Home > Publications Database > Aggregation-resistant alpha-synuclein tetramers are reduced in the blood of Parkinson's patients. > print

001     270708
005     20240808164337.0
024 7 _ |a pmc:PMC11250827
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024 7 _ |a 10.1038/s44321-024-00083-5
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024 7 _ |a pmid:38839930
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024 7 _ |a 1757-4676
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024 7 _ |a 1715-4684
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024 7 _ |a 1757-4684
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024 7 _ |a altmetric:164239994
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037 _ _ |a DZNE-2024-00880
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a de Boni, Laura
|0 0000-0001-7785-482X
|b 0
245 _ _ |a Aggregation-resistant alpha-synuclein tetramers are reduced in the blood of Parkinson's patients.
260 _ _ |a Heidelberg
|c 2024
|b EMBO Press
336 7 _ |a article
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336 7 _ |a ARTICLE
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336 7 _ |a Journal Article
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520 _ _ |a Synucleinopathies such as Parkinson's disease (PD) are defined by the accumulation and aggregation of the α-synuclein protein in neurons, glia and other tissues. We have previously shown that destabilization of α-synuclein tetramers is associated with familial PD due to SNCA mutations and demonstrated brain-region specific alterations of α-synuclein multimers in sporadic PD patients following the classical Braak spreading theory. In this study, we assessed relative levels of disordered and higher-ordered multimeric forms of cytosolic α-synuclein in blood from familial PD with G51D mutations and sporadic PD patients. We used an adapted in vitro-cross-linking protocol for human EDTA-whole blood. The relative levels of higher-ordered α-synuclein tetramers were diminished in blood from familial PD and sporadic PD patients compared to controls. Interestingly, the relative amount of α-synuclein tetramers was already decreased in asymptomatic G51D carriers, supporting the hypothesis that α-synuclein multimer destabilization precedes the development of clinical PD. Our data, therefore suggest that measuring α-synuclein tetramers in blood may have potential as a facile biomarker assay for early detection and quantitative tracking of PD progression.
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650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a alpha-Synuclein: metabolism
|2 MeSH
650 _ 2 |a alpha-Synuclein: blood
|2 MeSH
650 _ 2 |a Parkinson Disease: blood
|2 MeSH
650 _ 2 |a Parkinson Disease: metabolism
|2 MeSH
650 _ 2 |a Parkinson Disease: genetics
|2 MeSH
650 _ 2 |a Aged
|2 MeSH
650 _ 2 |a Male
|2 MeSH
650 _ 2 |a Female
|2 MeSH
650 _ 2 |a Middle Aged
|2 MeSH
650 _ 2 |a Protein Multimerization
|2 MeSH
650 _ 2 |a Protein Aggregates
|2 MeSH
650 _ 7 |a Parkinson’s disease
|2 Other
650 _ 7 |a Alpha-synuclein
|2 Other
650 _ 7 |a Blood
|2 Other
650 _ 7 |a Human
|2 Other
650 _ 7 |a Parkinson’s disease
|2 Other
650 _ 7 |a Tetramer
|2 Other
650 _ 7 |a alpha-Synuclein
|2 NLM Chemicals
650 _ 7 |a Protein Aggregates
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650 _ 7 |a SNCA protein, human
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700 1 _ |a Wallis, Amber
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700 1 _ |a Hays Watson, Aurelia
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700 1 _ |a Ruiz-Riquelme, Alejandro
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700 1 _ |a Leyland, Louise-Ann
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700 1 _ |a Bourinaris, Thomas
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700 1 _ |a Hannaway, Naomi
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700 1 _ |a Löhle, Matthias
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700 1 _ |a Hermann, Wiebke
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700 1 _ |a Schott, Björn-Hendrik
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700 1 _ |a Brockmann, Kathrin
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700 1 _ |a Haustein, Katrin
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700 1 _ |a Breuer, Peter
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700 1 _ |a Houlden, Henry
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700 1 _ |a Weil, Rimona S
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700 1 _ |a Bartels, Tim
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773 _ _ |a 10.1038/s44321-024-00083-5
|g Vol. 16, no. 7, p. 1657 - 1674
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