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Aβ的相关文献在1985年到2023年内共计39138443篇,主要集中在神经病学与精神病学、中国医学、基础医学 等领域,其中期刊论文246篇、会议论文1篇、专利文献39138196篇;相关期刊151种,包括解剖学杂志、中国老年学杂志、神经疾病与精神卫生等; 相关会议1种,包括全国老年性痴呆发病机理和药物作用靶位研讨会等;Aβ的相关文献由50000位作者贡献,包括不公告发明人、王伟、张伟等。

Aβ—发文量

期刊论文>

论文:246 占比:0.00%

会议论文>

论文:1 占比:0.00%

专利文献>

论文:39138196 占比:100.00%

总计:39138443篇

Aβ—发文趋势图

-研究学者

  • 不公告发明人
  • 王伟
  • 张伟
  • 王磊
  • 李伟
  • 张磊
  • 刘伟
  • 王勇
  • 张涛
  • 李强
  • 期刊论文
  • 会议论文
  • 专利文献

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    • Lorenzo Pini
    • 摘要: Dementia,for which there is no cure or effective treatment,is the leading cause of disability and death worldwide.Due to the high global prevalence and economic impact on families,caregivers,and communities,this condition represents one of the most significant public health challenges of our time.Dementia is an umbrella term describing a range of progressive neurodegenerative diseases,including Alzheimer’s disease(AD),which is the most common cause of cognitive and functional impairment among older adults.The presence of misfolded protein aggregates characterizes neurodegenerative disorders(e.g.,amyloid-beta()and tau in AD).
    • Evandro F.Fang; Alexander Anisimov
    • 摘要: The increase in the prevalence of individuals with Alzheimer's disease(AD)combined with the lack of a cure calls for the development of novel therapies against AD(Canter et al.,2016).The key disease-defining pathological features of AD are the accumulation of extracellular amyloid-beta()plaques(accompanied by increasing intracellular _(1-42))and higher intracellular neu rofi brilla ry tangles,comprised mostly of hyperphosphorylated tau protein/pTau(Goedert,2015;Hardy,2017).It is evident that the elderly are more predisposed to develop AD,and thus aging is considered to be the primary risk factor for AD.By extra polation,strategies that delay aging may also slow down(if not stop)AD.
    • Dalila Mango; Robert Nisticò
    • 摘要: Alzheimer's disease(AD)represents the most common form of dementia and is characterized by a progressive decline of cognitive functions.Complex multifactorial processes underlie AD pathophysiology,including amyloid-beta()toxicity,tau protein hyperphosphorylation,syna ptic dysfunction,oxidative stress,and neuroinflammation(J u and Tam,2022).
    • Annalisa Nobili; Marcello D’Amelio; Maria Teresa Viscomi
    • 摘要: Since their first description in the brains of patients suffering from Alzheimer’s disease(AD),more than 100 years ago,extracellular amyloid-β()plaques and intracellular neurofibrillary tangles have been the principal focus of AD research.However,this focus has led to the failure of several long and promising clinical trials,and the efficacy of new -targeting drugs to slow down the disease progression is still controversial despite being successful in reducing the load.
    • Frédéric Checler; Audrey Valverde
    • 摘要: The etiology of Alzheimer’s disease is far from being completely understood.Genetic approaches have helped in this matter and have greatly supported the view that theβ-amyloid precursor protein(βAPP)could be at the center of gravity of the pathology.Thus,mutations responsible for autosomal dominant aggressive forms of Alzheimer’s disease(AD)are all harbored by eitherβAPP itself or by its cleaving enzyme presenilins 1/2 referred to asγ-secretase.It was therefore convincing to note that fully independent gene products harboring AD-linked mutations,all concur to modulateβAPP proteolytic processing.These genetic clues combined with a bulk of anatomical observations and cellular manipulations pointed to the role of amyloid-β(),the main biochemical component of senile plaques that accumulate at late stages of AD.Unfortunately,a series of clinical trials designed to either abolish production or neutralize it once produced have consistently failed(Checler et al.,2021).
    • Sudip Dhakal; Ian Macreadie
    • 摘要: Alzheimer's disease AD remains one of the significant causes of death and morbidity in the older population (2021).The cause of AD remains unclear despite there being numerous hypotheses.Perhaps the most widely accepted hypothesis is the amyloid cascade hypothesis which is based on the accumulation of amyloid beta () in neurons (Dhakal et al., 2019).
    • Jason HY Yeung; Henry J Waldvogel; Richard LM Faull; Andrea Kwakowsky
    • 摘要: Alzheimer’s disease(AD)constitutes the largest proportion of dementia worldwide,with a significant associated medical burden.The major pathological hallmarks of AD include the gradual accumulation and deposition of amyloid-beta()plaques and hyperphosphorylated tau protein(Revett et al.,2013).Whilst investigations centered around the tau and hypothesis have been the main focus for the previous decades,the lack of therapeutic solutions has pushed for research into other potential therapeutic targets.
    • 朱仲康; 刘羽茜; 王冰; 张林; 王艳杰; 王哲; 柳春; 赵丹玉
    • 摘要: 目的研究六味地黄丸含药血清对诱导SH-SY5Y细胞的自噬影响及其机制,探讨阿尔茨海默病的病理机制及补肾填精法的作用机制。方法30只大鼠随机分成对照组和六味地黄丸组两组,分别予以等量的双蒸水和含六味地黄丸粉末水溶液进行灌胃,末次灌胃结束后取血并分离血清备用。将SHSY5Y细胞分为对照组、模型组和药物组,对照组和模型组给予含空白血清的完全培养液,药物组给予含含药血清的完全培养液,模型组和药物组加入1-42寡聚体,培养48 h。应用CCK-8法对各组进行细胞增殖率分析;免疫荧光法分析各组细胞内沉积情况;Western Blot法检测各组细胞BACE1、p62、LC3-Ⅰ、LC3-Ⅱ、Beclin1蛋白表达情况。结果CCK-8结果显示,与对照组相比,模型组细胞增殖率显著降低(P<0.01);与模型组相比,药物组细胞增殖率显著增高(P<0.01)。与对照组相比,模型组细胞内的沉积显著增加(P<0.01);与模型组相比,药物组细胞内的沉积显著减少(P<0.01)。Western Blot结果显示,与对照组相比,模型组细胞的BACE1、Beclin1的蛋白表达量和LC3-Ⅱ/LC3-Ⅰ的比值显著升高(P<0.01),p62的蛋白表达量显著降低(P<0.01);与模型组相比,药物组细胞的Beclin1的蛋白表达量和LC3-Ⅱ/LC3-Ⅰ的比值显著升高(P<0.01),BACE1和p62的蛋白表达量显著降低(P<0.01)。结论六味地黄丸含药血清可以增加诱导的SH-SY5Y细胞自噬相关基因的表达,上调自噬水平,减轻细胞损伤,对细胞具有明显的保护作用。
    • Jae Man Lee; Sang Ryong Kim
    • 摘要: Microglial activation in Alzheimer’s disease(AD):In 1907,Dr.Alois Alzheimer,a Bavarian-born German psychiatrist and neuropathologist,published an article describing the clinical and neuropathological features of an unclassified psychiatric disorder.The disorder was later named AD and is currently the most common brain disorder(Takata et al.,2021).AD involves the accumulation of amyloid-β()and hyperphosphorylated tau proteins in the brain,which are associated with senile plaques and neurofibrillary tangles,respectively(Vergara et al.,2019;Takata et al.,2021).AD is characterized by cognitive impairment and memory loss with hippocampal neurodegeneration(Kim et al.,2021).
    • 韩富华; 刘剑刚; 孙林娟; 乔丹丹; 詹敏
    • 摘要: 阿尔茨海默病(Alzheimei’s disease,AD)是一种以进行性记忆丧失、认知障碍和人格改变为特征的神经退行性疾病,一直以来,β淀粉样蛋白(βamyloid protein,)沉积及其神经毒性被普遍认为是AD发病的中心机制[1]。近年研究证实,蛋白沉积与线粒体功能障碍密切相关[2]。细胞中的线粒体含量是线粒体自噬和线粒体生成的净平衡,线粒体生成已经得到了清晰的认识,但是至今为止,对脑组织中的线粒体自噬尚不完全了解,目前还不知道这两种相反的机制在脑细胞活动期间如何维持平衡。本文概述了近年来自噬以及线粒体自噬在AD中的研究进展,阐述了_(42)蛋白与线粒体自噬的相互作用在AD病理过程中的重要影响。
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