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Tytuł pozycji:

Biofluid Markers for Prodromal Parkinson's Disease: Evidence From a Catecholaminergic Perspective

Tytuł :
Biofluid Markers for Prodromal Parkinson's Disease: Evidence From a Catecholaminergic Perspective
Autorzy :
Yannick Vermeiren
Yael Hirschberg
Inge Mertens
Peter P. De Deyn
Pokaż więcej
Temat :
biomarker
catecholamines
cerebrospinal fluid
DHPG/MHPG
DOPAC
extracellular vesicles
Neurology. Diseases of the nervous system
RC346-429
Źródło :
Frontiers in Neurology, Vol 11 (2020)
Wydawca :
Frontiers Media S.A., 2020.
Rok publikacji :
2020
Kolekcja :
LCC:Neurology. Diseases of the nervous system
Typ dokumentu :
article
Opis pliku :
electronic resource
Język :
English
ISSN :
1664-2295
Relacje :
https://www.frontiersin.org/article/10.3389/fneur.2020.00595/full; https://doaj.org/toc/1664-2295
DOI :
10.3389/fneur.2020.00595
Dostęp URL :
https://doaj.org/article/660930a5ac744d2382a69b8e61c0ae8e
Numer akcesji :
edsdoj.660930a5ac744d2382a69b8e61c0ae8e
Czasopismo naukowe
Parkinson's disease (PD) is the most frequent of all Lewy body diseases, a family of progressive neurodegenerative disorders characterized by intra-neuronal cytoplasmic inclusions of α-synuclein. Its most defining features are bradykinesia, tremor, rigidity and postural instability. By the time PD manifests with motor signs, 70% of dopaminergic midbrain neurons are lost, and the disease is already in the middle or late stage. However, there are various non-motor symptoms occurring up to 20 years before the actual parkinsonism that are closely associated with profound deficiency of myocardial noradrenaline content and peripheral sympathetic denervation, as evidenced by neuroimaging experiments in recent years. Additionally, there is an inherent autotoxicity of catecholamines in the neuronal cells in which they are produced, forming toxic catecholaldehyde intermediates that make α-synuclein prone to aggregation, initiating a cascade of events that ultimately leads to neuronal death. The etiopathogenesis of PD and related synucleinopathies thus may well be a prototypical example of a catecholamine-regulated neurodegeneration, given that the synucleinopathy in PD spreads in synergy with central and peripheral catecholaminergic dysfunction from the earliest phases onward. That is why catecholamines and their metabolites, precursors, or derivatives in cerebrospinal fluid or plasma could be of particular interest as biomarkers for prodromal and de novo PD. Because there is great demand for such markers, this mini-review summarizes all catecholamine-related studies to date, in addition to providing profound neurochemical evidence on a systemic and cellular level to further emphasize this hypothesis and with emphasis on extracellular vesicles as a novel diagnostic and therapeutic incentive.

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