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Tytuł pozycji:

Monoaminergic impairment in Down syndrome with Alzheimer's disease compared to early-onset Alzheimer's disease.

Tytuł:
Monoaminergic impairment in Down syndrome with Alzheimer's disease compared to early-onset Alzheimer's disease.
Autorzy:
Dekker AD; Department of Neurology and Alzheimer Research Center, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.; Laboratory of Neurochemistry and Behaviour, Institute Born-Bunge, University of Antwerp, Wilrijk, Antwerp, Belgium.
Vermeiren Y; Department of Neurology and Alzheimer Research Center, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.; Laboratory of Neurochemistry and Behaviour, Institute Born-Bunge, University of Antwerp, Wilrijk, Antwerp, Belgium.
Carmona-Iragui M; Department of Neurology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau, Universitat Autonoma de Barcelona, Barcelona, Spain.; Down Medical Center, Catalan Down Syndrome Foundation, Barcelona, Spain.
Benejam B; Down Medical Center, Catalan Down Syndrome Foundation, Barcelona, Spain.
Videla L; Down Medical Center, Catalan Down Syndrome Foundation, Barcelona, Spain.
Gelpi E; Neurological Tissue Bank-Biobanc, Hospital Clinic Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer, Barcelona, Spain.
Aerts T; Laboratory of Neurochemistry and Behaviour, Institute Born-Bunge, University of Antwerp, Wilrijk, Antwerp, Belgium.
Van Dam D; Department of Neurology and Alzheimer Research Center, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.; Laboratory of Neurochemistry and Behaviour, Institute Born-Bunge, University of Antwerp, Wilrijk, Antwerp, Belgium.
Fernández S; Down Medical Center, Catalan Down Syndrome Foundation, Barcelona, Spain.
Lleó A; Department of Neurology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau, Universitat Autonoma de Barcelona, Barcelona, Spain.
Videla S; Down Medical Center, Catalan Down Syndrome Foundation, Barcelona, Spain.; Faculty of Health and Life Sciences, Department of Experimental and Health Sciences, Universitat Pompeu Fabra, Barcelona, Spain.
Sieben A; Laboratory of Neurochemistry and Behaviour, Institute Born-Bunge, University of Antwerp, Wilrijk, Antwerp, Belgium.
Martin JJ; Laboratory of Neurochemistry and Behaviour, Institute Born-Bunge, University of Antwerp, Wilrijk, Antwerp, Belgium.
Blesa R; Department of Neurology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau, Universitat Autonoma de Barcelona, Barcelona, Spain.
Fortea J; Department of Neurology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau, Universitat Autonoma de Barcelona, Barcelona, Spain.; Down Medical Center, Catalan Down Syndrome Foundation, Barcelona, Spain.
De Deyn PP; Department of Neurology and Alzheimer Research Center, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.; Laboratory of Neurochemistry and Behaviour, Institute Born-Bunge, University of Antwerp, Wilrijk, Antwerp, Belgium.; Department of Neurology and Memory Clinic, Hospital Network Antwerp (ZNA) Middelheim and Hoge Beuken, Antwerp, Belgium.
Corporate Authors:
Netherlands Brain Bank
Źródło:
Alzheimer's & dementia (Amsterdam, Netherlands) [Alzheimers Dement (Amst)] 2017 Nov 23; Vol. 10, pp. 99-111. Date of Electronic Publication: 2017 Nov 23 (Print Publication: 2018).
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Publication: 2020- : [Hoboken, NJ] : Wiley on behalf of the Alzheimer's Association
Original Publication: [Amsterdam] : Elsevier B.V., [2015]-
References:
Behav Genet. 2006 May;36(3):405-15. (PMID: 16485178)
Alzheimers Res Ther. 2015 Feb 11;7(1):7. (PMID: 25717350)
J Neural Transm (Vienna). 2007;114(8):1041-5. (PMID: 17401539)
J Neural Transm Suppl. 1999;57:221-32. (PMID: 10666678)
J Neurol Neurosurg Psychiatry. 1989 Feb;52(2):193-200. (PMID: 2539435)
J Neurol Neurosurg Psychiatry. 1987 Jun;50(6):775-8. (PMID: 2440994)
J Alzheimers Dis. 2014;41(3):819-33. (PMID: 24685637)
Neurobiol Aging. 2003 Jan-Feb;24(1):1-23. (PMID: 12493547)
Curr Alzheimer Res. 2016;13(1):18-29. (PMID: 26651341)
Ann Neurol. 1987 Apr;21(4):408-11. (PMID: 2437853)
Neurosci Lett. 1996 Jan 12;203(1):29-32. (PMID: 8742039)
Ann Neurol. 1992 Nov;32(5):667-76. (PMID: 1449247)
Brain Res. 1983 Nov 28;280(1):119-26. (PMID: 6228286)
Cortex. 2015 Dec;73:36-61. (PMID: 26343344)
Intellect Dev Disabil. 2008 Jun;46(3):215-28. (PMID: 18578579)
Ment Retard Dev Disabil Res Rev. 2007;13(3):237-46. (PMID: 17910085)
Arch Pathol Lab Med. 2001 Apr;125(4):489-92. (PMID: 11260621)
Lancet Neurol. 2014 Jun;13(6):614-29. (PMID: 24849862)
Amyloid. 2002 Jun;9(2):88-102. (PMID: 12440481)
J Neuroinflammation. 2013 Jul 16;10:84. (PMID: 23866266)
J Alzheimers Dis. 2016 Jun 15;53(3):1079-96. (PMID: 27314528)
Lancet. 1981 Jul 4;2(8236):39-40. (PMID: 6113408)
Am J Med Genet Suppl. 1990;7:274-81. (PMID: 2149962)
Neurosci Biobehav Rev. 2013 Sep;37(8):1363-79. (PMID: 23707776)
Proc Natl Acad Sci U S A. 2011 Sep 6;108(36):14968-73. (PMID: 21873225)
Nat Rev Neurosci. 2015 Sep;16(9):564-74. (PMID: 26243569)
Arch Neurol. 2003 Mar;60(3):337-41. (PMID: 12633144)
J Neurol Sci. 1987 Aug;80(1):79-89. (PMID: 2956368)
Psychol Med. 2010 Apr;40(4):611-9. (PMID: 19671216)
Lancet. 1985 Dec 14;2(8468):1368-9. (PMID: 2866421)
Neurobiol Dis. 1996 Feb;3(1):16-32. (PMID: 9173910)
J Neurol Neurosurg Psychiatry. 1987 Mar;50(3):341-4. (PMID: 2951499)
Prog Neuropsychopharmacol Biol Psychiatry. 1992;16(6):883-90. (PMID: 1381103)
Alzheimers Dement (Amst). 2017 Mar 20;8:1-10. (PMID: 28413821)
Acta Neuropathol. 2012 Jan;123(1):1-11. (PMID: 22101365)
Curr Alzheimer Res. 2016;13(1):68-83. (PMID: 26391048)
J Chromatogr A. 2014 Aug 1;1353:28-39. (PMID: 24857034)
Free Radic Biol Med. 2018 Jan;114:102-109. (PMID: 28935420)
Alzheimers Dement. 2017 Nov;13(11):1251-1260. (PMID: 28463681)
J Ment Defic Res. 1985 Jun;29 ( Pt 2):125-35. (PMID: 2411933)
J Pharmacol Exp Ther. 2003 Jun;305(3):800-11. (PMID: 12649306)
Pediatrics. 2007 Dec;120(6):e1465-71. (PMID: 17998315)
Alzheimers Dement. 2015 Jan;11(1):58-69. (PMID: 24795085)
J Neurol Sci. 1988 Jan;83(1):15-24. (PMID: 2964513)
Histopathology. 1988 Aug;13(2):125-37. (PMID: 2971602)
Prog Neurobiol. 2017 Apr;151:101-138. (PMID: 27084356)
J Alzheimers Dis. 2015;43(3):871-91. (PMID: 25125467)
Neurobiol Aging. 2014 Dec;35(12 ):2691-2700. (PMID: 24997673)
Alzheimers Dement. 2011 Jul;7(4):386-395.e6. (PMID: 21784349)
Alzheimers Dement. 2015 Jun;11(6):700-9. (PMID: 25510383)
JAMA Psychiatry. 2013 Nov;70(11):1199-205. (PMID: 24048210)
Life Sci. 1997;60(15):1231-7. (PMID: 9096240)
J Ment Defic Res. 1987 Sep;31 ( Pt 3):259-69. (PMID: 2445990)
Clin Chem. 2015 May;61(5):734-43. (PMID: 25869575)
Alzheimers Dement. 2015 May;11(5):549-60. (PMID: 25282381)
Alzheimers Dement. 2012 Jul;8(4):312-36. (PMID: 22748938)
J Alzheimers Dis. 2017;55(4):1489-1496. (PMID: 27858714)
Contributed Indexing:
Keywords: Alzheimer's disease; Cerebrospinal fluid; Dementia; Dopamine; Down syndrome; MHPG; Monoamines; Neurotransmitter; Noradrenaline; Plasma; Serotonin; Trisomy 21
Entry Date(s):
Date Created: 20180522 Latest Revision: 20220317
Update Code:
20240104
PubMed Central ID:
PMC5956808
DOI:
10.1016/j.dadm.2017.11.001
PMID:
29780859
Czasopismo naukowe
Introduction: People with Down syndrome (DS) are at high risk for Alzheimer's disease (AD). Defects in monoamine neurotransmitter systems are implicated in DS and AD but have not been comprehensively studied in DS.
Methods: Noradrenaline, adrenaline, and their metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG); dopamine and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid; and serotonin and its metabolite 5-hydroxyindoleacetic acid were quantified in 15 brain regions of DS without AD (DS, n = 4), DS with AD (DS+AD, n = 17), early-onset AD (EOAD, n = 11) patients, and healthy non-DS controls (n = 10) in the general population. Moreover, monoaminergic concentrations were determined in cerebrospinal fluid (CSF)/plasma samples of DS (n = 37/149), DS with prodromal AD (DS+pAD, n = 13/36), and DS+AD (n = 18/40).
Results: In brain, noradrenergic and serotonergic compounds were overall reduced in DS+AD versus EOAD, while the dopaminergic system showed a bidirectional change. For DS versus non-DS controls, significantly decreased MHPG levels were noted in various brain regions, though to a lesser extent than for DS+AD versus EOAD. Apart from DOPAC, CSF/plasma concentrations were not altered between groups.
Discussion: Monoamine neurotransmitters and metabolites were evidently impacted in DS, DS+AD, and EOAD. DS and DS+AD presented a remarkably similar monoaminergic profile, possibly related to early deposition of amyloid pathology in DS. To confirm whether monoaminergic alterations are indeed due to early amyloid β accumulation, future avenues include positron emission tomography studies of monoaminergic neurotransmission in relation to amyloid deposition, as well as relating monoaminergic concentrations to CSF/plasma levels of amyloid β and tau within individuals.

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