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A phase 1 open-label pilot study of low-dose interleukine-2 immunotherapy in patients with Alzheimer’s disease

Translational Neurodegeneration 2023年第1期12卷 130-133页

作者： Alireza Faridar Abdulmunaim M.Eid Aaron D.Thome Weihua Zhao David R.Beers Maria B.Pascual Mohammad O.Nakawah Gustavo C.Roman Charles S.Davis Michael Grundman Joseph C.Masdeu Stanley H.Appel Department of Neurology Houston Methodist Research Institute6565 Fannin StreetSuite P3-201HoustonTXUSA csd biostatistics Inc.Oro ValleyAZUSA Global R&D Partners LLCSan DiegoCAUSA University of California San Diego San DiegoCAUSA

Regulatory T cells(Tregs)constitute a subset of T cells that play a protective role by suppressing inflammation[1].We previously documented that the Treg immu-nomodulatory mechanisms are compromised in AD patients[2],resulting in an activation of peripheral monocytes,associated with upregulation of inflamma-tory mediators[3].Preclinical studies have suggested variable effects of Treg modification on the neurode-generative *** some studies propose that the Treg population might obstruct a selective gateway for immune cell trafficking to the CNS,thereby compromis-ing reparative immune responses[4,5],an increasing number of preclinical studies,including ours,indicate that systemic Treg expansion through interleukine-2(IL-2)administration or ex vivo expanded Treg administra-tion effectively modulates neuroinflammation and allevi-ates AD pathology[6,7].IL-2,originally described as the main T-cell growth factor,has been used in standard high doses for activation of cytotoxic T cells and NK cells[8].

关键词： inflammation patients doses

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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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