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Investigation of a Chinese pedigree with early-onset familial Alzheimer’s disease caused by presenilin 1 p.M233T mutation
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作者 吴思 《中国医学文摘:内科学分册(英文版)》 2019年第2期122-123,共2页
Objective To analyze the clinical presentation andgenotype of a Chinese pedigree with early-onset familialAlzheimer's disease. Methods A pedigree with early-onsetfamilial Alzheimer's disease was recruited. The... Objective To analyze the clinical presentation andgenotype of a Chinese pedigree with early-onset familialAlzheimer's disease. Methods A pedigree with early-onsetfamilial Alzheimer's disease was recruited. The clinicaldata of the proband who was admitted to ShengjingHospital in March 2018 and the family members werecollected. The DNA sequences of 53 dementia relatedgenes were screened using next-generation sequencingtechnology in the blood sample of the proband. The point mutation discovered in the proband was also investigatedin some family members. Results There were five memberswith Alzheimer's disease in the pedigree,includingthe proband,a 42 years old female. The onset age of apedigree member was 33 years and that of the probandwas 37 years. A point mutation from T to C at position698 (M233T) in the exon 7 of presenilin 1 (PS1) genewas found in the proband and two other family memberswho were clinically normal. Conclusion The M233T mutationof PS1 gene can lead to early-onset familialAlzheimer's disease. This family is the first pedigree withM233T mutation of PS1 gene in China,which deservesclinical attention. 展开更多
关键词 Alzheimer a CHINESE PEDIGREE EARLY-ONSET FAMILIAL Alzheimer’s disease
Features of connected speech in patients with mild Alzheimer’s disease
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作者 李妍 《中国医学文摘:内科学分册(英文版)》 2019年第2期125-126,共2页
Objective To explore the features of connectedspeech produced by Chinese mild Alzheimer's disease(AD) patients. Methods Thirty Chinese mild AD patients( eight males and 22 females,and the age was(72. 73 ± 7. ... Objective To explore the features of connectedspeech produced by Chinese mild Alzheimer's disease(AD) patients. Methods Thirty Chinese mild AD patients( eight males and 22 females,and the age was(72. 73 ± 7. 78 ) years) and 30 age-and educationmatchednormal controls from three communities were recruitedin Xuanwu Hospital from January 2018 to May2018. All subjects completed tasks of picture naming,semantic fluency (animal),and Cookie Theft picture description.Picture description was analyzed for speechproduction ( total word output,speech rate,sound errors),lexical content (number of nouns and verbs,proportionof pronouns and verbs,semantic errors),informationcontent (information unit,idea density,efficiency),syntactic structure and complexity (mean length ofutterance,words in sentences,syntactic errors). Differencesbetween the groups were calculated. Associationbetween picture naming,semantic fluency,and measuresin picture descriptions was analyzed. 展开更多
关键词 ALZHEIMER FEATURES CONNECTED speech MILD Alzheimer’s disease
Effect of acupuncture on the ultrastructure of neurons and astrocytes in the hippocampal dentate gyrus in rats with Alzheimer’s disease induced by Aβ1-42
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作者 汤双红 《中国医学文摘:内科学分册(英文版)》 2019年第2期65-66,共2页
Objective To observe the effects of acupuncture at'Baihui'(GV 20) and'Shenshu'(BL 23) on the ultrastructure of hippocampal dentate gyrus in rats with Alzheimer’s disease. Methods Forty SPF Wistar male... Objective To observe the effects of acupuncture at'Baihui'(GV 20) and'Shenshu'(BL 23) on the ultrastructure of hippocampal dentate gyrus in rats with Alzheimer’s disease. Methods Forty SPF Wistar male rats were randomly divided into normal group,sham operation group,model group and acupuncture group,10 rats in each one. 展开更多
关键词 the ULTRASTRUCTURE of NEURONS and ASTROCYTES Alzheimer’s disease INDUCED by A Alzheimer
Mesenchymal stem cell-derived exosomes promote neurogenesis and cognitive function recovery in a mouse model of Alzheimer’s disease 预览
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作者 Edwin E. Reza-Zaldivar Mercedes A. Hernández-Sapiéns +6 位作者 Yanet K. Gutiérrez-Mercado Sergio Sandoval-ávila Ulises Gomez-Pinedo Ana L. Márquez-Aguirre Estefanía Vázquez-Méndez Eduardo Padilla-Camberos Alejandro A. Canales-Aguirre 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第9期1626-1634,共9页
Studies have shown that mesenchymal stem cell-derived exosomes can enhance neural plasticity and improve cognitive impairment.The purpose of this study was to investigate the effects of mesenchymal stem cell-derived e... Studies have shown that mesenchymal stem cell-derived exosomes can enhance neural plasticity and improve cognitive impairment.The purpose of this study was to investigate the effects of mesenchymal stem cell-derived exosomes on neurogenesis and cognitive capacity in a mouse model of Alzheimer’s disease.Alzheimer’s disease mouse models were established by injection of beta amyloid 1?42 aggregates into dentate gyrus bilaterally.Morris water maze and novel object recognition tests were performed to evaluate mouse cognitive deficits at 14 and 28 days after administration.Afterwards,neurogenesis in the subventricular zone was determined by immunofluorescence using doublecortin and PSA-NCAM antibodies.Results showed that mesenchymal stem cells-derived exosomes stimulated neurogenesis in the subventricular zone and alleviated beta amyloid 1?42-induced cognitive impairment,and these effects are similar to those shown in the mesenchymal stem cells.These findings provide evidence to validate the possibility of developing cell-free therapeutic strategies for Alzheimer’s disease.All procedures and experiments were approved by Institutional Animal Care and Use Committee(CICUAL)(approval No.CICUAL 2016-011)on April 25,2016. 展开更多
关键词 Alzheimer’s DISEASE neurodegenerative DISEASE COGNITIVE impairment memory Alzheimer’s DISEASE MOUSE model mesenchymal stem cell EXOSOMES NEUROGENESIS COGNITIVE improvement cell-free therapy neural regeneration
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Alteration of functional connectivity in patients with Alzheimer’s disease revealed by resting-state functional magnetic resonance imaging 预览
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作者 Jie Zhao Yu-Hang Du +2 位作者 Xue-Tong Ding Xue-Hu Wang Guo-Zun Men 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第2期285-292,共8页
The main symptom of patients with Alzheimer’s disease is cognitive dysfunction. Alzheimer’s disease is mainly diagnosed based on changes in brain structure. Functional connectivity reflects the synchrony of function... The main symptom of patients with Alzheimer’s disease is cognitive dysfunction. Alzheimer’s disease is mainly diagnosed based on changes in brain structure. Functional connectivity reflects the synchrony of functional activities between non-adjacent brain regions, and changes in functional connectivity appear earlier than those in brain structure. In this study, we detected resting-state functional connectivity changes in patients with Alzheimer’s disease to provide reference evidence for disease prediction. Functional magnetic resonance imaging data from patients with Alzheimer’s disease were used to show whether particular white and gray matter areas had certain functional connectivity patterns and if these patterns changed with disease severity. In nine white and corresponding gray matter regions, correlations of normal cognition, early mild cognitive impairment, and late mild cognitive impairment with blood oxygen level-dependent signal time series were detected. Average correlation coefficient analysis indicated functional connectivity patterns between white and gray matter in the resting state of patients with Alzheimer’s disease. Functional connectivity pattern variation correlated with disease severity, with some regions having relatively strong or weak correlations. We found that the correlation coefficients of five regions were 0.3–0.5 in patients with normal cognition and 0–0.2 in those developing Alzheimer’s disease. Moreover, in the other four regions, the range increased to 0.45–0.7 with increasing cognitive impairment. In some white and gray matter areas, there were specific connectivity patterns. Changes in regional white and gray matter connectivity patterns may be used to predict Alzheimer’s disease;however, detailed information on specific connectivity patterns is needed. All study data were obtained from the Alzheimer’s Disease Neuroimaging Initiative Library of the Image and Data Archive Database. 展开更多
关键词 Alzheimer's disease blood oxygen level-dependent signal correlation coefficient FUNCTIONAL connectivity pattern FUNCTIONAL magnetic resonance imaging gray MATTER RESTING state white MATTER
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Action of trichostatin A on Alzheimer’s disease-like pathological changes in SH-SY5Y neuroblastoma cells 预览
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作者 Li-Hua Li Wen-Na Peng +2 位作者 Yu Deng1 Jing-Jing Li Xiang-Rong Tian 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第2期293-301,共9页
The histone deacetylase inhibitor, trichostatin A, is used to treat Alzheimer’s disease and can improve learning and memory but its underlying mechanism of action is unknown. To determine whether the therapeutic effe... The histone deacetylase inhibitor, trichostatin A, is used to treat Alzheimer’s disease and can improve learning and memory but its underlying mechanism of action is unknown. To determine whether the therapeutic effect of trichostatin A on Alzheimer’s disease is associated with the nuclear factor erythroid 2-related factor 2(Nrf2) and Kelch-like epichlorohydrin-related protein-1(Keap1) signaling pathway, amyloid β-peptide 25–35(Aβ25–35) was used to induce Alzheimer’s disease-like pathological changes in SH-SY5 Y neuroblastoma cells. Cells were then treated with trichostatin A. The effects of trichostatin A on the expression of Keap1 and Nrf2 were detected by real-time quantitative polymerase chain reaction, western blot assays and immunofluorescence. Total antioxidant capacity and autophagy activity were evaluated by total antioxidant capacity assay kit and light chain 3-I/II levels, respectively. We found that trichostatin A increased cell viability and Nrf2 expression, and decreased Keap1 expression in SH-SY5 Y cells. Furthermore, trichostatin A increased the expression of Nrf2-related target genes, such as superoxide dismutase, NAD(P)H quinone dehydrogenase 1 and glutathione S-transferase, thereby increasing the total antioxidant capacity of SH-SY5 Y cells and inhibiting amyloid β-peptide-induced autophagy. Knockdown of Keap1 in SH-SY5 Y cells further increased trichostatin A-induced Nrf2 expression. These results indicate that the therapeutic effect of trichostatin A on Alzheimer’s disease is associated with the Keap1-Nrf2 pathway. The mechanism for this action may be that trichostatin A increases cell viability and the antioxidant capacity of SH-SY5 Y cells by alleviating Keap1-mediated inhibition Nrf2 signaling, thereby alleviating amyloid β-peptide-induced cell damage. 展开更多
关键词 Alzheimer's disease amyloid-β peptide autophagy KEAP1 signal neurocytotoxicity oxidative stress damage SH-SY5Y cells total antioxidant capacity TRANSCRIPTION factor Nrf2 TSA
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The local mammalian target of rapamycin (mTOR) modulation: a promising strategy to counteract neurodegeneration 预览
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作者 Diego Dolcetta Roberto Dominici 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第10期1711-1712,共2页
Alzheimer’s disease (AD) and the evolution of the “Amyloid Hypothesis”: The primary risk factor for dementia is aging, as the overwhelming majority of individuals who have the disease (~95%) are 65 years old or old... Alzheimer’s disease (AD) and the evolution of the “Amyloid Hypothesis”: The primary risk factor for dementia is aging, as the overwhelming majority of individuals who have the disease (~95%) are 65 years old or older, and the rate of development of AD doubles roughly every five years from that age, peaking at a nearly 50% population prevalence by the age of 85. The disease is progressive and irreversible, with an average time course of 8 to 10 years. Regardless of catastrophic forecasts for the next decades, its actual prevalence has huge family and social costs. 展开更多
关键词 Alzheimer’s disease primary risk factor family and SOCIAL COSTS
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Low-dose radiation and Alzheimer's disease:Neuronal effects and a potential modality for therapy?
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作者 Feng Li Liu Qiang +1 位作者 Wang Bing Cai Lu 《中华放射医学与防护杂志》 CAS CSCD 北大核心 2019年第8期581-589,共9页
Exposure to low-dose radiation(LDR,mostly less than 100 mGy)may reduce the vulnerability of exposed tissues to subsequent high-dose radiation(HDR)-induced damage,a phenomenon known as adaptive responses,which occurs v... Exposure to low-dose radiation(LDR,mostly less than 100 mGy)may reduce the vulnerability of exposed tissues to subsequent high-dose radiation(HDR)-induced damage,a phenomenon known as adaptive responses,which occurs via mechanisms including anti-inflammation and anti-oxidation.Alzheimer′s disease(AD)is a type of dementia that causes problems with memory,thinking,and behavior.Using the available literature,this review will examine whether there is any effect of LDR on AD.The available evidence shows that although LDR can alter the expression of some genes related to AD such as Apbb1,Lrp1,and Il1α,these alterations do not cause AD-like syndromes in animals,suggesting that LDR may also simultaneously upregulate several protective mechanisms that prevent the eventual development of AD.Furthermore,LDR seems capable of improving the symptoms of AD,as evidenced by the experience of an 81-year-old female AD patient.This patient was diagnosed with AD more than 10 years ago and gradually progressed to advanced AD in 2015,despite routine treatment.The patient then received about 12 computed tomography scans(about 40 mGy each)up until Nov.2017,which significantly improved her quality of life and reduced several AD symptoms.The improvement in this patient′s medical condition led to a few recent clinical trials investigating the effects of LDR on AD.To date,there is no efficient therapy available for AD,thus whether exposure to LDR at 100 mGy can provide a preventive or therapeutic effect for AD is an important issue.If LDR is a potential treatment for AD,as suggested by this reported case,this non-invasive approach would also bear the merit that it would be unlikely to cause a significant radiation health risk,as the LDR could be delivered locally to the head without any impact on other organs. 展开更多
关键词 LOW-DOSE radiation Alzheimer's disease Adaptive response HORMESIS NEURONAL STIMULATION
Potential preventive disease-modifying pharmacological strategies to delay late onset Alzheimer’s disease 预览
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作者 Miren Ettcheto Oriol Busquets Antoni Camins 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第10期1721-1725,共5页
Alzheimer’s disease(AD)is a progressive neurodegenerative disease that was histopathologically characterized in the brain by the presence of extracellular senile plaques made of amyloid β peptides and intracellular ... Alzheimer’s disease(AD)is a progressive neurodegenerative disease that was histopathologically characterized in the brain by the presence of extracellular senile plaques made of amyloid β peptides and intracellular neurofibrillary tangles composed of hyperphosphorylated Tau protein.Over the years,AD has been classified in two subgroups:early onset or familial AD and late onset or sporadic AD.On the one hand,familial AD has been described to be the result of genetic mutations that cause,in some cases,for the overproduction of amyloid β.On the other,the cause of late onset or sporadic AD is still unclear even though several hypotheses have been proposed to explain the process of severe and progressive memory and cognitive loss.In the present review,some of the current hypotheses that try to explain the origin of late onset or sporadic AD have been summarized.Also,their potential implication in the development of new drugs for the presymptomatic treatment of late onset or sporadic AD has been considered. 展开更多
关键词 Alzheimer's DISEASE BETA-SECRETASE NEUROINFLAMMATION Tau amyloid N-METHYL-D-ASPARTATE glutamate
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Effects of Acupuncture on Alzheimer's Disease: Evidence from Neuroimaging Studies
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作者 YU Chao-chao MA Chao-yang +4 位作者 WANG Hua KONG Li-hong ZHAO Yan SHEN Feng WU Miao 《中国结合医学杂志:英文版》 SCIE CAS CSCD 2019年第8期631-640,共10页
As the worldwide population ages, the prevalence of Alzheimer's disease (AD) increases. However, the results of promising medications have been unsatisfactory. Chinese acupuncture has a long history of treating de... As the worldwide population ages, the prevalence of Alzheimer's disease (AD) increases. However, the results of promising medications have been unsatisfactory. Chinese acupuncture has a long history of treating dementia, but lack of evidence from well-designed randomized controlled trials that validate its efficacy and safety, as well as its lack of clear underlying mechanisms, contribute to its limited application in clinical practice. In recent years, brain imaging technologies, such as functional magnetic resonance imaging and positron emission tomography, have been used to assess brain responses to acupuncture in a dynamic, visual, and objective way. These techniques are frequently used to explore neurological mechanisms of responses to acupuncture in AD and provide neuroimaging evidence as well as starting points to elucidate the possible mechanisms. This review summarizes the existing brain imaging evidence that explains the effects of acupuncture for AD and analyzes brain responses to acupuncture at cognitive-related acupoints [Baihui (GV 20), Shenmen (HT 7), Zusanli (ST 36), Neiguan (PC 6), and Taixi (KI 3)] from perspectives of acupoint specificity and acupoint combinations. Key issues and directions to consider in future studies are also put forward. This review should deepen our understanding of how brain imaging studies can be used to explore the underlying mechanisms of acupuncture in AD. 展开更多
关键词 ACUPUNCTURE Alzheimer's disease brain response ACUPOINT SPECIFICITY NEUROIMAGING
Folate/Vitamin B Alleviates Hyperhomocysteinemia-Induced Alzheimer-Like Pathologies in Rat Retina
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作者 Jing Guo Shaozhou Ni +2 位作者 Qihang Li Jian-Zhi Wang Ying Yang 《神经科学通报:英文版》 SCIE CAS CSCD 2019年第2期325-335,共11页
Hyperhomocysteinemia(Hhcy) is an independent risk factor for Alzheimer’s disease(AD). Visual dysfunction is commonly found and is positively correlated with the severity of cognitive defects in AD patients. Our previ... Hyperhomocysteinemia(Hhcy) is an independent risk factor for Alzheimer’s disease(AD). Visual dysfunction is commonly found and is positively correlated with the severity of cognitive defects in AD patients. Our previous study demonstrated that Hhcy induces memory deficits with AD-like tau and amyloid-b(Ab) pathologies in the hippocampus, and supplementation with folate and vitamin B12(FB) prevents the Hhcy-induced AD-like pathologies in the hippocampus. Here, we investigated whether Hhcy also induces AD-like pathologies in the retina and the effects of FB. An Hhcy rat model was produced by vena caudalis injection of homocysteine for14 days, and the effects of FB were assessed by simultaneous supplementation with FB in drinking water. We found that Hhcy induced vessel damage with Ab and taupathologies in the retina, while simultaneous supplementation with FB remarkably attenuated the Hhcy-induced tau hyperphosphorylation at multiple AD-related sites and Ab accumulation in the retina. The mechanisms involved downregulation of amyloid precursor protein(APP), presenilin-1, beta-site APP-cleaving enzyme 1, and protein phosphatase-2 A. Our data suggest that the retina may serve as a window for evaluating the effects of FB on hyperhomocysteinemia-induced Alzheimer-like pathologies. 展开更多
关键词 HYPERHOMOCYSTEINEMIA Alzheimer’s disease RETINA Folate VITAMIN B12
A high methionine,low folate and vitamin B6/B12 containing diet can be associated with memory loss by epigenetic silencing of netrin-1 预览
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作者 Anuradha Kalani Pankaj Chaturvedi +3 位作者 Komal Kalani Pradip K.Kamat Poonam Chaturvedi Neetu Tyagi 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第7期1247-1254,共8页
Memory-epigenetics which is the loss of memory due to epigenetic modifications can be due to the silencing of genes involved in cognitive functions and this is the basis of the current study.We hypothesize that a diet... Memory-epigenetics which is the loss of memory due to epigenetic modifications can be due to the silencing of genes involved in cognitive functions and this is the basis of the current study.We hypothesize that a diet containing high methionine and low vitamins can lead to memory impairment by increasing global DNA methylation and therefore,silencing the netrin-1 gene,which encodes the glycoprotein involved in neurogenesis,axonal guidance and maintenance of the synaptic plasticity.Wild type(C57BL/6J)mice were fed with a diet containing excess methionine(1.2%),low-folate(0.08 mg/kg),vitamin B6(0.01 mg/kg),and B12(10.4 mg/kg)for 6 weeks.Mice were examined weekly for the long-term memory function,using a passive avoidance test,which determined loss of fear-motivated long-term memory starting from the fourth week of diet.Similarly,an increase in brain%5-methyl cytosine was observed starting from the 4th week of diet in mice.Mice fed with a high methionine,low folate and vitamins containing diet showed a decrease in netrin-1 protein expression and an increase in netrin-1 gene promotor methylation,as determined by methylation-sensitive restriction enzyme-polymerase chain reaction analysis.The increase in methylation of netrin-1 gene was validated by high-resolution melting and sequencing analysis.Furthermore,the association of netrin-1 with memory was established by administering netrin that considerably restored long-term fear motivated memory.Taken together,these results suggest that a diet rich in methionine and lacking in folate and vitamin B6/B12 can induce defects in learning and memory.Furthermore,the data indicates that decrease in netrin-1 expression due to hyper-methylation of its gene can be associated with memory loss.The animal procedures were approved by the Institutional Animal Care and Use Committee,University of Louisville,USA(No.A3586-01)on February 2,2018. 展开更多
关键词 Alzheimer’s disease EPIGENETICS memory METHIONINE 5-methylcytosine METHYLATION NETRIN-1
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The Glutamatergic Postrhinal Cortex–Ventrolateral Orbitofrontal Cortex Pathway Regulates Spatial Memory Retrieval
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作者 Xinyang Qi Zhanhong Jeff Du +7 位作者 Lin Zhu Xuemei Liu Hua Xu Zheng Zhou Cheng Zhong Shijiang Li Liping Wang Zhijun Zhang 《神经科学通报:英文版》 SCIE CAS CSCD 2019年第3期447-460,共14页
A deficit in spatial memory has been taken as an early predictor of Alzheimer’s disease(AD) or mild cognitive impairment(MCI). The uncinate fasciculus(UF) is a long-range white-matter tract that connects the anterior... A deficit in spatial memory has been taken as an early predictor of Alzheimer’s disease(AD) or mild cognitive impairment(MCI). The uncinate fasciculus(UF) is a long-range white-matter tract that connects the anterior temporal lobe with the orbitofrontal cortex(OFC)in primates. Previous studies have shown that the UF impairment associated with spatial memory deficits may be an important pathological change in aging and AD, but its exact role in spatial memory is not well understood. The pathway arising from the postrhinal cortex(POR) and projecting to the ventrolateral orbitofrontal cortex(vlOFC)performs most of the functions of the UF in rodents.Although the literature suggests an association between spatial memory and the regions connected by the POR–vlOFC pathway, the function of the pathway in spatialmemory is relatively unknown. To further illuminate the function of the UF in spatial memory, we dissected the POR–vlOFC pathway in mice. We determined that the POR–vlOFC pathway is a glutamatergic structure, and that glutamatergic neurons in the POR regulate spatial memory retrieval. We also demonstrated that the POR–vlOFC pathway specifically transmits spatial information to participate in memory retrieval. These findings provide a deeper understanding of UF function and dysfunction related to disorders of memory, as in MCI and AD. 展开更多
关键词 Spatial memory Postrhinal CORTEX Ventrolateral orbitofrontal CORTEX MILD COGNITIVE IMPAIRMENT Alzheimer's disease
精神行为异常与阿尔茨海默病的关系及干预方法 预览
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作者 汤占斌 李国忠 《脑与神经疾病杂志》 2019年第5期327-330,I0001共5页
1. AD 患者的精神行为异常通过pubmed 搜索检索到的研究中,只有21.4%将精神神经症状(neuropsychiatric symptoms,NPSs)作为主要研究对象,只有17.7%做了特定的努力来测试药物或非药物干预对NPSs 的影响[1]。痴呆的精神行为异常(behaviora... 1. AD 患者的精神行为异常通过pubmed 搜索检索到的研究中,只有21.4%将精神神经症状(neuropsychiatric symptoms,NPSs)作为主要研究对象,只有17.7%做了特定的努力来测试药物或非药物干预对NPSs 的影响[1]。痴呆的精神行为异常(behavioral andpsychological symptoms of dementia,BPSD)在阿尔茨海默病(Alzheimer disease,AD)患者中的发病率较高,患者的精神行为异常症状可以是幻觉、妄想、躁动、易怒、睡眠障碍、抑郁等。 展开更多
关键词 精神行为异常 阿尔茨海默病 干预方法 Alzheimer 精神神经症状 非药物干预 pubmed BPSD
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The Theory of Dove-like Particles 预览
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作者 SUN Zuodong 《美中医学:英文版》 2019年第2期73-99,共27页
Objective:Alzheimer‘s disease(AD)has been reported for more than 100 years since its first discovery in 1906.There has been no significant progress in the study of its real causes and pathogenesis.The viewpoint of th... Objective:Alzheimer‘s disease(AD)has been reported for more than 100 years since its first discovery in 1906.There has been no significant progress in the study of its real causes and pathogenesis.The viewpoint of this paper is a heuristic viewpoint based on brain cell activation theory under such background.In this paper,the pathogenesis of sporadic AD is discussed at molecular level by applying the principles of cell physics and biology.The purpose of this paper is to harmonize the existing theories of etiology of AD and to solve the source problems that have plagued the research field of neurodegenerative diseases for a long time.Method:(1)Discuss the relationship with the existing hypothesis:the Aβprotein hypothesis,the tau protein hypothesis,the presenilin(PS)hypothesis,the apolipoprotein E(ApoE)hypothesis,the cholinergic hypothesis,the inflammatory hypothesis;(2)Demonstration:biophysical proof,medical pathological proof,biological model proof;(3)Interpretation:ion channel and blood-brain barrier,potassium ion and potassium channel,ion pump and epilepsy and cancer,A beta protein and spots and plaques,related AD solutions.Result:(1)Abeta is not the cause of AD,but the remains of brain cells after abnormal apoptosis;(2)The K^+concentration difference of 0.00001%which causes the great change of membrane potential is the effective concentration,which can not be neglected;(3)Abnormal impairment of potassium channels and early entry of sodium ions to occupy potassium positions are related to epilepsy,cancer and HeLa cells;(4)AD is a physical disease,especially transcranial magnetoelectricity stimulation,should be the first choice for treatment,which can activate abnormal neurons accurately without interfering with normal neurons.Conclusion:(1)Basic contents:excess cations are transferred from extracellular to intracellular.They compete position with potassium ions on the inner surface of cell membranes,thus abatementing the membrane potential,making action potential unable to activate calcium channels normally, 展开更多
关键词 Alzheimer ETIOLOGY CATIONIC PLACEMENT AMYLOID PLAQUE cell REMAINS physical mean.
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Brain networks modeling for studying the mechanism underlying the development of Alzheimer’s disease 预览
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作者 Shuai-Zong Si Xiao Liu +2 位作者 Jin-Fa Wang Bin Wang Hai Zhao 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第10期1805-1813,共9页
Alzheimer’s disease is a primary age-related neurodegenerative disorder that can result in impaired cognitive and memory functions.Although connections between changes in brain networks of Alzheimer’s disease patien... Alzheimer’s disease is a primary age-related neurodegenerative disorder that can result in impaired cognitive and memory functions.Although connections between changes in brain networks of Alzheimer’s disease patients have been established,the mechanisms that drive these alterations remain incompletely understood.This study,which was conducted in 2018 at Northeastern University in China,included data from 97 participants of the Alzheimer’s Disease Neuroimaging Initiative(ADNI)dataset covering genetics,imaging,and clinical data.All participants were divided into two groups:normal control(n=52;20 males and 32 females;mean age 73.90±4.72 years)and Alzheimer’s disease(n=45,23 males and 22 females;mean age 74.85±5.66).To uncover the wiring mechanisms that shaped changes in the topology of human brain networks of Alzheimer’s disease patients,we proposed a local naive Bayes brain network model based on graph theory.Our results showed that the proposed model provided an excellent fit to observe networks in all properties examined,including clustering coefficient,modularity,characteristic path length,network efficiency,betweenness,and degree distribution compared with empirical methods.This proposed model simulated the wiring changes in human brain networks between controls and Alzheimer’s disease patients.Our results demonstrate its utility in understanding relationships between brain tissue structure and cognitive or behavioral functions.The ADNI was performed in accordance with the Good Clinical Practice guidelines,US 21 CFR Part 50-Protection of Human Subjects,and Part 56-Institutional Review Boards(IRBs)/Research Good Clinical Practice guidelines Institutional Review Boards(IRBs)/Research Ethics Boards(REBs). 展开更多
关键词 nerve REGENERATION Alzheimer's disease graph theory functional magnetic resonance imaging network model link prediction NAIVE Bayes topological structures ANATOMICAL distance global EFFICIENCY local EFFICIENCY neural REGENERATION
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Nerve growth factor catches copper in neuronal inning 预览
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作者 Diego La Mendola 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第4期665-666,共2页
The physiological effect of neurotrophic factors and their role in Alzheimer’s disease(AD):Neurotrophins(NTs)are a family of homologues proteins that play an essential role in neuronal cells growth,survival and diffe... The physiological effect of neurotrophic factors and their role in Alzheimer’s disease(AD):Neurotrophins(NTs)are a family of homologues proteins that play an essential role in neuronal cells growth,survival and differentiation.These proteins include the nerve growth factor(NGF),the brain derived neurotrophic factor(BDNF),NT-3 and NT-3,also known as NT-4/5. 展开更多
关键词 ALZHEIMER COPPER differentiation.
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More than anti-malarial agents:therapeutic potential of artemisinins in neurodegeneration 预览
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作者 Bing-Wen Lu Larry Baum +2 位作者 Kwok-Fai So Kin Chiu Li-Ke Xie 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第9期1494-1498,共5页
Artemisinin,also called qinghaosu,is originally derived from the sweet wormwood plant(Artemisia annua),which is used in traditional Chinese medicine.Artemisinin and its derivatives(artemisinins)have been widely used f... Artemisinin,also called qinghaosu,is originally derived from the sweet wormwood plant(Artemisia annua),which is used in traditional Chinese medicine.Artemisinin and its derivatives(artemisinins)have been widely used for many years as anti-malarial agents,with few adverse side effects.Interestingly,evidence has recently shown that artemisinins might have a therapeutic value for several other diseases beyond malaria,including cancers,inflammatory diseases,and autoimmune disorders.Neurodegeneration is a challenging age-associated neurological disorder characterized by deterioration of neuronal structures as well as functions,whereas neuroinflammation has been considered to be an underlying factor in the development of various neurodegenerative disorders,including Alzheimer’s disease.Recently discovered properties of artemisinins suggested that they might be used to treat neurodegenerative disorders by decreasing oxidation,inflammation,and amyloid beta protein(Aβ).In this review,we will introduce artemisinins and highlight the possible mechanisms of their neuroprotective activities,suggesting that artemisinins might have therapeutic potential in neurodegenerative disorders. 展开更多
关键词 ARTEMISININ inflammation neuroinflammation NEURODEGENERATION Alzheimer’s DISEASE Parkinson’s DISEASE ANTI-OXIDATION neuroprotection neural regeneration
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Why microglia kill neurons after neural disorders?The friendly fire hypothesis 预览
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作者 Walace Gomes-Leal 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第9期1499-1502,共4页
Neuroinflammation plays a fundamental role on the pathophysiology of acute and chronic neural disorders.Microglia activation is a major event following central nervous system inflammation displaying different phenotyp... Neuroinflammation plays a fundamental role on the pathophysiology of acute and chronic neural disorders.Microglia activation is a major event following central nervous system inflammation displaying different phenotypes with beneficial and detrimental actions(a Janus face).The reason for this apparent duality is unknown.We have previously shown that following experimental middle cerebral artery occlusion in the rat brain,microglia seem to support and impair adult neurogenesis in the same ischemic striatum.Based on these results,we raised the hypothesis that in the same pathologic environment,gradients of different ligands distributed over different anatomical niches might contribute to both detrimental and beneficial microglial phenotypes.These ligands(“danger signals”)are released by dying cells and bind to microglial receptors in their membranes.Activation of different microglial receptors induces downstream biochemical pathways culminating in a spectrum of microglial phenotypes like M1 and M2 and others.In this paper,we first review the immune functions of microglia and the role of toll-like receptors on the fight against infections.We then briefly revise the dual role of microglia after neural disorders.We then propose a novel hypothesis to explain the Janus face of microglia during the pathophysiology of central nervous system diseases:the“friendly fire hypothesis”.According to this idea“danger signals”or danger associated molecular patterns released by stressed,damaged and/or dying cells during stroke,trauma and other diseases might activate microglial pattern-recognition receptors(i.e.,toll like receptors)or other unidentified receptors normally activated by pathogens.This could activate the same genetic and biochemical machinery used by microglia to fight against pathogens even in the absence of infection.According to this notion,microglia may cause bystander neuronal damage with a kind of blind“friendly fire”,fighting against a non-existing infection during non-infectious disorders,like s 展开更多
关键词 stroke trauma Alzheimer’s disease NEUROINFLAMMATION GLIAL cells PHENOTYPES degeneration neuroprotection
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ASAF: altered spontaneous activity fingerprinting in Alzheimer's disease based on multisite fMRI
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作者 Jiachen Li Dan Jin +20 位作者 Ang Li Bing Liu Chengyuan Song Pan Wang Dawei Wang Kaibin Xu Hongwei Yang Hongxiang Yao Bo Zhou Alexandre Bejanin Gael Chetelat Tong Han Jie Lu Qing Wang Chunshui Yu Xinqing Zhang Yuying Zhou Xi Zhang Tianzi Jiang Yong Liu Ying Han 《科学通报:英文版》 SCIE EI CSCD 2019年第14期998-1010,共13页
Several monocentric studies have noted alterations in spontaneous brain activity in Alzheimer's disease (AD), although there is no consensus on the altered amplitude of low-frequency fluctuations in AD patients. T... Several monocentric studies have noted alterations in spontaneous brain activity in Alzheimer's disease (AD), although there is no consensus on the altered amplitude of low-frequency fluctuations in AD patients. The main aim of the present study was to identify a reliable and reproducible abnormal brain activity pattern in AD. The amplitude of local brain activity (AM), which can provide fast mapping of spontaneous brain activity across the whole brain, was evaluated based on multisite rs-fMRI data for 688 subjects (215 normal controls (NCs), 221 amnestic mild cognitive impairment (aMCI) 252 AD). Two-sample t-tests were used to detect group differences between AD patients and NCs from the same site. Differences in the AM maps were statistically analyzed via the Stouffer's meta-analysis. Consistent regions of lower spontaneous brain activity in the default mode network and increased activity in the bilateral hippocampus/parahippocampus, thalamus, caudate nucleus, orbital part of the middle frontal gyrus and left fusiform were observed in the AD patients compared with those in NCs. Significant correlations (P?<?0.05, Bonferroni corrected) between the normalized amplitude index and Mini-Mental State Examination scores were found in the identified brain regions, which indicates that the altered brain activity was associated with cognitive decline in the patients. Multivariate analysis and leave-one-site-out cross-validation led to a 78.49% prediction accuracy for single-patient classification. The altered activity patterns of the identified brain regions were largely correlated with the FDG-PET results from another independent study. These results emphasized the impaired brain activity to provide a robust and reproducible imaging signature of AD. 展开更多
关键词 Brain SPONTANEOUS activity Multisite Biomarkers Leave-one-site-out cross-validation Alzheimer's disease