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Food Science and Human Wellness 2022年第3期11卷 483-493页

作者： Kumju Youn Chi-Tang Ho Mira Jun Department of Food Science and Nutrition Dong-A UniversityBusan 49315Korea Department of Food Science Rutgers UniversityNJ 08901USA Department of Health Sciences The graduate School of Dong-A UniversityBusan 49315Korea

Alzheimer’s disease(AD)is the most common neurodegenerative disease characterized by cognitive decline and memory *** lines of evidence indicate that excessiveβ-amyloid peptide(Aβ)generation and aggregation play pivotal roles in the initiation of AD,leading to various biochemical alteration including oxidative damage,mitochondrial dysfunction,neuroinflammation,signaling pathway and finally resulting in neuronal *** has a complex pathogenic mechanism,and a single-target approach for anti-AD strategy is thus full of *** overcome these limitations,the present study focused to review on one of multiple target-compounds,(-)-epigallocatechin-3-gallate(EGCG)for the prevention and treatment of *** is a main bioactive polyphenol in green tea and has been reported to exert potent neuroprotective properties in a wide array of both cellular and animal models in *** review demonstrated multiple neuroprotective efficacies of EGCG by focusing on the involvement of Aβ-evoked damage and its Aβ***,to understand its mechanism of action on the brain,the permeability of the blood-brain barrier was also discussed.

关键词： Alzheimer’s disease β-amyloid peptide Green tea EGCG Neuroinflammation

Effects of Yizhi Capsule (益智胶囊) on Learning and Memory Disorder and β-amyloid peptide Induced Neurotoxicity in Rats

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Chinese Journal of Integrated Traditional and Western Medicine 2006年第2期12卷 137-141页

作者：吴航宇徐江平李琳朱柏华 Department of Pharmacology First Military Medical University Guangzhou (510515) Qixing Pharmaceutical Co. Ltd. Guangzhou

To explore the effects of Yizhi Capsule （益智胶囊, YZC） on learning and memory disorder and β-amyloid peptide induced neurotoxicity in rats. Methods： Various doses of YZC were administered to Sprague-Dawley （SD） rats for 8 consecutive days, twice a day. On the 8th day of the experiment, scopolamine hydrobromide was intraperitoneally injected to every rat and Morris water maze test and shuttle dark avoidance test were carried out respectively to explore the changes of learning and memory capacities in the rats. Resides, after the cerebral cortical neurons of newborn SD rats aged within 3 days were cultured in vitro for 7 days, drug serum containing YZC was added to the cultured neurons before or after β amyloid peptide25-35 （Aβ25-35） intoxication to observe the protective effect of YZC on neurotoxicity by MTT assay and to determine the LDH content in the supernatant. Results： Compared with those untreated with YZC, the rats having received YZC treatment got superiority in shorter time of platform seeking in Morris water maze test, as well as elongated latent period and less times of error in shuttle dark avoidance test. On the cultured neurons, YZC drug serum could effectively increase the survival rate of Aβ25-35 intoxicated neurons and reduce the LDH contents in cultured supernatant. Conclusion： YZC has an action of improving learning and memory disorder, and good protective effect on Aβ25-35 induced neurotoxicity in SD rats. KEY WORDS

关键词： learning and memory disorder β-amyloid peptide neurotoxicity

Estrogens enhance β-amyloid peptide degradation through upregulation of neprilysin

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Estrogens enhance β-amyloid peptide degradation through upr...

The effect of chronic cerebral hypoperfusion on β-amyloid peptide in rats' blood and brain

中国神经科学学会第四次会员代表大会暨第八届全国学术会议

作者： Kai-Wei LIANG,Liu-Qing YANG,Chen YIN,Zhi-Min XIAO,Jian HUANG~* State Key Lab of Virology,College of Life Sciences,Wuhan University,Wuhan 430072,China

＜正＞Postmenopausal estrogen-depletion is a known risk factor for Alzheimer’s disease（AD）,a human disorder linked to high levels ofβ-amyloid peptide（Ap） in brain *** studies suggest that estrogen negatively regulates the level of Aβin the brain,but the molecular mechanism is ***,we provide evidence that estrogen promotes degradation of Aβby stimulating of the primary Aβdegrading enzyme,*** in SH-SY5Y neuroblastoma cells demonstrate that ligand-activated estrogen receptor（ER） regulates expression of neprilysin mRNA and protein through physical interactions between ER and estrogen response elements（EREs） in the neprilysin *** results were confirmed by in vitro gel shift and in vivo chromatin immunoprecipitation analysis,which demonstrates specific binding of ERa and ERb to two putative EREs in the neprilysin *** EREs also enhance ERa- and ERb-dependent reporter gene expression in a yeast model ***,the study described here provides a putative mechanism by which estrogen positively regulates expression of neprilysin to promote degradation of Ap,reducing risk for *** results may lead to novel approaches to prevent or treat AD.

关键词： Alzheimer’s disease neprilysin β-amyloid peptide estrogen receptor estrogen response element

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The effect of chronic cerebral hypoperfusion on β-amyloid p...

Role of BACE1 in Alzheimer’s synaptic function

中国神经科学学会第四次会员代表大会暨第七届全国学术会议

作者： An-Feng XING,Le-Rong REN,Ye DING,Jue WANG,Liang LI Department of Pathology,School of Basic Medical Sciences,Capital Medical University,Beijing 100069,China

Objective To investigate the effect of chronic cerebral hypoperfusion on β-amyloid peptide(Aβ) which plays a very important role in the onset of Alzheimer’s disease,chronic cerebral hypoperfusion rat model was employed to observe the changes of Aβin rats’s blood and brain,the distributions of Aβsubtype in the brain,the rats’ learning and memory capability and the amyloidosis of the blood *** Male Sprague-Dawley rats,approximately 10 months of age,were randomly divided into model groups(M groups) and control groups(C groups).Permanent bilateral carotid occlusion(2-VO) was done to lead to sustained chronic cerebral ischemia to the model ***-matched control groups were performed surgery without bilateral carotid *** rats were devided into 10 d group,30 d group,90 d group and 180 d *** the following experiments were fulfilled:(1) Spatial learning and memory capability were tested by Morris water maze;(2) Weight and volume of the rats’ brain was measured;(3) Radioimmunoassay was employed to test the levels of Aa in serum,cortex and hippocampus;(4) The expression of APP in the extract from homogenate of hippocampus and cortex of rats were evaluated by western-blot;(5) Histomorphology:Hematoxylin-eosin staining(HE) was processed to observe the general morphological changes of the rats’s brain;Immunohistochemistry was processed to observe the distribution and expression of APP,Aβ and Aβ;And the amyloidosis of the blood vessels was observed by Congo red ***(1) Escaping latency time and swimming distance was postponed initially in model group after 30 days of hypoperfusion compared with control group(P<0.05).More significant differences were found between model groups and control groups after 90 and 180 d of hypoperfusion(P<0.05 and P<0.01,respectively). (2) The weight of the rats’ brain in 10 d model group was more than that of control group(P<0.05).(3) The content of Aβin the serum was more signigicantly increased in 10 d、30 d、90

关键词： chronic cerebral hypoperfusion Alzheimer’s disease β-amyloid peptide β-amyloid precursor protein

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Translational Neurodegeneration 2017年第1期6卷 217-224页

作者： Brati Das Riqiang Yan Department of Neurosciences Lerner Research InstituteCleveland Clinic9500 Euclid Avenue/NC30ClevelandOH 44195USA

Alzheimer’s disease(AD)is the most common age-dependent disease of dementia,and there is currently no cure *** hallmark pathologies of AD are the presence of amyloid plaques and neurofibrillary *** the exact etiology of AD remains a mystery,studies over the past 30 have shown that abnormal generation or accumulation of β-amyloid peptides(Aβ)is likely to be a predominant early event in AD pathological development.Aβ is generated from amyloid precursor protein(APP)via proteolytic cleavage by β-site APP cleaving enzyme 1(BACE1).Chemical inhibition of BACE1 has been shown to reduce Aβ in animal studies and in human *** BACE1 inhibitors are currently being tested in clinical trials to treat AD patients,it is highly important to understand whether BACE1 inhibition will significantly impact cognitive functions in AD *** review summarizes the recent studies on BACE1 synaptic *** knowledge will help to guide the proper use of BACE1 inhibitors in AD therapy.

关键词： amyloid deposition β-amyloid peptide BACE1 Secretase BACE1 substrates Synaptic functions

Stepping closer to treating Alzheimer’s disease patients with BACE1 inhibitor drugs

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Translational Neurodegeneration 2016年第1期5卷 107-117页

作者： Riqiang Yan Department of Neurosciences Lerner Research InstituteCleveland Clinic Foundation9500 Euclid Avenue/NC30ClevelandOH 44195USA

Alzheimer’s disease(AD)is the most common age-dependent neurodegenerative disease which impairs cognitive function and gradually causes patients to be unable to lead normal daily *** the etiology of AD remains an enigma,excessive accumulation ofβ-amyloid peptide(Aβ)is widely believed to induce pathological changes and cause dementia in brains of AD ***1 was discovered to initiate the cleavage of amyloid precursor protein(APP)at theβ-secretase *** after this cleavage doesγ-secretase further cleave the BACE1-cleaved C-terminal APP fragment to release Aβ.Hence,blocking BACE1 proteolytic activity will suppress Aβ*** to the linkage of Aβto the potential cause of AD,extensive discovery and development efforts have been directed towards potent BACE1 inhibitors for AD *** the recent breakthrough in developing brain-penetrable BACE1 inhibitors,targeting amyloid deposition-mediated pathology for AD therapy has now become more *** review will summarize various strategies that have successfully led to the discovery of BACE1 drugs,such as MK8931,AZD-3293,JNJ-54861911,E2609 and *** drugs are currently in clinical trials and their updated states will be *** the promise of reducing Aβgeneration and deposition with no alarming safety concerns,the amyloid cascade hypothesis in AD therapy may finally become validated.

关键词： Alzheimer’s disease amyloid plaques amyloid precursor protein Secretase BACE1 Aspartyl protease Drug discovery Clinical trials amyloid deposition β-amyloid peptide Fragment based drug discovery Verubecestat

Otophylloside B Protects Against AβToxicity in Caenorhabditis elegans Models of Alzheimer’s Disease

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Natural Products and Bioprospecting 2017年第2期7卷 207-214页

作者： Jie Yang Xiao-Bing Huang Qin-Li Wan Ai-Jun Ding Zhang-Lin Yang Ming-Hua Qiu Hua-Ving Sun Shu-Hua Qi Huai-Rong Luo State Key Laboratory of Phytochemistry and Plant Resources in West China Yunnan Key Laboratory of Natural Medicinal ChemistryKunming Iastitute of BotanyChinese Academy of SciencesKunming 650201Yunnan.China University of Chinese Academy of Sciences Beijing 100049China The Second Affiliated Hospital of Kunming Medical University Kunming 650101YunnanChina Key Laboratory for Aging and Regenerative Medicine Department of Pharmacology.School of PharmacySouthwest Medical UniversityLuzhou 646000SichuanChina Guangdong Key Laboratory of Marine Material Medical South China Sea Institute of OceanologyChinese Academy of SciencesGuangzhou 510301China

Alzheimer’s disease(AD)is a major public health concern worldwide and the few drugs currently available only treat the ***,there is a strong need to find more effective anti-AD *** otophyllum is a traditional Chinese medicine for treating epilepsy,and otophylloside B(Ot B),isolated from ***,is the essential active *** previously identified anti-aging effects of Ot B,we evaluated Ot B for AD prevention in *** models of AD and found that Ot B extended lifespan,increased heat stress-resistance,delayed body paralysis,and increased the chemotaxis ***,these results indicated thatOt B protects against Aβ*** mechanistic studies revealed that Ot B decreased Aβdeposition by decreasing the expression of Aβat the mRNA *** analyses showed that Ot B mediated its effects by increasing the activity of heat shock transcription factor(HSF)by upregulating the expression of hsf-1 and its target genes,hsp-12.6,hsp-16.2 and *** B also increased the expression of sod-3 by partially activating DAF-16,while SKN-1 was not essential in Ot B-mediated protection against Aβtoxicity.

关键词： Alzheimer’s disease Caenorhabditis elegans Otophylloside B β-amyloid peptide HSF-1

Chronic treatment with anesthetic propofol attenuates β-amyloid protein levels in brain tissues of aged mice

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Translational Neurodegeneration 2014年第1期3卷 46-52页

作者： Yiying Zhang Haijun Shao Yuanlin Dong Celeste A Swain Buwei Yu Weiming Xia Zhongcong Xie Geriatric Anesthesia Research Unit Department of AnesthesiaCritical Care and Pain MedicineMassachusetts General Hospital and Harvard Medical School14913th St.Room 4310CharlestownMA 02129-2060USA Department of Anesthesiology Ruijin HospitalShanghai Jiao Tong University School of Medicine200025 ShanghaiP.R.China Department of Veterans Affairs Medical Research and Development Service and Geriatric ResearchEducation and Clinical CenterBedfordMA 01730UK

Alzheimer’s disease(AD)is the most common form of *** the present time,however,AD still lacks effective *** recent studies showed that chronic treatment with anesthetic propofol attenuated brain caspase-3 activation and improved cognitive function in aged *** ofβ-amyloid protein(Aβ)is a major component of the neuropathogenesis of AD dementia and cognitive *** therefore set out to determine the effects of chronic treatment with propofol on Aβlevels in brain tissues of aged ***(50 mg/kg)was administrated to aged(18 month-old)wild-type mice once a week for 8 *** brain tissues of mice were harvested one day after the final propofol *** harvested brain tissues were then subjected to enzyme-linked immunosorbent assay(ELISA)and Western blot *** we report that the propofol treatment reduced Aβ(Aβ40 and Aβ42)levels in the brain tissues of the aged ***,the propofol treatment decreased the levels ofβ-site amyloid precursor protein cleaving enzyme(the enzyme for Aβgeneration),and increased the levels of neprilysin(the enzyme for Aβdegradation)in the brain tissues of the aged *** results suggested that the chronic treatment with propofol might reduce brain Aβlevels potentially via decreasing brain levels ofβ-site amyloid precursor protein cleaving enzyme,thus decreasing Aβgeneration;and via increasing brain neprilysin levels,thus increasing Aβ*** preliminary findings from our pilot studies have established a system and postulated a new hypothesis for future research.

关键词： Aging Alzheimer’s disease Neurodegeneration β-amyloid peptide Anesthesia Propofol

Osthole improves synaptic plasticity in the hippocampus and cognitive function of Alzheimer's disease rats via regulating glutamate

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Neural Regeneration Research 2012年第30期7卷 2325-2332页

作者： Xiaohua Dong Li Zhang Wei Li Xianyong Meng Department of Pharmacology College of Pharmacy Hebei Medical University Shijiazhuang 050017 Hebei Province China Department of Pharmacology School of Medicine Hebei North University Zhangjiakou 075000 Hebei Province China Department of Orthopedics the First Attached Hospital Hebei North University Zhangjiakou 075000 Hebei Province China

Osthole, an effective monomer in Chinese medicinal herbs, can cross the blood-brain barrier and protect against brain injury, with few toxic effects. In this study, a rat model of Alzheimer＇s disease was established after intracerebroventricular injection of β-amyloid peptide （25-35）. Subsequently the rats were intraperitoneally treated with osthole （12.5 or 25.0 mg/kg） for 14 successive days. Results showed that osthole treatment significantly improved cognitive impairment and protected hippocampal neurons of AIzheimer＇s disease rats. Also, osthole treatment alleviated suppressed long-term potentiation in the hippocampus of Alzheimer＇s disease rats. In these osthole-treated Alzheimer＇s disease rats, the level of glutamate decreased, but there was no significant change in y-amino-butyric acid. These experimental findings suggest that osthole can improve learning and memory impairment, and increase synaptic plasticity in Alzheimer＇s disease rats. These effects of osthole may be because of its regulation of central glutamate and y-amino-butyric acid levels.

关键词： osthole Alzheimer's disease learning and memory long-term potentiation glutamate y-amino-butyric acid β-amyloid peptide brain hippocampus neural regeneration

Brain-derived neurotrophic factor prevents beta-amyloid-induced apoptosis of pheochromocytoma cells by regulating Bax/Bcl-2 expression

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Neural Regeneration Research 2012年第5期7卷 347-351页

作者： Zhikun Sun Xingrong Ma Hongqi Yang Jiahua Zhao Jiewen Zhang Department of Neurology Henan Provincial People＇s Hospital Zhengzhou 450003 Henan Province China Department of Neurology the First Affiliated Hospital Zhengzhou University Zhengzhou 450052 Henan Province China

Brain-derived neurotrophic factor was utilized in the present study to treat cell injury models induced by aggregated β-amyloid（25 35）. Methylthiazolyldiphenyl-tetrazolium bromide assay and western blot analysis showed that brain-derived neurotrophic factor provided neuroprotection against cellular apoptosis by suppressing the decline in β-amyloid（25 35）-induced cell activity and the increasing ratio of Bax/Bcl-2. After treating pheochromocytoma cells with tyrosine kinase receptor B receptor inhibitor K252a, brain-derived neurotrophic factor reverses the above- mentioned changes. The experimental findings suggested that brain-derived neurotrophic factor prevented β-amyloid peptide-induced cellular apoptosis by modulating Bax/Bcl-2 expression, and this effect was associated with binding to the specific tyrosine kinase receptor B receptor.

关键词： Alzheimer's disease apoptosis β-amyloid peptide Bax brain-derived neurotrophic factor Bcl-2 tyrosine kinase receptor B