Mitochondrial dynamics in Parkinson's disease: a role for alpha-synuclein?

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00159816%3A_____%2F17%3A00067442" target="_blank" >RIV/00159816:_____/17:00067442 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1242/dmm.026294" target="_blank" >http://dx.doi.org/10.1242/dmm.026294</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1242/dmm.026294" target="_blank" >10.1242/dmm.026294</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Mitochondrial dynamics in Parkinson's disease: a role for alpha-synuclein?

Popis výsledku v původním jazyce

The distinctive pathological hallmarks of Parkinson&apos;s disease are the progressive death of dopaminergic neurons and the intracellular accumulation of Lewy bodies enriched in a-synuclein protein. Several lines of evidence from the study of sporadic, familial and pharmacologically induced forms of human Parkinson&apos;s disease also suggest that mitochondrial dysfunction plays an important role in disease progression. Although many functions have been proposed for a-synuclein, emerging data from human and animal models of Parkinson&apos;s disease highlight a role for a-synuclein in the control of neuronal mitochondrial dynamics. Here, we review the a-synuclein structural, biophysical and biochemical properties that influence relevant mitochondrial dynamic processes such as fusion-fission, transport and clearance. Drawing on current evidence, we propose that a-synuclein contributes to the mitochondrial defects that are associated with the pathology of this common and progressive neurodegenerative disease.

Název v anglickém jazyce

Mitochondrial dynamics in Parkinson's disease: a role for alpha-synuclein?

Popis výsledku anglicky

The distinctive pathological hallmarks of Parkinson&apos;s disease are the progressive death of dopaminergic neurons and the intracellular accumulation of Lewy bodies enriched in a-synuclein protein. Several lines of evidence from the study of sporadic, familial and pharmacologically induced forms of human Parkinson&apos;s disease also suggest that mitochondrial dysfunction plays an important role in disease progression. Although many functions have been proposed for a-synuclein, emerging data from human and animal models of Parkinson&apos;s disease highlight a role for a-synuclein in the control of neuronal mitochondrial dynamics. Here, we review the a-synuclein structural, biophysical and biochemical properties that influence relevant mitochondrial dynamic processes such as fusion-fission, transport and clearance. Drawing on current evidence, we propose that a-synuclein contributes to the mitochondrial defects that are associated with the pathology of this common and progressive neurodegenerative disease.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

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OECD FORD obor

10601 - Cell biology

Projekt

<a href="/cs/project/EF15_003%2F0000492" target="_blank" >EF15_003/0000492: Mapování molekulární podstaty procesů stárnutí pro vývoj nových léčebných metod</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2017

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Disease Models &amp; Mechanisms

ISSN

1754-8403

e-ISSN

—

Svazek periodika

10

Číslo periodika v rámci svazku

9

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

13

Strana od-do

1075-1087

Kód UT WoS článku

000409446400003

EID výsledku v databázi Scopus

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