected mice. These findings suggest that CT might be a candidate for functional food on cognitive improvement.

scholarly journals Autophagy attenuates postoperative cognitive dysfunction by up-regulating cystatin C in aged rats undergoing splenectomy

2019 ◽  
Author(s):  
Bi Xing-hua ◽  
Zhou Long-yuan ◽  
Cai Chang ◽  
Qi Yong ◽  
Yan Li
Keyword(s):  
Learning And Memory ◽  
Cognitive Dysfunction ◽  
Cystatin C ◽  
Postoperative Cognitive Dysfunction ◽  
The Other ◽  
Inflammatory Factors ◽  
Aged Rats ◽  
Tnf Α ◽  
Neuro Inflammation ◽  
Related Proteins

Abstract B ackground : This study aimed to explore whether autophagy can attenuate postoperative cognitive dysfunction (POCD) by up-regulating cystatin C (CysC) in aged rats undergoing splenectomy. Methods : Rats were randomized into four groups ( n = 10 per group): normal control (CON), surgery (SUR), surgery + rapamycin (autophagy inducer) at 1.0 mg/kg/d (RAP), and surgery + 3-methyladenine (autophagy inhibitor) at 3.0 mg/kg/d (3-MA). Treatments were carried out for four weeks. Postoperative learning and memory were assessed using the Morris water maze. Hippocampal expression of the autophagy-related proteins ATG5, LC-3B, Beclin1, and p62 as well as Cys C was assayed using Western blotting and real-time polymerase chain reaction. Results: SUR animals showed higher levels of autophagy and higher expression of autophagy proteins and Cys C than CON animals. These levels were even higher in RAP animals, which also showed lower levels of the inflammatory factors IL-1β, IL-6 and TNF-α than the other groups. Learning and memory functions were higher in RAP animals than in the other groups on days 5 and 7. Effects of 3-MA were opposite to those of RAP. Conclusion : Autophagy improves learning and memory in aged rats following splenectomy, which may involve up-regulation of Cys C and attenuation of neuro-inflammation.

scholarly journals SIRT1 Regulates Cognitive Performance and Ability of Learning and Memory in Diabetic and Nondiabetic Models

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Yue Cao ◽  
Zi Yan ◽  
Tong Zhou ◽  
Guixia Wang
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Learning And Memory ◽  
Cognitive Dysfunction ◽  
Therapeutic Potential ◽  
Future Research ◽  
Cognitive Improvement ◽  
Age Related

Type 2 diabetes mellitus is a complex age-related metabolic disease. Cognitive dysfunction and learning and memory deficits are main characteristics of age-related metabolic diseases in the central nervous system. The underlying mechanisms contributing to cognitive decline are complex, especially cognitive dysfunction associated with type 2 diabetes mellitus. SIRT1, as one of the modulators in insulin resistance, is indispensable for learning and memory. In the present study, deacetylation, oxidative stress, mitochondrial dysfunction, inflammation, microRNA, and tau phosphorylation are considered in the context of mechanism and significance of SIRT1 in learning and memory in diabetic and nondiabetic murine models. In addition, future research directions in this field are discussed, including therapeutic potential of its activator, resveratrol, and application of other compounds in cognitive improvement. Our findings suggest that SIRT1 might be a potential therapeutic target for the treatment of cognitive impairment induced by type 2 diabetes mellitus.

scholarly journals Autophagy attenuates postoperative cognitive dysfunction by up-regulating cystatin C in aged rats undergoing splenectomy

2019 ◽  
Author(s):  
Bi Xing-hua ◽  
Zhou Long-yuan ◽  
Cai Chang ◽  
Qi Yong ◽  
Yan Li
Keyword(s):  
Learning And Memory ◽  
Cognitive Dysfunction ◽  
Cystatin C ◽  
Postoperative Cognitive Dysfunction ◽  
The Other ◽  
Aged Rats ◽  
Chain Reaction ◽  
Tnf Α ◽  
Polymerase Chain ◽  
Related Proteins

Abstract Background: This study aimed to explore whether autophagy can attenuate postoperative cognitive dysfunction (POCD) by up-regulating cystatin C in aged rats undergoing splenectomy. Methods: Rats were randomized into four groups (n = 10 per group): normal control (CON), surgery (SUR), surgery + rapamycin (autophagy inducer) at 1.0 mg/kg/d (RAP), and surgery + 3-methyladenine (autophagy inhibitor) at 3.0 mg/kg/d (3-MA). Treatments were carried out for four weeks. Learning and memory were assessed postoperatively using the Morris water maze. Hippocampal expression of the autophagy-related proteins ATG5, LC-3B, Beclin1, and p62 as well as Cys C was assayed using Western blotting and real-time polymerase chain reaction. Results: SUR animals showed higher levels of autophagy and higher expression of autophagy proteins and Cys C than CON animals. These levels were even higher in RAP animals, which also showed lower levels of the inflammatory cytokines IL-1β, IL-6 and TNF-α than the other groups. Learning and memory functions were higher in RAP animals than in the other groups on days 5 and 7. Effects of 3-MA were opposite to those of RAP. Conclusion: Autophagy improves learning and memory in aged rats following splenectomy, which may involve up-regulation of Cys C and attenuation of neuroinflammation.

scholarly journals Danggui-Shaoyao-San Improves Learning and Memory in Female SAMP8 via Modulation of Estradiol

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Yan Huang ◽  
Zeng-yao Hu ◽  
Hui Yuan ◽  
Lei Shu ◽  
Gang Liu ◽  
...  
Keyword(s):  
Blood Plasma ◽  
Learning And Memory ◽  
Cognitive Dysfunction ◽  
Morris Water Maze ◽  
Cognitive Abilities ◽  
Water Maze ◽  
Test Session ◽  
Cognitive Improvement ◽  
Improvement Effect ◽  
Step Down

Previous studies showed that Danggui-Shaoyao-San (DSS), a traditional Chinese medicinal prescription, could alleviate cognitive dysfunction of Alzheimer’s disease (AD) patients. However, the mechanisms remain unclear; we have now examined the effect of DSS on SAMP8 and elucidated the possible mechanism. Animals were treated with DSS for 2 months, and step-down test and Morris water maze (MWM) test were used to evaluated cognitive abilities. The estradiol (E2), NO, and glycine in blood plasma or in hippocampus were detected to explore the possible mechanisms. The latency of SAMP8 in step-down test was shorter than that of age-matched SAMR1, and DSS increased the latency especially in female animals. In MWM test, we got similar results; SAMP8 spent more time to find the platform, and DSS decreased the time before finding the platform, with little effect on swim velocity, during the training sessions. During test session, DSS increased the time spent in target quadrant especially in female SAMP8. In female SAMP8, plasma E2, NO, and glycine were elevated in plasma or hippocampus tissue. In conclusion, DSS could ameliorate deterioration of cognition in SAMP8, especially in female animals. Increasing E2, NO, and glycine might contribute to the cognitive improvement effect of DSS in female SAMP8.

scholarly journals Amyloid Beta-Protein and Neural Network Dysfunction

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Fernando Peña-Ortega
Keyword(s):  
Neural Network ◽  
Cognitive Dysfunction ◽  
Amyloid Beta ◽  
Network Dynamics ◽  
Basic Knowledge ◽  
Specific Cell ◽  
Amyloid Beta Protein ◽  
Neural Network Dynamics

Understanding the neural mechanisms underlying brain dysfunction induced by amyloid beta-protein (Aβ) represents one of the major challenges for Alzheimer’s disease (AD) research. The most evident symptom of AD is a severe decline in cognition. Cognitive processes, as any other brain function, arise from the activity of specific cell assemblies of interconnected neurons that generate neural network dynamics based on their intrinsic and synaptic properties. Thus, the origin of Aβ-induced cognitive dysfunction, and possibly AD-related cognitive decline, must be found in specific alterations in properties of these cells and their consequences in neural network dynamics. The well-known relationship between AD and alterations in the activity of several neural networks is reflected in the slowing of the electroencephalographic (EEG) activity. Some features of the EEG slowing observed in AD, such as the diminished generation of different network oscillations, can be induced in vivo and in vitro upon Aβ application or by Aβ overproduction in transgenic models. This experimental approach offers the possibility to study the mechanisms involved in cognitive dysfunction produced by Aβ. This type of research may yield not only basic knowledge of neural network dysfunction associated with AD, but also novel options to treat this modern epidemic.

scholarly journals Berberine Promotes TREM2-Dependent Phagocytosis of Amyloid-β By Microglia

2021 ◽  
Author(s):  
Yang-Yang Wang ◽  
Zhen-Ting Huang ◽  
Qian Zou ◽  
Yin-Shuang Pu ◽  
Ming-Hao Yuan ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Spatial Learning ◽  
Microglial Activation ◽  
Amyloid Β ◽  
Spatial Learning And Memory ◽  
Pathological Feature ◽  
Bv2 Cells ◽  
Aβ Clearance

Abstract Background: The production and accumulation of amyloid-β (Aβ) is the most important pathological feature of Alzheimer’s Disease (AD), and the deficiency of Aβ clearance contributes to the progression of AD. TREM2-dependent microglial activation may be the key to Aβ clearance. BBR plays the neuroprotective role in the progression of AD by inhibiting Aβ production and promoting Aβ degradation. However, the specific relationship between BBR and microglial activation remains unclear. Thus, we aimed to investigate whether BBR can inhibit the pathological progression of Aβ in AD by changing the phenotype of microglia.Methods: Western blot and Immunofluorescence staining were applied to detect the effects of BBR on the transformation of resting microglia to different phenotypes. ELISA, Immunohistochemistry and Immunofluorescence were used to detect the effect of BBR on microglial phagocytosis of Aβ. Morris water maze (MWM) test was applied to test the effect of BBR on the spatial learning and memory of experimental animals.Results: Firstly, BBR promoted the phagocytosis of Aβ1-42 by BV2 cells. Secondly, BBR promoted the changes of microglia to phenotypes M2 and DAM in vivo and in vitro, which were in close proximity to Aβ and reduced Aβ aggregation. Finally, BBR ameliorated spatial learning and memory impairment in APP/PS1 mice.Conclusion: BBR could enhance the phagocytosis of microglia, which decreased Aβ level and improved the spatial learning and memory of APP/PS1 mice.

scholarly journals Kiwifruit Alleviates Learning and Memory Deficits Induced by Pb through Antioxidation and Inhibition of Microglia Activation In Vitro and In Vivo

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Wei-Zhen Xue ◽  
Qian-Qian Yang ◽  
Yiwen Chen ◽  
Rong-Xin Zou ◽  
Dong Xing ◽  
...  
Keyword(s):  
Vitamin C ◽  
Learning And Memory ◽  
Cognitive Dysfunction ◽  
Memory Deficits ◽  
Postnatal Life ◽  
Lactation Period ◽  
Pb Exposure ◽  
Learning And Memory Deficits

Lead (Pb) exposure, in particular during early postnatal life, increases susceptibility to cognitive dysfunction and neurodegenerative outcomes. The detrimental effect of Pb exposure is basically due to an increasing ROS production which overcomes the antioxidant systems and finally leads to cognitive dysfunction. Kiwifruit is rich in the antioxidants like vitamin C and polyphenols. This study aims to investigate the effects and mechanism of kiwifruit to alleviate learning and memory deficits induced by Pb exposure. Sprague-Dawley (SD) rat pups acquired Pb indirectly through their mothers during lactation period and after postnatal day 21 (PND21) directly acquired Pb by themselves. Five kinds of kiwifruits were collected in this study and the amounts of vitamin C and polyphenols in them were measured and the antioxidation effects were determined. Among them, Qinmei kiwifruit (Qm) showed the strongest antioxidation effects in vitro. In vivo, Qm significantly repaired Pb-induced learning and memory deficits and dendritic spine loss. In addition, Pb compromised the enzymatic activity and transcriptional levels of SOD and GSH-Px and decreased the microglial activation, which, to some extent, could be reversed by Qm kiwifruit administration. The results suggest that kiwifruit could alleviate Pb-induced cognitive deficits possibly through antioxidative stress and microglia inactivation. Consequently, kiwifruit could be potentially regarded as the functional food favorable in the prevention and treatment of Pb intoxication.

scholarly journals Autophagy attenuates postoperative cognitive dysfunction by up-regulating cystatin C in aged rats undergoing splenectomy

2019 ◽  
Author(s):  
Bi Xing-hua ◽  
Zhou Long-yuan ◽  
Cai Chang ◽  
Qi Yong ◽  
Yan Li
Keyword(s):  
Learning And Memory ◽  
Cognitive Dysfunction ◽  
Cystatin C ◽  
Postoperative Cognitive Dysfunction ◽  
The Other ◽  
Inflammatory Factors ◽  
Aged Rats ◽  
Tnf Α ◽  
Neuro Inflammation ◽  
Related Proteins

Abstract B ackground : This study aimed to explore whether autophagy can attenuate postoperative cognitive dysfunction (POCD) by up-regulating cystatin C (CysC) in aged rats undergoing splenectomy. Methods : Rats were randomized into four groups ( n = 10 per group): normal control (CON), surgery (SUR), surgery + rapamycin (autophagy inducer) at 1.0 mg/kg/d (RAP), and surgery + 3-methyladenine (autophagy inhibitor) at 3.0 mg/kg/d (3-MA). Treatments were carried out for four weeks. Postoperative learning and memory were assessed using the Morris water maze. Hippocampal expression of the autophagy-related proteins ATG5, LC-3B, Beclin1, and p62 as well as Cys C was assayed using Western blotting and real-time polymerase chain reaction. Results: SUR animals showed higher levels of autophagy and higher expression of autophagy proteins and Cys C than CON animals. These levels were even higher in RAP animals, which also showed lower levels of the inflammatory factors IL-1β, IL-6 and TNF-α than the other groups. Learning and memory functions were higher in RAP animals than in the other groups on days 5 and 7. Effects of 3-MA were opposite to those of RAP. Conclusion : Autophagy improves learning and memory in aged rats following splenectomy, which may involve up-regulation of Cys C and attenuation of neuro-inflammation.

Rapid, Refined, and Robust Method for Expression, Purification, and Characterization of Recombinant Human Amyloid-beta M1-42

2019 ◽  
Author(s):  
Priya Prakash ◽  
Travis Lantz ◽  
Krupal P. Jethava ◽  
Gaurav Chopra
Keyword(s):  
Amyloid Beta ◽  
Western Blots ◽  
Force Microscopy ◽  
E Coli ◽  
Atomic Force ◽  
Set Up ◽  
Short Time

Amyloid plaques found in the brains of Alzheimer’s disease (AD) patients primarily consists of amyloid beta 1-42 (Ab42). Commercially, Ab42 is synthetized using peptide synthesizers. We describe a robust methodology for expression of recombinant human Ab(M1-42) in Rosetta(DE3)pLysS and BL21(DE3)pLysS competent E. coli with refined and rapid analytical purification techniques. The peptide is isolated and purified from the transformed cells using an optimized set-up for reverse-phase HPLC protocol, using commonly available C18 columns, yielding high amounts of peptide (~15-20 mg per 1 L culture) in a short time. The recombinant Ab(M1-42) forms characteristic aggregates similar to synthetic Ab42 aggregates as verified by western blots and atomic force microscopy to warrant future biological use. Our rapid, refined, and robust technique to purify human Ab(M1-42) can be used to synthesize chemical probes for several downstream in vitro and in vivo assays to facilitate AD research.

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