Peripheral alpha-synuclein levels in patients with genetic and non-genetic forms of Parkinson's disease.


Journal

Parkinsonism & related disorders
ISSN: 1873-5126
Titre abrégé: Parkinsonism Relat Disord
Pays: England
ID NLM: 9513583

Informations de publication

Date de publication:
04 2020
Historique:
received: 22 09 2019
revised: 11 02 2020
accepted: 19 03 2020
pubmed: 3 4 2020
medline: 30 3 2021
entrez: 3 4 2020
Statut: ppublish

Résumé

Variations of α-synuclein levels have been reported in serum and plasma in Parkinson's Disease (PD) Patients. Serum and plasma were obtained from PD patients without known mutations (GU-PD, n = 124)), carriers of the A53T/G209A point mutation in the α-synuclein gene (SNCA) (n = 29), and respective age-/sex-matched controls. Levels of total α-synuclein were assessed using an in-house ELISA assay. A statistically significant increase of α-synuclein levels was found in serum, but not plasma, from GU-PD patients compared to healthy controls. A statistically significant decrease of α-synuclein levels was found in serum and plasma from symptomatic A53T mutation carriers compared to healthy controls. Plasma α-synuclein levels were modestly negatively correlated with UPDRS part III score and disease duration in A53T-PD patients. Increased α-synuclein levels in serum of GU-PD patients suggest a systemic deregulation of α-synuclein homeostasis in PD. The opposite results in A53T-PD highlight the complexity of α-synuclein homeostatic regulation in PD, and suggest the possibility of reduced expression of the mutant allele.

Sections du résumé

BACKGROUND
Variations of α-synuclein levels have been reported in serum and plasma in Parkinson's Disease (PD) Patients.
METHODS
Serum and plasma were obtained from PD patients without known mutations (GU-PD, n = 124)), carriers of the A53T/G209A point mutation in the α-synuclein gene (SNCA) (n = 29), and respective age-/sex-matched controls. Levels of total α-synuclein were assessed using an in-house ELISA assay.
RESULTS
A statistically significant increase of α-synuclein levels was found in serum, but not plasma, from GU-PD patients compared to healthy controls. A statistically significant decrease of α-synuclein levels was found in serum and plasma from symptomatic A53T mutation carriers compared to healthy controls. Plasma α-synuclein levels were modestly negatively correlated with UPDRS part III score and disease duration in A53T-PD patients.
CONCLUSION
Increased α-synuclein levels in serum of GU-PD patients suggest a systemic deregulation of α-synuclein homeostasis in PD. The opposite results in A53T-PD highlight the complexity of α-synuclein homeostatic regulation in PD, and suggest the possibility of reduced expression of the mutant allele.

Identifiants

pubmed: 32234683
pii: S1353-8020(20)30070-5
doi: 10.1016/j.parkreldis.2020.03.014
pii:
doi:

Substances chimiques

SNCA protein, human 0
alpha-Synuclein 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

35-40

Informations de copyright

Copyright © 2020 Elsevier Ltd. All rights reserved.

Auteurs

Evangelia Emmanouilidou (E)

Center of Basic Research, Biomedical Research Foundation of the Academy of Athens, Athens, Greece; Laboratory of Biochemistry, Department of Chemistry, National and Kapodistrian University of Athens, Athens, Greece.

Nikolaos Papagiannakis (N)

Center of Clinical Research, Experimental Surgery and Translational Research, Biomedical Research Foundation of the Academy of Athens, Athens, Greece; First Department of Neurology, National and Kapodistrian University of Athens Medical School, Athens, Greece; Second Department of Neurology, National and Kapodistrian University of Athens Medical School, Athens, Greece.

Stella Kouloulia (S)

Laboratory of Analytical Chemistry, Department of Chemistry, National and Kapodistrian University of Athens, Greece.

Aikaterini Galaziou (A)

Laboratory of Analytical Chemistry, Department of Chemistry, National and Kapodistrian University of Athens, Greece.

Roubina Antonellou (R)

Second Department of Neurology, National and Kapodistrian University of Athens Medical School, Athens, Greece.

Dimitra Papadimitriou (D)

Department of Neurology, Henry Dunant Hospital Center, Greece.

Aglaia Athanasiadou (A)

Department of Biology, University of Patras Medical School, Greece.

Maria Bozi (M)

Second Department of Neurology, National and Kapodistrian University of Athens Medical School, Athens, Greece.

Christos Koros (C)

First Department of Neurology, National and Kapodistrian University of Athens Medical School, Athens, Greece.

Matina Maniati (M)

Center of Clinical Research, Experimental Surgery and Translational Research, Biomedical Research Foundation of the Academy of Athens, Athens, Greece.

Kostas Vekrellis (K)

Center of Basic Research, Biomedical Research Foundation of the Academy of Athens, Athens, Greece.

Penelope C Ioannou (PC)

Laboratory of Analytical Chemistry, Department of Chemistry, National and Kapodistrian University of Athens, Greece.

Leonidas Stefanis (L)

Center of Clinical Research, Experimental Surgery and Translational Research, Biomedical Research Foundation of the Academy of Athens, Athens, Greece; First Department of Neurology, National and Kapodistrian University of Athens Medical School, Athens, Greece; Second Department of Neurology, National and Kapodistrian University of Athens Medical School, Athens, Greece. Electronic address: lstefanis@bioacademy.gr.

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Classifications MeSH