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A pancreatic player in dementia:pathological role for islet Amyloid polypeptide accumulation in the brain

Neural Regeneration Research 2023年第10期18卷 2141-2146页

作者： Angelina S.Bortoletto Ronald J.Parchem Center for Cell and Gene Therapy Stem Cell and Regenerative Medicine CenterDepartment of NeuroscienceDepartment of Molecular and Cellular BiologyTranslational Biology and Molecular Medicine ProgramMedical Scientist Training ProgramBaylor College of MedicineHoustonTXUSA

Type 2 diabetes mellitus patients have a markedly higher risk of developing dementia.While multiple factors contribute to this predisposition,one of these involves the increased secretion of amylin,or islet Amyloid polypeptide,that accompanies the pathophysiology of type 2 diabetes mellitus.Islet Amyloid polypeptide accumulation has undoubtedly been implicated in various forms of dementia,including Alzheimer’s disease and vascular dementia,but the exact mechanisms underlying islet Amyloid polypeptide’s causative role in dementia are unclear.In this review,we have summarized the literature supporting the various mechanisms by which islet Amyloid polypeptide accumulation may cause neuronal damage,ultimately leading to the clinical symptoms of dementia.We discuss the evidence for islet Amyloid polypeptide deposition in the brain,islet Amyloid polypeptide interaction with other Amyloids implicated in neurodegeneration,neuroinflammation caused by islet Amyloid polypeptide deposition,vascular damage induced by islet Amyloid polypeptide accumulation,and islet Amyloid polypeptide-induced cytotoxicity.There are very few therapies approved for the treatment of dementia,and of these,clinical responses have been controversial at best.Therefore,investigating new,targetable pathways is vital for identifying novel therapeutic strategies for treating dementia.As such,we conclude this review by discussing islet Amyloid polypeptide accumulation as a potential therapeutic target not only in treating type 2 diabetes mellitus but as a future target in treating or even preventing dementia associated with type 2 diabetes mellitus.

关键词： Alzheimer’s disease amylin Amyloid dementia diabetes human islet Amyloid polypeptide islet Amyloid polypeptide protofibrils type 2 diabetes mellitus vascular dementia

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Neuroprotective effect of hydroxy-α-sanshool against β-Amyloid-induced damage in differentiated PC12 cells

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Chinese Medical Journal 2023年第17期136卷 2140-2142页

作者： Shufang Shan Siquan Zhou Guochen Ma Xiaoyu Wang Jingyuan Xiong Guo Cheng Laboratory of Molecular Translational Medicine Center for Translational MedicineKey Laboratory of Birth Defects and Related Diseases of Women and Children(Sichuan University)Ministry of EducationDepartment of PediatricsWest China Second University HospitalSichuan UniversityChengduSichuan 610041China Healthy Food Evaluation Research Center West China School of Public Health and West China Fourth HospitalSichuan UniversityChengduSichuan 610041China

To the Editor:Alzheimer’s disease(AD)is a chronic neurodegenerative disorder that accounts for approximately 70%of global dementia cases and leads to cognitive and behavioral impairments.[1]Neuritic plaques and neurofibrillary tangles are the pathological hallmarks of AD and are related to the accumulation of b-Amyloid(Ab)peptides in cerebral tissues and cytoskeletal changes,which arise from the hyperphosphorylation of microtubule-associated tau proteins in neurons.Oxidative stress is among the earliest events in AD pathogenesis.The accumulation of Ab could promote the production of reactive oxygen species(ROS)and consequently lipid peroxidation,protein oxidation,and tau hyperphosphorylation,exerting toxic effects on synapses and neurons.In turn,oxidative stress could increase Ab production.Therefore,antioxidant therapy is becoming a popular strategy for treating AD.

关键词： protective Amyloid peroxidation

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Misfolded Amyloid-βstrains and their potential roles in the clinical and pathological variability of Alzheimer’s disease

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Neural Regeneration Research 2023年第1期18卷 119-120页

作者： Sara Kelley Nelson Perez-Urrutia Rodrigo Morales Department of Neurology University of Texas Health Science Center at HoustonHoustonTXUSA Centro Integrativo de Biologia y Quimica Aplicada(CIBQA) Universidad Bernardo O’HigginsSantiagoChile

Potential causes for the clinical and pathological variability observed in Alzheimer’s disease(AD):AD is an age-related neurodegenerative disorder characterized by the impairment of cognitive functions such as memory,learning,and reasoning.These commonly described clinical symptoms are due to particular pathological changes in the brain,including inflammation,synaptic loss,and neuronal death.These changes are a consequence of the accumulation of abnormally folded Amyloid-β(Aβ)and tau proteins in specific areas of the central nervous system.Considering the progressive aging of the world’s population,the number of people affected by AD is expected to substantially and consistently increase in the coming years.This positions AD as one of the main public health challenges in the near future.

关键词： clinical Alzheimer Amyloid

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Heat shock factor 1 is a direct anti-Amyloid factor:connecting neurodegeneration and uncontrolledgrowth

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Neural Regeneration Research 2022年第3期17卷 559-560页

作者： Zijian Tang Chengkai Dai Mouse Cancer Genetics Program Center for Cancer ResearchNational Cancer InstituteFrederickMDUSA

Worldwide,more than 40 million people are afflicted with Alzheimer's disease(AD)(Esquerda-Canals et al.,2017).AD is a devastating neurodegenerative disroder characterized by progressive decline in cognitive abilities.A hallmark of AD and other neurodegenerative disorders in humans is the aggregation of proteins into Amyloid fibrils and their deposition into plaques and intracellular inclusions(Iadanza et al.)。

关键词： Amyloid al. Alzheimer

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Association between QRS voltages and Amyloid burden in patients with cardiac Amyloidosis

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Chinese Medical Journal 2024年第3期137卷 365-367页

作者： Jing-Hui Li Changcheng Li Yucong Zheng Kai Yang Yan Huang Huixin Zhang Xianmei Li Xiuyu Chen Linlin Dai Tian Lan Yang Sun Minjie Lu Shihua Zhao Department of Magnetic Resonance Imaging Fuwai HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100037China Department of Radiology Taian City Central Hospital(The Affiliated Taian City Central Hospital of Qingdao University)Tai’anShandong 271099China Department of Radiology Tsinghua University HospitalTsinghua UniversityBeijing 100084China Department of Radiology The Fifth People’s Hospital of Huai’anHuai’anJiangsu 223001China Department of Radiology Geriatric Hospital of Nanjing Medical UniversityNanjingJiangsu 210000China Department of Cardiology Peking Union Medical College HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100730China Department of Pathology Fuwai HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100037China

To the Editor:Cardiac Amyloidosis(CA)is an infiltrative cardiomyopathy characterized by extracellular deposition of misfolded insoluble Amyloid fibrils.^([1])Electrocardiography(ECG)is an essential diagnostic test characterized by low QRS voltages in CA,observed in 20–74%of patients.^([2])Cipriani et al^([3])reported that low QRS voltages could independently predict cardiovascular death.But the mechanisms underlying low QRS voltages in CA remain unclear.

关键词： Amyloid patients death.

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Rationally designed Amyloid inhibitors based on Amyloid-related structural studies

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Chinese Chemical Letters 2023年第2期34卷 7-17页

作者： Jinjian Hu Yufen Zhao Yanmei Li Department of Chemistry Key Lab of Bioorganic Phosphorus Chemistry&Chemical BiologyTsinghua UniversityBeijing 100084China Beijing Institute for Brain Disorders Beijing 100069China Center for Synthetic and Systems Biology Tsinghua UniversityBeijing 100084China Institute of Drug Discovery Technology Ningbo UniversityNingbo 315221China

Amyloid proteins correlate with a series of degenerative diseases. Targeting Amyloid aggregation has remained a hot topic in therapeutic studies. Numerous inhibitors have been developed, but very few have been approved for marketing. Meanwhile, the growing knowledge of Amyloid structural characteristics provides a basis for the rational design of inhibitors. Here we introduce the high-resolution structural findings of Amyloid fibrils in recent years and discuss the reported strategies toward rationally designed inhibitors based on Amyloid-related structural studies.

关键词： Amyloid Amyloid structure Degenerative disease Amyloid inhibitor Rational design

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LL-37 and CsgC exemplify the crosstalk between anti-Amyloid, antimicrobial, and anti-biofilm protein activities

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Neural Regeneration Research 2023年第5期18卷 1027-1028页

作者： Jaime Santos Salvador Ventura Irantzu Pallares Institut de Biotecnologia i Biomedicina Departament de Bioquímica i Biologia Molecular Universitat Autònoma de Barcelona

Protein misfolding and aggregation into Amyloid fibrils is the main pathological hallmark of neurodegenerative diseases,including Alzheimer’s,Parkinson’s,Huntington’s,and prion diseases(Chiti and Dobson,2017).These insoluble fibrillar deposits possess a common structure characterized by a cross-β-sheet conformation in which β-strands run transversely to the fiber axis and form an intermolecular network of hydrogen bonds.

关键词： Amyloid Huntington diseases

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APOE ε4-dependent effects on the early Amyloid pathology in induced neurons of patients with Alzheimer’s disease

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Translational Neurodegeneration 2022年第1期11卷 248-261页

作者： Hongwon Kim Siyoung Kim Byounggook Cho Jaein Shin Jongpil Kim Department of Biomedical Engineering Dongguk UniversityPildong-ro 1-gil 30Jung-GuSeoul 04620Republic of Korea Laboratory of Stem Cells&Gene Editing Department of ChemistryDongguk UniversityPildong-ro 1-gil 30Jung-GuSeoul 04620Republic of Korea.

Background: The ε4 allele of apolipoprotein E (APOE ε4) is the strongest known genetic risk factor for late-onset Alzheimer’s disease (AD), associated with Amyloid pathogenesis. However, it is not clear how APOE ε4 accelerates Amyloid-beta (Aβ) deposition during the seeding stage of Amyloid development in AD patient neurons. Methods: AD patient induced neurons (iNs) with an APOE ε4 inducible system were prepared from skin fibroblasts of AD patients. Transcriptome analysis was performed using RNA isolated from the AD patient iNs expressing APOE ε4 at Amyloid-seeding and Amyloid-aggregation stages. Knockdown of IGFBP3 was applied in the iNs to investigate the role of IGFBP3 in the APOE ε4-mediated Amyloidosis. Results: We optimized Amyloid seeding stage in the iNs of AD patients that transiently expressed APOE ε4. Remarka-bly, we demonstrated that Aβ pathology was aggravated by the induction of APOE ε4 gene expression at the Amyloid early-seeding stage in the iNs of AD patients. Moreover, transcriptome analysis in the early-seeding stage revealed that IGFBP3 was functionally important in the molecular pathology of APOE ε4-associated AD. Conclusions: Our findings suggest that the presence of APOE ε4 at the early Aβ-seeding stage in patient iNs is critical for aggravation of sporadic AD pathology. These results provide insights into the importance of APOE ε4 expression for the progression and pathogenesis of sporadic AD.

关键词： Alzheimer’s disease Direct conversion Apolipoprotein E Induced neuron Amyloid Presenilin

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Mechanosensitivity of N-methyl-D-aspartate receptors(NMDAR)is the key through which Amyloid beta oligomers activate them

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Neural Regeneration Research 2022年第6期17卷 1263-1264页

作者： Giulia Fani Fabrizio Chiti Department of Experimental and Clinical Biomedical Sciences Section of BiochemistryUniversity of FlorenceFlorenceItaly

Alzheimer’s disease(AD)is one of the major forms of dementia,accounting for 60 to 80%of the cases of dementia,affecting approximately 50 million people worldwide,which is why it has become an object of great interest in both the medical and social fields(Source:Alzheimer’s Association).One of the main histopathological hallmarks of AD is the formation and accumulation of senile plaques in the brain parenchyma,mainly composed by fibrillar aggregates of the Amyloidβ(Aβ)peptide.This peptide is generated by the cleavage of the membrane protein named Amyloidβprecursor protein,and its secretion in the extracellular space leads to its aggregation into Amyloid fibrils.Various intermediates of this process of aggregation have been identified,and it was found that prefibrillar,soluble oligomeric forms of Aβare more likely to be the pathological species(Benilova et al.,2012).

关键词： Amyloid Alzheimer Aβ

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Plasma Amyloid-beta oligomer and phosphorylated tau:diagnostic tools for progressive Alzheimer's disease

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Neural Regeneration Research 2023年第11期18卷 2391-2392页

作者： Seong Soo A.An John P.Hulme Department of Bionano Technology Gachon Bionano Research InstituteGachon UniversitySeongnam-siGyeonggi-doSouth Korea

Introduction:Spanning the three stages of the Alzheimer’s disease (AD) continuum,Amyloid-beta(Aβ40and Aβ42) oligomers (AβO’s) and tau protein constitute a set of biomarkers ideally suited for the non-invasive monitoring of AD (Wolgin et al.,2022).AD progression is correlated with the presence of low molecular weight oligomers and not Amyloid plaques.Moreover,low molecular weight AβO is present in the beginning and later stages of disease even when the plaque burden becomes prevalent.Furthermore.

关键词： Amyloid tau Alzheimer

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