Mitochondrial Dysfunctions in Neurodegenerative Diseases: Relevance to Alzheimer's Disease

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11110%2F14%3A10284461" target="_blank" >RIV/00216208:11110/14:10284461 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1155/2014/175062" target="_blank" >http://dx.doi.org/10.1155/2014/175062</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1155/2014/175062" target="_blank" >10.1155/2014/175062</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Mitochondrial Dysfunctions in Neurodegenerative Diseases: Relevance to Alzheimer's Disease

Popis výsledku v původním jazyce

Mitochondrial dysfunctions are supposed to be responsible for many neurodegenerative diseases dominating in Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD). A growing body of evidence suggests that defects in mitochondrial metabolism and particularly of electron transport chain may play a role in pathogenesis of AD. Structurally and functionally damaged mitochondria do not produce sufficient ATP and are more prominent in producing proapoptotic factors and reactive oxygen species (ROS), and this can be an early stage of several mitochondrial disorders, including neurodegenerative diseases. Mitochondrial dysfunctions may be caused by both mutations in mitochondrial or nuclear DNA that code mitochondrial components and byenvironmental causes. In the following review, common aspects of mitochondrial impairment concerned about neurodegenerative diseases are summarized including ROS production, impaired mitochondrial dynamics, and apoptosis. Also, damaged f

Název v anglickém jazyce

Mitochondrial Dysfunctions in Neurodegenerative Diseases: Relevance to Alzheimer's Disease

Popis výsledku anglicky

Mitochondrial dysfunctions are supposed to be responsible for many neurodegenerative diseases dominating in Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD). A growing body of evidence suggests that defects in mitochondrial metabolism and particularly of electron transport chain may play a role in pathogenesis of AD. Structurally and functionally damaged mitochondria do not produce sufficient ATP and are more prominent in producing proapoptotic factors and reactive oxygen species (ROS), and this can be an early stage of several mitochondrial disorders, including neurodegenerative diseases. Mitochondrial dysfunctions may be caused by both mutations in mitochondrial or nuclear DNA that code mitochondrial components and byenvironmental causes. In the following review, common aspects of mitochondrial impairment concerned about neurodegenerative diseases are summarized including ROS production, impaired mitochondrial dynamics, and apoptosis. Also, damaged f

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

FL - Psychiatrie, sexuologie

OECD FORD obor

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Projekt

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Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2014

Kód důvěrnosti údajů

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

Název periodika

BioMed Research International

ISSN

2314-6133

e-ISSN

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Svazek periodika

neuveden

Číslo periodika v rámci svazku

May

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

9

Strana od-do

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Kód UT WoS článku

000336295900001

EID výsledku v databázi Scopus

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