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Stabilization of Monomeric Tau Protein by All D-Enantiomeric Peptide Ligands as Therapeutic Strategy for Alzheimer's Disease and Other Tauopathies.

التفاصيل البيبلوغرافية
العنوان: Stabilization of Monomeric Tau Protein by All D-Enantiomeric Peptide Ligands as Therapeutic Strategy for Alzheimer's Disease and Other Tauopathies.
المؤلفون: Altendorf T; Institut für Biologische Informationsprozesse, IBI-7, Forschungszentrum Jülich, 52425 Jülich, Germany.; Institut für Physikalische Biologie, Heinrich-Heine-Universität Düsseldorf, 40225 Düsseldorf, Germany., Gering I; Institut für Biologische Informationsprozesse, IBI-7, Forschungszentrum Jülich, 52425 Jülich, Germany., Santiago-Schübel B; Zentralinstitut für Engineering, Elektronik und Analytik, ZEA-3, Forschungszentrum Jülich, 52425 Jülich, Germany., Aghabashlou Saisan S; Institut für Biologische Informationsprozesse, IBI-7, Forschungszentrum Jülich, 52425 Jülich, Germany., Tamgüney G; Institut für Biologische Informationsprozesse, IBI-7, Forschungszentrum Jülich, 52425 Jülich, Germany., Tusche M; Institut für Biologische Informationsprozesse, IBI-7, Forschungszentrum Jülich, 52425 Jülich, Germany., Honold D; Institut für Biologische Informationsprozesse, IBI-7, Forschungszentrum Jülich, 52425 Jülich, Germany., Schemmert S; Institut für Biologische Informationsprozesse, IBI-7, Forschungszentrum Jülich, 52425 Jülich, Germany., Hoyer W; Institut für Physikalische Biologie, Heinrich-Heine-Universität Düsseldorf, 40225 Düsseldorf, Germany., Mohrlüder J; Institut für Biologische Informationsprozesse, IBI-7, Forschungszentrum Jülich, 52425 Jülich, Germany., Willbold D; Institut für Biologische Informationsprozesse, IBI-7, Forschungszentrum Jülich, 52425 Jülich, Germany.; Institut für Physikalische Biologie, Heinrich-Heine-Universität Düsseldorf, 40225 Düsseldorf, Germany.
المصدر: International journal of molecular sciences [Int J Mol Sci] 2023 Jan 21; Vol. 24 (3). Date of Electronic Publication: 2023 Jan 21.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: MDPI Country of Publication: Switzerland NLM ID: 101092791 Publication Model: Electronic Cited Medium: Internet ISSN: 1422-0067 (Electronic) Linking ISSN: 14220067 NLM ISO Abbreviation: Int J Mol Sci Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Basel, Switzerland : MDPI, [2000-
مواضيع طبية MeSH: Alzheimer Disease*/drug therapy , Alzheimer Disease*/metabolism , Tauopathies*/drug therapy , Tauopathies*/metabolism, Humans ; tau Proteins/metabolism ; Amyloid/metabolism ; Peptides/pharmacology ; Peptides/therapeutic use
مستخلص: Alzheimer's disease and other tauopathies are the world's leading causes of dementia and memory loss. These diseases are thought to be caused by the misfolding and aggregation of the intracellular tau protein, ultimately leading to neurodegeneration. The tau protein is involved in a multitude of different neurodegenerative diseases. During the onset of tauopathies, tau undergoes structural changes and posttranslational modifications and aggregates into amyloid fibrils that are able to spread with a prion-like behavior. Up to now, there is no therapeutic agent which effectively controls or reverses the disease. Most of the therapeutics that were developed and underwent clinical trials targeted misfolded or aggregated forms of tau. In the current manuscript, we present the selection and characterization of two all D-enantiomeric peptides that bind monomeric tau protein with a low nanomolar K D , stabilize tau in its monomeric intrinsically disordered conformation, and stop the conversion of monomers into aggregates. We show that the effect of the two all D-enantiomeric peptides is strong enough to stop ongoing tau aggregation in vitro and is able to significantly reduce tau fibril assembly in cell culture. Both compounds may serve as new lead components for the development of therapeutic agents against Alzheimer's disease and other tauopathies.
References: J Biol Chem. 2019 Mar 29;294(13):4728-4737. (PMID: 30745358)
Neurosci Lett. 2000 Feb 4;279(3):129-32. (PMID: 10688046)
Rejuvenation Res. 2010 Apr-Jun;13(2-3):210-3. (PMID: 19954305)
Proc Natl Acad Sci U S A. 2000 May 9;97(10):5129-34. (PMID: 10805776)
Science. 1996 Mar 29;271(5257):1854-7. (PMID: 8596952)
Bioinformatics. 2016 Jan 1;32(1):9-16. (PMID: 26342231)
Neuron. 2014 Jun 18;82(6):1271-88. (PMID: 24857020)
J Pharmacol Exp Ther. 1990 May;253(2):884-91. (PMID: 2338660)
Neurology. 1984 Jul;34(7):939-44. (PMID: 6610841)
Mol Biosyst. 2009 Aug;5(8):783-6. (PMID: 19603110)
Appl Biochem Biotechnol. 2010 Mar;160(6):1699-722. (PMID: 19582595)
J Alzheimers Dis. 2018;61(1):265-281. (PMID: 29154274)
Acta Neuropathol. 2020 Oct;140(4):417-447. (PMID: 32728795)
Nature. 2017 Jul 13;547(7662):185-190. (PMID: 28678775)
Int J Mol Sci. 2021 Jun 18;22(12):. (PMID: 34207233)
eNeuro. 2020 May 28;7(3):. (PMID: 32393582)
J Neurosci. 2017 Aug 9;37(32):7561-7563. (PMID: 28821682)
J Am Chem Soc. 2021 Aug 25;143(33):13056-13064. (PMID: 34374536)
Proc Natl Acad Sci U S A. 1987 Oct;84(19):6953-7. (PMID: 3477820)
Chembiochem. 2003 Sep 5;4(9):811-5. (PMID: 12964153)
J Neurochem. 2008 Mar;104(6):1433-9. (PMID: 18088381)
J Biol Chem. 2001 Dec 21;276(51):48165-74. (PMID: 11606569)
J Biotechnol. 2012 Oct 15;161(2):121-5. (PMID: 22728425)
Alzheimers Res Ther. 2022 Jan 21;14(1):15. (PMID: 35063014)
J Cell Biol. 1985 Nov;101(5 Pt 1):1799-807. (PMID: 2997236)
J Alzheimers Dis. 2019;71(3):715-732. (PMID: 31476157)
Proc Natl Acad Sci U S A. 2016 Dec 13;113(50):E8187-E8196. (PMID: 27911827)
Chembiochem. 2021 Nov 3;22(21):3049-3059. (PMID: 34375027)
Alzheimers Dement (N Y). 2020 Mar 20;6(1):e12001. (PMID: 32211506)
ACS Chem Neurosci. 2021 Jul 7;12(13):2520-2528. (PMID: 34138531)
J Vis Exp. 2013 Nov 12;(81):e50934. (PMID: 24300849)
Proc Natl Acad Sci U S A. 1988 Jun;85(12):4506-10. (PMID: 3132715)
ChemMedChem. 2008 Dec;3(12):1848-52. (PMID: 19016284)
Nat Chem. 2018 Feb;10(2):170-176. (PMID: 29359764)
J Mol Recognit. 2003 Sep-Oct;16(5):260-4. (PMID: 14523938)
Sci Transl Med. 2019 May 1;11(490):. (PMID: 31043574)
Sci Rep. 2019 Apr 5;9(1):5715. (PMID: 30952881)
فهرسة مساهمة: Keywords: Alzheimer’s disease; all D-enantiomeric peptides; mirror-image phage display; tau aggregation; tauopathies
المشرفين على المادة: 0 (tau Proteins)
0 (Amyloid)
0 (Peptides)
تواريخ الأحداث: Date Created: 20230211 Date Completed: 20230214 Latest Revision: 20230214
رمز التحديث: 20230214
مُعرف محوري في PubMed: PMC9917023
DOI: 10.3390/ijms24032161
PMID: 36768484
قاعدة البيانات: MEDLINE
الوصف
تدمد:1422-0067
DOI:10.3390/ijms24032161