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中国神经科学学会第十届全国学术会议

作者： Qi-Ying SUN Harald Hampel kaj blennow Simone Lista Allan Levey Bei-Sha TANG Rena LI Yong SHEN Center for Advanced Therapeutic Strategies for Brain Disorders Roskamp Institute Department of Neurology Xiangya HospitalCentral south university Department of Psychiatry Alzheimer Memorial CenterUniversity of Munich Department of Neurology University of Belgrade Clinical Neurochemistry Lab Department of Neuroscience and Physiology University of GothenburgSahlgren's University Hospital

Objective Evidence suggests that the tumor necrosis factor receptor(TNFR)-signaling pathway contributes to the pathogenesis of Alzheimer’s disease(AD).TNF-α converting enzyme(TACE/AD AM-17) can cleave both pro-TNF-α and TNF ***,we have shown that TACE activity in the cerebrospinal fluid(CSF) from subjects with mild cognitive impairment(MCI) and AD patients is significantly higher than that from cognitively healthy controls(HC).However,it is not clear whether TACE activity could be detected and whether TACE activity is higher than that in HC *** We examined TACE expression and ist enzamatic activity in the frontal cortex of postmortem AD cases and control ***,we also analyzed a large set of clinical sample of 64patients with AD,88 subjects with MCI,and 50 age-matched HC recruited from three distinct academic *** In the frontal cortex of AD patients,TACE protein levels and enzymatic activity tended to be higher than in HC,although the difference was not statistically *** TACE protein levels did not differ significantly in the three study groups(AD,MCI,and HC).However,plasma TACE activity was significantly higher in subjects with MCI and AD patients than in ***,in MCI and AD groups we found a significant correlation between plasma TACE activity and CSF T-tau and Aβ *** AD patients,the levels of plasma TACE activity correlated significantly and negatively with *** These findings further support the role of the TNF-α receptor complex in AD-related neuroinflammation and propose TACE plasma activity as a promising hypothesis-driven biomarker candidate for detection,diagnosis,and prognosis of prodromal and clinical AD.

关键词： mild cognitive impairment Alzheimer’s disease tumor necrosis factor converting enzyme plasma biomarker

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A phase 1b randomized clinical trial of CT1812 to measure Aβoligomer displacement in Alzheimer’s disease using an indwelling CSF catheter

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Translational Neurodegeneration 2023年第1期12卷 568-571页

作者： Kelsie M.LaBarbera Yvette I.Sheline Nicholas J.Izzo Carla M.Yuede Lora Waybright Raymond Yurko Hannah M.Edwards Woodrow D.Gardiner kaj blennow Henrik Zetterberg Anne Börjesson-Hanson Roger Morgan Charles S.Davis Robert J.Guttendorf Lon S.Schneider Steven DeKosky Harry LeVine III Michael Grundman Anthony O.Caggiano John R.Cirrito Susan M.Catalano Mary E.Hamby Cognition Therapeutics Inc. PittsburghPAUSA University of Pennsylvania PhiladelphiaUSA Washington University St.LouisUSA University of Gothenburg MölndalSweden Department of Psychiatry and Neurochemistry Institute of Neuroscience and PhysiologyThe Sahlgrenska Academy at the University of GothenburgMölndalSweden Clinical Neurochemistry Laboratory Sahlgrenska University HospitalMölndalSweden Department of Neurodegenerative Disease UCL Institute of NeurologyQueen SquareLondonUK UK Dementia Research Institute at UCL LondonUK Hong Kong Center for Neurodegenerative Diseases Clear Water BayHong KongChina Wisconsin Alzheimer’s Disease Research Center University of Wisconsin School of Medicine and Public HealthUniversity of Wisconsin-MadisonMadisonWIUSA Karolinska University Hospital StockholmSweden MedSurgPI LLCRaleighNCUSA CSD Biostatistics Inc.Oro ValleyAZUSA Aclairo Pharmaceutical Development Group IncViennaVAUSA Keck School of Medicine of USC Los AngelesCAUSA McKnight Brain Institute University of FloridaGainesvilleFLUSA Sanders-Brown Center on Aging University of KentuckyLexingtonKYUSA Global R&D Partners LLCSan DiegoCAUSA Department of Neurosciences University of CaliforniaSan DiegoUSA

Trial Registration:May 11th,2018 *** Identifier:NCT03522129 https://clini caltr ***/ct2/show/*** therapies for Alzheimer’s disease(AD)target a wide range of mechanisms,yet promising dis-ease-modifying therapies remain a huge unmet *** evidence indicates that the oligomeric form of amyloid-beta(Aβ)is a toxic species contributing to AD through synaptic damage and neuronal toxicity[1].

关键词： Alzheimer Aβ damage

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