Matches in SemOpenAlex for { <https://semopenalex.org/work/W2090955970> ?p ?o ?g. }
- W2090955970 endingPage "915" @default.
- W2090955970 startingPage "839" @default.
- W2090955970 abstract "Alzheimer’s disease (AD), Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS) are the most common human adult-onset neurodegenerative diseases. They are characterized by prominent age-related neurodegeneration in selectively vulnerable neural systems. Some forms of AD, PD, and ALS are inherited, and genes causing these diseases have been identified. Nevertheless, the mechanisms of the neuronal cell death are unresolved. Morphological, biochemical, genetic, as well as cell and animal model studies reveal that mitochondria could have roles in this neurodegeneration. The functions and properties of mitochondria might render subsets of selectively vulnerable neurons intrinsically susceptible to cellular aging and stress and overlying genetic variations, triggering neurodegeneration according to a cell death matrix theory. In AD, alterations in enzymes involved in oxidative phosphorylation, oxidative damage, and mitochondrial binding of Aβ and amyloid precursor protein have been reported. In PD, mutations in putative mitochondrial proteins have been identified and mitochondrial DNA mutations have been found in neurons in the substantia nigra. In ALS, changes occur in mitochondrial respiratory chain enzymes and mitochondrial cell death proteins. Transgenic mouse models of human neurodegenerative disease are beginning to reveal possible principles governing the biology of selective neuronal vulnerability that implicate mitochondria and the mitochondrial permeability transition pore. This review summarizes how mitochondrial pathobiology might contribute to neuronal death in AD, PD, and ALS and could serve as a target for drug therapy." @default.
- W2090955970 created "2016-06-24" @default.
- W2090955970 creator A5024878520 @default.
- W2090955970 date "2010-03-25" @default.
- W2090955970 modified "2023-09-30" @default.
- W2090955970 title "Mitochondrial and Cell Death Mechanisms in Neurodegenerative Diseases" @default.
- W2090955970 cites W132441100 @default.
- W2090955970 cites W141294482 @default.
- W2090955970 cites W142080826 @default.
- W2090955970 cites W1482301804 @default.
- W2090955970 cites W1484249060 @default.
- W2090955970 cites W1506642042 @default.
- W2090955970 cites W1518893426 @default.
- W2090955970 cites W1522890520 @default.
- W2090955970 cites W1524061838 @default.
- W2090955970 cites W1532440724 @default.
- W2090955970 cites W1542061701 @default.
- W2090955970 cites W1551906701 @default.
- W2090955970 cites W1564677510 @default.
- W2090955970 cites W1572812739 @default.
- W2090955970 cites W1573108780 @default.
- W2090955970 cites W1578633669 @default.
- W2090955970 cites W1589415602 @default.
- W2090955970 cites W1599584623 @default.
- W2090955970 cites W1606105957 @default.
- W2090955970 cites W1607531254 @default.
- W2090955970 cites W1616121322 @default.
- W2090955970 cites W1618846043 @default.
- W2090955970 cites W1630502818 @default.
- W2090955970 cites W1656708631 @default.
- W2090955970 cites W1680974060 @default.
- W2090955970 cites W1780295430 @default.
- W2090955970 cites W179329376 @default.
- W2090955970 cites W1836761553 @default.
- W2090955970 cites W1873062439 @default.
- W2090955970 cites W1877873625 @default.
- W2090955970 cites W1909302202 @default.
- W2090955970 cites W1911014954 @default.
- W2090955970 cites W1937707692 @default.
- W2090955970 cites W1940436875 @default.
- W2090955970 cites W1963947961 @default.
- W2090955970 cites W1965111978 @default.
- W2090955970 cites W1965217295 @default.
- W2090955970 cites W1965521454 @default.
- W2090955970 cites W1965732243 @default.
- W2090955970 cites W1966093955 @default.
- W2090955970 cites W1966134982 @default.
- W2090955970 cites W1966798559 @default.
- W2090955970 cites W1967464880 @default.
- W2090955970 cites W1967573239 @default.
- W2090955970 cites W1968112618 @default.
- W2090955970 cites W1968210150 @default.
- W2090955970 cites W1968257316 @default.
- W2090955970 cites W1968942251 @default.
- W2090955970 cites W1969455851 @default.
- W2090955970 cites W1969850018 @default.
- W2090955970 cites W1970094644 @default.
- W2090955970 cites W1970714345 @default.
- W2090955970 cites W1971125884 @default.
- W2090955970 cites W1971335269 @default.
- W2090955970 cites W1971639674 @default.
- W2090955970 cites W1972260106 @default.
- W2090955970 cites W1972533526 @default.
- W2090955970 cites W1972812522 @default.
- W2090955970 cites W1972953195 @default.
- W2090955970 cites W1973851166 @default.
- W2090955970 cites W1975449325 @default.
- W2090955970 cites W1975742456 @default.
- W2090955970 cites W1975860435 @default.
- W2090955970 cites W1975995347 @default.
- W2090955970 cites W1976226379 @default.
- W2090955970 cites W1976664378 @default.
- W2090955970 cites W1976720365 @default.
- W2090955970 cites W1977069725 @default.
- W2090955970 cites W1977258127 @default.
- W2090955970 cites W1978008790 @default.
- W2090955970 cites W1978119032 @default.
- W2090955970 cites W1978163054 @default.
- W2090955970 cites W1978518304 @default.
- W2090955970 cites W1978559408 @default.
- W2090955970 cites W1978733364 @default.
- W2090955970 cites W1978900577 @default.
- W2090955970 cites W1979179771 @default.
- W2090955970 cites W1979496463 @default.
- W2090955970 cites W1979995768 @default.
- W2090955970 cites W1980601652 @default.
- W2090955970 cites W1980898980 @default.
- W2090955970 cites W1980959570 @default.
- W2090955970 cites W1981288814 @default.
- W2090955970 cites W1981360487 @default.
- W2090955970 cites W1982029249 @default.
- W2090955970 cites W1982577723 @default.
- W2090955970 cites W1982967923 @default.
- W2090955970 cites W1983030859 @default.
- W2090955970 cites W1983668432 @default.
- W2090955970 cites W1984308009 @default.
- W2090955970 cites W1984547206 @default.
- W2090955970 cites W1985773900 @default.