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sleep as a window to understand and regulate alzheimer's disease:emerging roles of thalamic reticular nucleus

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Neural Regeneration Research 2025年第6期20卷 1711-1712页

作者： Haoqi sun shiqian shen Robert J.Thomas M.Brandon Westover Can Zhang Department of Neurology Beth Israel Deaconess Medical CenterHarvard Medical SchoolBostonMAUSA Center for Translational Pain Research Department of AnesthesiaCritical Care and Pain MedicineMassachusetis General HospitalHarvard Medical SchoolBostonMAUSA Division of Pulmonary Critical Care and Sleep MedicineDepartment of MedicineBeth Israel Deaconess Medical CenterHarvard Medical SchoolBostonMAUSA Genetics and Aging Research Unit McCance Center for Brain HealthMass General Institute for Neurodegenerative DiseaseDepartment of NeurologyMassachusetts General HospitalHarvard Medical SchoolBostonMAUSA

Introduction:alzheimer 's disease(AD) is a common neurodegenerative disorder and the primary cause of dementia. Considerable evidence supports the “amyloid hypothesis,” stating that the pathogenesis of AD is primarily caused by the deposition of amyloid-β(Aβ), which drives tau phosphorylation, neuroinflammation, and neurodegeneration in the brain. The amyloid hypothesis is strengthened by the significant and moderate benefit of lecanemab, a humanized antibody through an anti-amyloid mechanism,showing slowed clinical decline(van Dyck et al.,2023). The recent positive results of anti-amyloid trials have brought back focus on the amyloid hypothesis through biochemical, genetic, and pharmacological approaches(Zhang, 2023).

关键词： alzheimer inflammation hypothesis

Development of a potential PET probe for HDAC6 imaging in alzheimer's disease

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Acta Pharmaceutica sinica B 2022年第10期12卷 3891-3904页

作者： Ping Bai Prasenjit Mondal Frederick A.Bagdasarian Nisha Rani Yan Liu Ashley Gomm Darcy R.Tocci se Hoon Choi Hsiao-Ying Wey Rudolph E.Tanzi Can Zhang Changning Wang Athinoula A.Martinos Center for Biomedical Imaging Department of RadiologyMassachusetts General HospitalHarvard Medical SchoolCharlestownMA 02129USA Genetics and Aging Research Unit McCance Center for Brain HealthMassGeneral Institute for Neurodegenerative DiseaseDepartment of NeurologyMassachusetts General HospitalHarvard Medical SchoolCharlestownMA 02129USA

Although the epigenetic regulatory protein histone deacetylase 6(HDAC6)has been recently implicated in the etiology of alzheimer’s disease(AD),little is known about the role of HDAC6 in the etiopathogenesis of AD and whether HDAC6 can be a potential therapeutic target for ***,we performed positron emission tomography(PET)imaging in combination with histopathological analysis to better understand the underlying pathomechanisms of HDAC6 in *** first developed[^(18)F]PB118 which was demonstrated as a valid HDAC6 radioligand with excellent brain penetration and high specificity to *** studies of[^(18)F]PB118 in 5xFAD mice showed significantly increased radioactivity in the brain compared to WT animals,with more pronounced changes identified in the cortex and *** translatability of this radiotracer for AD in a potential human use was supported by additional studies,including similar uptake profiles in non-human primates,an increase of HDAC6 in ADrelated human postmortem hippocampal tissues by Western blotting protein analysis,and our ex vivo histopathological analysis of HDAC6 in postmortem brain tissues of our ***,our findings show that HDAC6 may lead to AD by mechanisms that tend to affect brain regions particularly susceptible to AD through an association with amyloid pathology.

关键词： HDAC6 alzheimer’s disease Radiotracer PET imaging Epigenetic

Exploration of C-terminal CX3CL1 for reducing age-dependent neurodegeneration

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Neural Regeneration Research 2023年第12期18卷 2667-2668页

作者： Jacob Hudobenko Manoshi Gayen Marc RBenoit Neeraj singh Riqiang Yan Department of Neuroscience University of Connecticut HealthFarmingtonCTUSA

Owing to the increasing life expectancy, the prevalence of age-dependent neurodegenerative diseases will exert an enormous toll on our aging population, their caregivers and the healthcare system. It is anticipated th... 详细信息

关键词： diseases alzheimer prevalence

RNAi-mediated knock-down of Dab and Numb attenuate Ab levels via g-secretase mediated APP processing

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Translational Neurodegeneration 2012年第1期1卷 45-54页

作者： Zhongcong Xie Yuanlin Dong Uta Maeda Weiming Xia Rudolph E Tanzi Department of Neurology Genetics and Aging Research UnitMassGeneral Institute for Neurodegenerative DiseaseMassachusetts General Hospital and Harvard Medical SchoolCharlestownMA 02129-2060USA Department of Anesthesia and Critical Care Geriatric Anesthesia Research UnitMassachusetts General Hospital and Harvard Medical SchoolCharlestownMA 02129-2060USA Center for Neurological Diseases Harvard Institute of Medicine and Harvard Medical SchoolBostonMA 02115USA Graduate student Department of PsychologyUniversity of Southern CaliforniaLos AngelesCA 90089USA.

Amyloid-b-protein(Ab),the key component of senile plaques in alzheimer’s disease(AD)brain,is produced from amyloid precursor protein(APP)by cleavage of b-secretase and then *** adaptor proteins with phosphotyrosine-binding(PTB)domains,including Dab(gene:DAB)and Numb(gene:NUMB),can bind to and interact with the conserved YENPTY-motif in the APP *** we describe,for the first time,the effects of RNAi knock-down of Dab and Numb expression on APP processing and Ab *** knock-down of Dab and Numb in H4 human neuroglioma cells stably transfected to express either FL-APP(H4-FL-APP cells)or APP-C99(H4-APP-C99 cells)increased levels of APP-C-terminal fragments(APP-CTFs)and lowered Ab levels in both cell lines by inhibiting g-secretase cleavage of ***,RNAi knock-down of APP also reduced levels of Numb in H4-APP *** findings suggest that pharmacologically blocking interaction of APP with Dab and Numb may provide novel therapeutic strategies of *** notion of attenuating g-secretase cleavage of APP via the APP adaptor proteins,Dab and Numb,is particularly attractive with regard to therapeutic potential,given that side effects of gsecretase inhibition owing to impaired proteolysis of other g-secretase substrates,***,might be avoided.

关键词： APP impaired attractive

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

Converging multi-modality datasets to build efficient drug repositioning pipelines against alzheimer’s disease and related dementias

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Medical Review 2022年第1期2卷 110-113页

作者： Zheng Yin stephen T.C.Wong Department of systems Medicine and Bioengineering Houston Methodist Cancer Center and Ting Tsung&Wei Fong Chao Center for BRAINHouston Methodist Research InstituteWeill Cornell MedicineHouston 77030TXUSA

alzheimer’s disease and related dementias(AD/ADRD)affects more than 50 million people worldwide but there is no clear therapeutic option affordable for the general patient ***,drug repositioning studies featuring collaborations between academic institutes,medical centers,and hospitals are generating novel therapeutics candidates against these devastating diseases and filling in an important area for healthcare that is poorly represented by pharmaceutical *** drug repositioning studies converge expertise from bioinformatics,chemical informatics,medical informatics,artificial intelligence,high throughput and high-content screening and systems *** also take advantage of multi-scale,multi-modality datasets,ranging from transcriptomic and proteomic data,electronical medical records,and medical imaging to social media information of patient behaviors and emotions and epidemiology profiles of disease populations,in order to gain comprehensive understanding of disease mechanisms and drug *** proposed a recursive drug repositioning paradigm involving the iteration of three processing steps of modeling,prediction,and validation to identify known drugs and bioactive compounds for AD/*** recursive paradigm has the potential of quickly obtaining a panel of robust novel drug candidates for AD/ADRD and gaining in-depth understanding of disease mechanisms from those repositioned drug candidates,subsequently improving the success rate of predicting novel hits.

关键词： alzheimer’s disease drug repositioning modeling multi-omics prediction systems biology validation.

Extracellular Elastin Molecule Modulates alzheimer’s AβDynamics In Vitro and In Vivo by Affecting Microglial Activities

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CCs Chemistry 2021年第7期3卷 1830-1837页

作者： Jingjing Li Yao sun Yingxia Liang Jun Ma Bo Li Chao Ma Rudolph ETanzi Hongjie Zhang Kai Liu Can Zhang state Key Laboratory of Rare Earth Resource Utilization Changchun Institute of Applied ChemistryChinese Academy of SciencesChangchun Genetics and Aging Research Unit McCance Center for Brain HealthMass General Institute for Neurodegenerative DiseaseDepartment of NeurologyMassachusetts General Hospital and Harvard Medical SchoolCharlestownMA school of Engineering and Applied sciences&Department of Physics Harvard UniversityMA Department of Chemistry Tsinghua UniversityBeijing

alzheimer’s disease(AD)is a neurodegenerative disorder,and the etiology of AD has not been completely *** remains unknown how the components from the brain’s extracellular matrix(ECM),particularly fibrous entities,may influence the pathogenesis of ***,we report that treatment with elastin-like polypeptides(ELPs),a component of the brain ECM,significantly increases the extracellular levels of AD-related amyloid-beta(Aβ)peptides and decreases intracellular Aβlevels in human microglial cell model HMC3 cells(HMC3).

关键词： alzheimer’s disease Aβpeptides elastin-like polypeptides microglia phagocytosis

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维生素E与老年痴呆症机制研究（英文）

维生素E与老年痴呆症机制研究（英文）

Blood:血管系统变化可能会导致阿兹海默症

中国营养学会第十次特殊营养学术会议

作者：莫焕镳乔治亚州立大学营养系

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来源： cnki会议评论

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现代生物医学进展 2017年第15期17卷 I0003-I0003页

作者： Zu-Lin Chen Alexey s. Revenko Pradeep singh A. Robert MacLeod Erin H. Norris sidney strickland Patricia and John Rosenwald Laboratory of Neurobiology and Genetics The Rockefeller University New York NY Department of Antisense Drug Discovery Ionis Pharmaceuticals Inc. Carlsbad CA Patricia and John Rosenwald Laboratory of Neurobiology and Genetics The Rockefeller University New York NY Department of Antisense Drug Discovery Ionis Pharmaceuticals Inc. Carlsbad CA Patricia and John Rosenwald Laboratory of Neurobiology and Genetics The Rockefeller University New York NY Patricia and John Rosenwald Laboratory of Neurobiology and Genetics The Rockefeller University New York NY and

随着人口老龄化的趋势不断上升，阿兹海默症的发病成为越来越重要的健康问题。最近，科学家们试图利用各种手段清除患者大脑中造成疾病的斑块，但是药物的结果往往不尽如人意。来自洛克菲勒大学的科学家们利用一项最新的技术对阿兹海默... 详细信息

随着人口老龄化的趋势不断上升，阿兹海默症的发病成为越来越重要的健康问题。最近，科学家们试图利用各种手段清除患者大脑中造成疾病的斑块，但是药物的结果往往不尽如人意。来自洛克菲勒大学的科学家们利用一项最新的技术对阿兹海默症发病的生物学机制进行了解。意想不到的是，他们发现了一种常见于血栓以及炎症反应中的血浆成分在一些患者体内也检查得到。这并不是第一次将阿兹海默症与心血管疾病联系在了一起。”有大量证据表明锻炼身体能够帮助维持血管的健康以及血流的稳定，同时也能够有效避免阿兹海默症的发生”，神经生物学家sidney strickland说道：”另外。我们知道阿兹海默症会影响血管系统，就像糖尿病那样，提高人们血管疾病的发生风险”。

关键词：血管系统心血管疾病健康问题人口老龄化生物学机制血浆成分炎症反应生物学家