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Relation of plasma β-amyloid, clusterin, and tau with cerebral microbleeds: Framingham Heart Study.

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  • معلومة اضافية
    • المصدر:
      Publisher: Wiley Periodicals, Inc on behalf of American Neurological Association Country of Publication: United States NLM ID: 101623278 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2328-9503 (Electronic) Linking ISSN: 23289503 NLM ISO Abbreviation: Ann Clin Transl Neurol Subsets: MEDLINE
    • بيانات النشر:
      Original Publication: [Hoboken, NJ] : Wiley Periodicals, Inc on behalf of American Neurological Association, [2014]-
    • الموضوع:
    • نبذة مختصرة :
      Objective: Cerebral microbleeds (CMBs) are associated with higher risk of stroke and dementia, predating clinical diagnosis by several years. CMB are considered markers of cerebral small vessel disease (CSVD): hypertensive (deep CMB) and cerebral amyloid angiopathy (lobar CMB). We related plasma β-Amyloid (40, 42 and their ratio), clusterin, and tau levels to CMB to elucidate their role as biomarkers for the angiopathies represented by CMB.
      Methods: Dementia, stroke, and other neurological disease-free Framingham Heart Study participants with available CMB and biomarker measurements were included. We related biomarker levels (standardized for analyses) to CMB presence overall and stratified by brain topography (any, lobar, deep), using multivariable logistic regression analyses.
      Results: CMB were observed in 208 (5.7%) participants (mean age 57 years, 54% women). After multivariable adjustment, Aβ1-40 was associated with any CMB (OR (95%CI) 1.20 (0.99, 1.45) P = 0.062)) and lobar CMB (OR (95%CI) 1.33 (1.05, 1.68) P = 0.019), but not with deep CMB. Log-Aβ1-42 levels were not associated with CMB overall. Clusterin was related to mixed CMB (1.70 [1.05, 2.74], P = 0.031). Tau levels were associated with any CMB (OR (95%CI) 1.26 (1.07, 1.49) P = 0.006), lobar CMB (OR (95%CI) 1.26 (1.05, 1.52) P = 0.013), and with deep CMB (OR (95% CI) 1.46 (1.13, 1.89) P = 0.004).
      Interpretation: We found that plasma Aβ1-40 and Tau are associated with CMB but further studies are needed to confirm their role in hemorrhage prone CSVD represented by CMB and as indicators of ongoing subclinical neuronal injury.
      (© 2020 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.)
    • References:
      Semin Neurol. 2016 Jun;36(3):233-43. (PMID: 27214698)
      Neuroradiol J. 2017 Aug;30(4):330-335. (PMID: 28463092)
      Ann Neurol. 2004 Apr;55(4):570-5. (PMID: 15048897)
      PLoS One. 2014 Jul 30;9(7):e103351. (PMID: 25076422)
      Alzheimers Dement. 2015 Mar;11(3):249-57.e1. (PMID: 25217292)
      Sci Rep. 2016 May 31;6:26801. (PMID: 27241045)
      Acta Neuropathol. 2003 Jan;105(1):14-7. (PMID: 12471455)
      Neuromolecular Med. 2016 Mar;18(1):99-108. (PMID: 26661731)
      Mol Neurobiol. 2012 Apr;45(2):314-26. (PMID: 22274961)
      Curr Alzheimer Res. 2017;14(6):686-694. (PMID: 26502812)
      Alzheimers Dement (Amst). 2016 Jul 09;3:103-9. (PMID: 27453932)
      Int J Stroke. 2018 Jul;13(5):454-468. (PMID: 29338604)
      Alzheimers Dement. 2018 Apr;14(4):535-562. (PMID: 29653606)
      Stroke. 2018 Apr;49(4):884-890. (PMID: 29540613)
      Neurol Ther. 2017 Jul;6(Suppl 1):25-36. (PMID: 28733956)
      J Am Heart Assoc. 2018 Jul 13;7(14):. (PMID: 30006491)
      Alzheimers Dement (Amst). 2017 Sep 12;8:179-187. (PMID: 28948206)
      Lancet Neurol. 2009 Feb;8(2):165-74. (PMID: 19161908)
      Alzheimers Res Ther. 2017 Nov 23;9(1):91. (PMID: 29169407)
      Stroke. 2014 May;45(5):1492-4. (PMID: 24713533)
      Lancet Neurol. 2010 Jul;9(7):689-701. (PMID: 20610345)
      Stroke. 1997 Mar;28(3):491-9. (PMID: 9056601)
      Neurology. 1996 Mar;46(3):673-7. (PMID: 8618665)
      Proc Natl Acad Sci U S A. 2017 Aug 15;114(33):8681-8682. (PMID: 28765369)
      Neurology. 2016 Oct 25;87(17):1827-1835. (PMID: 27694257)
    • Grant Information:
      R01 NS017950 United States NS NINDS NIH HHS; R01 AG054076 United States AG NIA NIH HHS; RF1 AG059421 United States AG NIA NIH HHS; HHSN268201500001C United States HL NHLBI NIH HHS; R01 HL076784 United States HL NHLBI NIH HHS; K24 HL004334 United States HL NHLBI NIH HHS; R01 AG008122 United States AG NIA NIH HHS; R01 AG033193 United States AG NIA NIH HHS; HHSN268201500001I United States HL NHLBI NIH HHS; R01 HL067288 United States HL NHLBI NIH HHS; R03 AG048180 United States AG NIA NIH HHS; R01 AG028321 United States AG NIA NIH HHS; P30 AG066546 United States AG NIA NIH HHS; U01 AG052409 United States AG NIA NIH HHS; K23 AG038444 United States AG NIA NIH HHS; P30 AG010129 United States AG NIA NIH HHS
    • الرقم المعرف:
      0 (Amyloid beta-Peptides)
      0 (Biomarkers)
      0 (CLU protein, human)
      0 (Clusterin)
      0 (MAPT protein, human)
      0 (tau Proteins)
    • الموضوع:
      Date Created: 20200627 Date Completed: 20210722 Latest Revision: 20240922
    • الموضوع:
      20240922
    • الرقم المعرف:
      PMC7359126
    • الرقم المعرف:
      10.1002/acn3.51066
    • الرقم المعرف:
      32588552