Lag-time in Alzheimer's disease patients: a potential plasmatic oxidative stress marker associated with ApoE4 isoform.

Age-associated diseases Alzheimer’s disease Oxidative stress Vascular dysfunction

Journal

Immunity & ageing : I & A
ISSN: 1742-4933
Titre abrégé: Immun Ageing
Pays: England
ID NLM: 101235427

Informations de publication

Date de publication:
2019
Historique:
received: 17 12 2018
accepted: 14 03 2019
entrez: 16 4 2019
pubmed: 16 4 2019
medline: 16 4 2019
Statut: epublish

Résumé

In the brain, Oxidative Stress (OS) contribute to structural and functional changes associated with vascular aging, such as endothelial dysfunction, extracellular matrix degradation, resulting in age-related reduced vasodilatation in response to agonists. For this reason, OS is considered a key factor in Alzheimer's Disease (AD) development and recent evidence correlated oxidative stress with vascular lesion in the pathogenesis of AD, but the mechanism still need to be fully clarified. The etiology of AD is still not completely understood and is influenced by several factors including Apolipoprotein E (ApoE) genotype. In particular, the Apo ε4 isoform is considered a risk factor for AD development. This study was aimed to evaluate the possible relationship between three plasmatic OS marker and Apo ε4 carrier status. Plasmatic soluble receptor for advanced glycation end products (sRAGE) levels, plasma antioxidant total defenses (by lag-time method) and plasmatic Reactive Oxygen species (ROS) levels were evaluated in 25 AD patients and in 30 matched controls. ROS were significantly higher while plasma antioxidant total defenses and sRAGE levels were significantly lower in AD patients compared to controls. In AD patients lag-time values show a significant positive linear correlation with sRAGE levels and a (even not significant) negative correlation with ROS levels. Lag-time is significantly lower in ε4 carrier (

Identifiants

pubmed: 30984280
doi: 10.1186/s12979-019-0147-x
pii: 147
pmc: PMC6444862
doi:

Types de publication

Journal Article

Langues

eng

Pagination

7

Déclaration de conflit d'intérêts

The study was carried out in accordance with recommendation of ethical committee of Fondazione IRCCS Ca′ Granda Ospedale Maggiore Policlinico (approval number: 441/2016) All subjects gave written informed consent in accordance with the Declaration of Helsinki.Not applicable.The authors declare that they have no competing interests.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Références

Clin Biochem. 1999 Apr;32(3):171-7
pubmed: 10383076
Free Radic Biol Med. 1999 Sep;27(5-6):544-53
pubmed: 10490274
Neurobiol Dis. 2000 Feb;7(1):23-37
pubmed: 10671320
Neurobiol Aging. 2000 Mar-Apr;21(2):321-30
pubmed: 10867217
Neurology. 2000 Jun 27;54(12):2319-21
pubmed: 10881261
Haematologica. 2001 Jan;86(1):85-91
pubmed: 11146576
Brain Pathol. 2002 Jan;12(1):21-35
pubmed: 11770899
Arch Neurol. 2002 Jun;59(6):972-6
pubmed: 12056933
Neurobiol Aging. 2006 Feb;27(2):262-9
pubmed: 16399211
J Nephrol. 2008 Nov-Dec;21(6):924-30
pubmed: 19034878
Curr Neuropharmacol. 2009 Mar;7(1):65-74
pubmed: 19721819
J Alzheimers Dis. 2013;33(1):77-83
pubmed: 22914590
J Alzheimers Dis. 2013;33(3):823-9
pubmed: 23076075
Free Radic Res. 2013 Aug;47(8):569-76
pubmed: 23668794
Cell Signal. 2013 Nov;25(11):2185-97
pubmed: 23838007
Free Radic Biol Med. 2013 Dec;65:595-606
pubmed: 23933528
Oxid Med Cell Longev. 2013;2013:316523
pubmed: 23983897
Mol Neurobiol. 2016 Jan;53(1):648-661
pubmed: 25511446
Expert Opin Investig Drugs. 2015 Mar;24(3):393-9
pubmed: 25586103
Arch Toxicol. 2015 Oct;89(10):1669-80
pubmed: 26126631
Rev Neurosci. 2015;26(6):691-8
pubmed: 26226128
Neurobiol Dis. 2015 Oct;82:593-606
pubmed: 26311408
Tissue Barriers. 2015 Sep 11;4(1):e1090524
pubmed: 27141417
Curr Clin Pharmacol. 2016;11(2):118-27
pubmed: 27164965
Antioxid Redox Signal. 2016 Dec 1;25(16):886-901
pubmed: 27392670
J Neurol Sci. 2017 Feb 15;373:295-302
pubmed: 28131209
Br J Pharmacol. 2018 Apr;175(8):1279-1292
pubmed: 28430357
Int Psychogeriatr. 2017 Sep;29(9):1525-1534
pubmed: 28539135
Alzheimers Dement (Amst). 2017 Sep 06;8:196-207
pubmed: 28951883
Redox Biol. 2018 Apr;14:450-464
pubmed: 29080524
Biomark Med. 2018 Mar;12(3):201-203
pubmed: 29436240
Front Physiol. 2018 Jul 03;9:806
pubmed: 30018565
Biochem Mol Biol Int. 1994 Apr;32(5):983-94
pubmed: 8069247
Nat Genet. 1996 Sep;14(1):55-61
pubmed: 8782820
Free Radic Biol Med. 1997;23(1):134-47
pubmed: 9165306

Auteurs

Luca Massaccesi (L)

1Department of Biomedical Sciences for Health, Università degli Studi di Milano, Milan, Italy.

Emanuela Galliera (E)

1Department of Biomedical Sciences for Health, Università degli Studi di Milano, Milan, Italy.
2IRCCS Galeazzi Orthopaedic Institute, Milan, Italy.

Daniela Galimberti (D)

3Department of Pathophysiology and Transplantation, Università degli Studi di Milano, Centro "Dino Ferrari", Milan, Italy.
4U.O.S.D. Neurologia-Malattie Neurodegenerative, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.

Chiara Fenoglio (C)

3Department of Pathophysiology and Transplantation, Università degli Studi di Milano, Centro "Dino Ferrari", Milan, Italy.
4U.O.S.D. Neurologia-Malattie Neurodegenerative, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.

Marina Arcaro (M)

4U.O.S.D. Neurologia-Malattie Neurodegenerative, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.

Giancarlo Goi (G)

5Department of Biomedical, Surgical and Dental Sciences, Università degli Studi di Milano, Milan, Italy.

Alessandra Barassi (A)

6Department of Health's Science, Università degli Studi di Milano, Milan, Italy.

Massimiliano Marco Corsi Romanelli (MM)

1Department of Biomedical Sciences for Health, Università degli Studi di Milano, Milan, Italy.
7U.O.C SMEL-1 Patologia Clinica IRCCS Policlinico San Donato, San Donato, Milan, Italy.

Classifications MeSH