دورية أكاديمية
أعرض في EDS

Leveraging the preformed fibril model to distinguish between alpha-synuclein inclusion- and nigrostriatal degeneration-associated immunogenicity.

التفاصيل البيبلوغرافية
العنوان: Leveraging the preformed fibril model to distinguish between alpha-synuclein inclusion- and nigrostriatal degeneration-associated immunogenicity.
المؤلفون: Stoll AC; Department of Translational Neuroscience, Michigan State University, Grand Rapids, MI, USA; Department of Pharmacology and Toxicology, Michigan State University, East Lansing, MI, USA., Sortwell CE; Department of Translational Neuroscience, Michigan State University, Grand Rapids, MI, USA. Electronic address: sortwell@msu.edu.
المصدر: Neurobiology of disease [Neurobiol Dis] 2022 Sep; Vol. 171, pp. 105804. Date of Electronic Publication: 2022 Jun 25.
نوع المنشور: Journal Article; Review; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: Academic Press Country of Publication: United States NLM ID: 9500169 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1095-953X (Electronic) Linking ISSN: 09699961 NLM ISO Abbreviation: Neurobiol Dis Subsets: MEDLINE
أسماء مطبوعة: Publication: San Diego, CA : Academic Press
Original Publication: Oxford : Blackwell Science, c1994-
مواضيع طبية MeSH: Parkinson Disease*/pathology , alpha-Synuclein*/metabolism, Humans ; Inflammation/pathology ; Lewy Bodies/metabolism ; Substantia Nigra/metabolism
مستخلص: Neuroinflammation has become a well-accepted pathologic hallmark of Parkinson's disease (PD). However, it remains unclear whether inflammation, triggered by α-syn aggregation and/or degeneration, contributes to the progression of the disease. Studies examining neuroinflammation in PD are unable to distinguish between Lewy body-associated inflammation and degeneration-associated inflammation, as both pathologies are present simultaneously. Intrastriatal and intranigral injections of alpha-synuclein (α-syn) preformed fibrils (PFFs) results in two distinct pathologic phases: Phase 1: The accumulation and peak formation of α-syn inclusions in nigrostriatal system and, Phase 2: Protracted dopaminergic neuron degeneration. In this review we summarize the current understanding of neuroinflammation in the α-syn PFF model, leveraging the distinct Phase 1 aggregation phase and Phase 2 degeneration phase to guide our interpretations. Studies consistently demonstrate an association between pathologic α-syn aggregation in the substantia nigra (SN) and activation of the innate immune system. Further, major histocompatibility complex-II (MHC-II) antigen presentation is proportionate to inclusion load. The α-syn aggregation phase is also associated with peripheral and adaptive immune cell infiltration to the SN. These findings suggest that α-syn like aggregates are immunogenic and thus have the potential to contribute to the degenerative process. Studies examining neuroinflammation during the neurodegenerative phase reveal elevated innate, adaptive, and peripheral immune cell markers, however limitations of single time point experimental design hinder interpretations as to whether this neuroinflammation preceded, or was triggered by, nigral degeneration. Longitudinal studies across both the aggregation and degeneration phases of the model suggest that microglial activation (MHC-II) is greater in magnitude during the aggregation phase that precedes degeneration. Overall, the consistency between neuroinflammatory markers in the parkinsonian brain and in the α-syn PFF model, combined with the distinct aggregation and degenerative phases, establishes the utility of this model platform to yield insights into pathologic events that contribute to neuroinflammation and disease progression in PD.
(Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)
References: Glia. 1993 Jan;7(1):84-92. (PMID: 8423066)
Adv Neurol. 1993;60:600-8. (PMID: 8380528)
PLoS One. 2015 Jun 18;10(6):e0128651. (PMID: 26087293)
J Exp Med. 2012 May 7;209(5):975-86. (PMID: 22508839)
Methods Mol Biol. 2016;1382:367-82. (PMID: 26611600)
J Parkinsons Dis. 2012;2(4):249-67. (PMID: 23938255)
Nat Med. 2018 Jul;24(7):931-938. (PMID: 29892066)
Nat Cell Biol. 2002 Feb;4(2):160-4. (PMID: 11813001)
Proc Natl Acad Sci U S A. 2020 Mar 3;117(9):4971-4982. (PMID: 32075919)
Brain. 2019 Nov 1;142(11):3565-3579. (PMID: 31580415)
PLoS One. 2010 Jan 20;5(1):e8784. (PMID: 20098715)
Proc Natl Acad Sci U S A. 2011 Mar 8;108(10):4194-9. (PMID: 21325059)
J Proteome Res. 2021 Jul 2;20(7):3428-3443. (PMID: 34061533)
Acta Neuropathol. 2017 Dec;134(6):819-838. (PMID: 28803412)
Trends Immunol. 2020 Sep;41(9):820-835. (PMID: 32819809)
Mov Disord. 2021 Sep;36(9):2036-2047. (PMID: 33547846)
Front Mol Neurosci. 2014 May 13;7:42. (PMID: 24860424)
J Exp Med. 2016 Aug 22;213(9):1759-78. (PMID: 27503075)
J Neurosci. 2013 Jun 5;33(23):9592-600. (PMID: 23739956)
Nature. 2017 Jan 26;541(7638):481-487. (PMID: 28099414)
Ann Neurol. 2005 Feb;57(2):168-75. (PMID: 15668962)
Science. 2012 Nov 16;338(6109):949-53. (PMID: 23161999)
Neurosci Lett. 1994 Jan 3;165(1-2):208-10. (PMID: 8015728)
Front Immunol. 2018 Sep 19;9:2122. (PMID: 30283455)
J Cereb Blood Flow Metab. 2002 Feb;22(2):232-9. (PMID: 11823721)
Front Immunol. 2020 Jan 31;11:33. (PMID: 32082315)
Brain. 2013 Aug;136(Pt 8):2419-31. (PMID: 23884810)
Neurobiol Aging. 2021 Oct;106:12-25. (PMID: 34225000)
Proc Natl Acad Sci U S A. 2017 Sep 26;114(39):E8284-E8293. (PMID: 28900002)
J Neuroinflammation. 2008 Feb 27;5:8. (PMID: 18304357)
Sci Rep. 2020 Mar 17;10(1):4895. (PMID: 32184415)
Exp Mol Med. 2020 Sep;52(9):1517-1525. (PMID: 32973221)
Neurobiol Aging. 2003 Mar-Apr;24(2):197-211. (PMID: 12498954)
Neurobiol Dis. 2015 Oct;82:185-199. (PMID: 26093169)
J Neurosci. 2012 May 2;32(18):6391-410. (PMID: 22553043)
J Neuroinflammation. 2018 May 1;15(1):129. (PMID: 29716614)
Exp Neurol. 2006 Feb;197(2):275-83. (PMID: 16336966)
NPJ Parkinsons Dis. 2020 Jul 9;6:15. (PMID: 32665974)
Eur J Neurosci. 2002 Mar;15(6):991-8. (PMID: 11918659)
Acta Neuropathol Commun. 2017 Nov 21;5(1):85. (PMID: 29162163)
J Neurosci. 2014 Sep 10;34(37):12368-78. (PMID: 25209277)
Nat Protoc. 2014 Sep;9(9):2135-46. (PMID: 25122523)
Glia. 2022 May;70(5):935-960. (PMID: 35092321)
Acta Neuropathol Commun. 2014 Aug 07;2:90. (PMID: 25099483)
Brain. 2020 May 1;143(5):1476-1497. (PMID: 32355963)
Nature. 2017 Jun 29;546(7660):656-661. (PMID: 28636593)
Brain. 2005 Nov;128(Pt 11):2665-74. (PMID: 16219675)
J Neurosci. 2021 Mar 3;41(9):2039-2052. (PMID: 33472823)
Front Neurol. 2018 Jun 19;9:455. (PMID: 29971039)
Environ Health Perspect. 2011 Jun;119(6):807-14. (PMID: 21245015)
Nature. 2015 Jun 18;522(7556):340-4. (PMID: 26061766)
Front Immunol. 2018 Jan 25;8:1905. (PMID: 29422891)
J Parkinsons Dis. 2022;12(4):1133-1153. (PMID: 35213388)
Proc Natl Acad Sci U S A. 2009 Nov 24;106(47):20051-6. (PMID: 19892735)
Acta Neuropathol. 2011 Jun;121(6):695-704. (PMID: 21400129)
Acta Neuropathol. 2003 Dec;106(6):518-26. (PMID: 14513261)
Trends Neurosci. 2017 Jun;40(6):358-370. (PMID: 28527591)
Neurology. 1988 Aug;38(8):1285-91. (PMID: 3399080)
PLoS One. 2012;7(6):e38545. (PMID: 22701661)
J Neuroinflammation. 2019 Dec 3;16(1):250. (PMID: 31796095)
Front Chem. 2021 Jul 07;9:666585. (PMID: 34307295)
Neurosci Lett. 1994 Oct 24;180(2):147-50. (PMID: 7700568)
Neurobiol Dis. 2020 Feb;134:104708. (PMID: 31837424)
Neurobiol Aging. 2003 Mar-Apr;24(2):245-58. (PMID: 12498958)
NPJ Parkinsons Dis. 2021 Apr 12;7(1):35. (PMID: 33846345)
Cell Rep. 2016 Sep 20;16(12):3373-3387. (PMID: 27653697)
Front Immunol. 2020 Jul 16;11:1416. (PMID: 32765501)
Nature. 2018 May;557(7706):558-563. (PMID: 29743672)
Mol Neurodegener. 2017 May 29;12(1):40. (PMID: 28552073)
Neurobiol Dis. 2017 Sep;105:84-98. (PMID: 28576704)
Nat Neurosci. 2019 Aug;22(8):1248-1257. (PMID: 31346295)
J Neural Transm Suppl. 2000;(60):277-90. (PMID: 11205147)
Cell Rep. 2015 Mar 3;10(8):1252-60. (PMID: 25732816)
Neuron. 2013 Jul 24;79(2):347-60. (PMID: 23810541)
PLoS One. 2016 Sep 13;11(9):e0162717. (PMID: 27622765)
Acta Neuropathol Commun. 2017 Feb 2;5(1):12. (PMID: 28148299)
Sci Rep. 2017 Nov 28;7(1):16533. (PMID: 29184069)
Nat Commun. 2020 Apr 20;11(1):1875. (PMID: 32313102)
Neuroscience. 2020 Jun 15;437:64-75. (PMID: 32353461)
Neurobiol Dis. 2019 Oct;130:104525. (PMID: 31276792)
Exp Neurol. 1999 Mar;156(1):50-61. (PMID: 10192776)
Brain. 2013 Apr;136(Pt 4):1128-38. (PMID: 23466394)
J Neuroinflammation. 2020 Apr 16;17(1):119. (PMID: 32299492)
Mov Disord. 2010 Dec 15;25(16):2717-23. (PMID: 20939082)
Acta Neuropathol. 2020 Jun;139(6):977-1000. (PMID: 32356200)
Front Neuroanat. 2014 Oct 13;8:114. (PMID: 25352786)
NPJ Parkinsons Dis. 2015;1:. (PMID: 27148593)
J Biol Chem. 2008 Jun 13;283(24):16895-905. (PMID: 18343814)
Brain. 2005 Dec;128(Pt 12):2777-85. (PMID: 16081470)
Proc Natl Acad Sci U S A. 2020 Jan 21;117(3):1762-1771. (PMID: 31900358)
Neuron. 2011 Oct 6;72(1):57-71. (PMID: 21982369)
Mol Ther. 2017 Oct 4;25(10):2231-2235. (PMID: 28522034)
Neurosci Res. 2021 Sep;170:330-340. (PMID: 33316306)
Parkinsonism Relat Disord. 2021 Aug;89:41-47. (PMID: 34218047)
Acta Neuropathol. 1988;76(6):550-7. (PMID: 2974227)
Neurobiol Dis. 2021 Feb;149:105229. (PMID: 33352233)
Sci Transl Med. 2018 Oct 31;10(465):. (PMID: 30381407)
NPJ Parkinsons Dis. 2018 Jul 10;4:21. (PMID: 30003140)
Mov Disord. 2022 Aug;37(8):1739-1748. (PMID: 35524682)
J Neuroinflammation. 2005 Jun 03;2:14. (PMID: 15935098)
JAMA Neurol. 2016 Nov 01;73(11):1316-1324. (PMID: 27668667)
Neurobiol Dis. 2006 Feb;21(2):404-12. (PMID: 16182554)
معلومات مُعتمدة: R21 NS099416 United States NS NINDS NIH HHS; R21 NS111333 United States NS NINDS NIH HHS; R33 NS099416 United States NS NINDS NIH HHS; T32 GM092715 United States GM NIGMS NIH HHS
فهرسة مساهمة: Keywords: Aggregation; Astrocytes; Inclusions; Microglia; Neuroinflammation; Parkinson's disease; Synucleinopathy
المشرفين على المادة: 0 (alpha-Synuclein)
تواريخ الأحداث: Date Created: 20220628 Date Completed: 20220726 Latest Revision: 20240607
رمز التحديث: 20240607
مُعرف محوري في PubMed: PMC9803935
DOI: 10.1016/j.nbd.2022.105804
PMID: 35764290
قاعدة البيانات: MEDLINE
الوصف
تدمد:1095-953X
DOI:10.1016/j.nbd.2022.105804