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- W3028471102 endingPage "1091" @default.
- W3028471102 startingPage "1076" @default.
- W3028471102 abstract "Accumulative evidence has shown that mitochondrial dysfunction plays a pivotal role in the pathogenesis of Alzheimer's disease (AD). Mitochondrial impairment actively contributes to the synaptic and cognitive failure that characterizes AD. The presence of soluble pathological forms of tau like hyperphosphorylated at Ser396 and Ser404 and cleaved at Asp421 by caspase 3, negatively impacts mitochondrial bioenergetics, transport, and morphology in neurons. These adverse effects against mitochondria health will contribute to the synaptic impairment and cognitive decline in AD. Current studies suggest that mitochondrial failure induced by pathological tau forms is likely the result of the opening of the mitochondrial permeability transition pore (mPTP). mPTP is a mitochondrial mega-channel that is activated by increases in calcium and is associated with mitochondrial stress and apoptosis. This structure is composed of different proteins, where Ciclophilin D (CypD) is considered to be the primary mediator of mPTP activation. Also, new studies suggest that mPTP contributes to Aβ pathology and oxidative stress in AD. Further, inhibition of mPTP through the reduction of CypD expression prevents cognitive and synaptic impairment in AD mouse models. More importantly, tau protein contributes to the physiological regulation of mitochondria through the opening/interaction with mPTP in hippocampal neurons. Therefore, in this paper, we will discuss evidence that suggests an important role of pathological forms of tau against mitochondrial health. Also, we will discuss the possible role of mPTP in the mitochondrial impairment produced by the presence of tau pathology and its impact on synaptic function present in AD." @default.
- W3028471102 created "2020-05-29" @default.
- W3028471102 creator A5087894268 @default.
- W3028471102 creator A5091080441 @default.
- W3028471102 date "2020-11-09" @default.
- W3028471102 modified "2023-10-17" @default.
- W3028471102 title "The Role of Mitochondrial Impairment in Alzheimer´s Disease Neurodegeneration: The Tau Connection" @default.
- W3028471102 cites W1499506658 @default.
- W3028471102 cites W1511517753 @default.
- W3028471102 cites W1528220495 @default.
- W3028471102 cites W1542215809 @default.
- W3028471102 cites W1650328097 @default.
- W3028471102 cites W1675881254 @default.
- W3028471102 cites W1906905763 @default.
- W3028471102 cites W1918417411 @default.
- W3028471102 cites W1929269608 @default.
- W3028471102 cites W1967918005 @default.
- W3028471102 cites W1968257316 @default.
- W3028471102 cites W1968553823 @default.
- W3028471102 cites W1968937229 @default.
- W3028471102 cites W1969461857 @default.
- W3028471102 cites W1970302092 @default.
- W3028471102 cites W1970354788 @default.
- W3028471102 cites W1971090593 @default.
- W3028471102 cites W1972493045 @default.
- W3028471102 cites W1974068776 @default.
- W3028471102 cites W1983523416 @default.
- W3028471102 cites W1985351513 @default.
- W3028471102 cites W1986384924 @default.
- W3028471102 cites W1988664434 @default.
- W3028471102 cites W1989167108 @default.
- W3028471102 cites W1989331957 @default.
- W3028471102 cites W1990271214 @default.
- W3028471102 cites W1990752558 @default.
- W3028471102 cites W1991631628 @default.
- W3028471102 cites W1993418135 @default.
- W3028471102 cites W1994539511 @default.
- W3028471102 cites W1996917933 @default.
- W3028471102 cites W2002181764 @default.
- W3028471102 cites W2002984957 @default.
- W3028471102 cites W2006717582 @default.
- W3028471102 cites W2008584420 @default.
- W3028471102 cites W2014898742 @default.
- W3028471102 cites W2017363986 @default.
- W3028471102 cites W2020951538 @default.
- W3028471102 cites W2022285303 @default.
- W3028471102 cites W2022532556 @default.
- W3028471102 cites W2025449918 @default.
- W3028471102 cites W2027367467 @default.
- W3028471102 cites W2030126692 @default.
- W3028471102 cites W2030602441 @default.
- W3028471102 cites W2031280902 @default.
- W3028471102 cites W2031850537 @default.
- W3028471102 cites W2032105133 @default.
- W3028471102 cites W2032879521 @default.
- W3028471102 cites W2033166503 @default.
- W3028471102 cites W2033957230 @default.
- W3028471102 cites W2037202999 @default.
- W3028471102 cites W2045085957 @default.
- W3028471102 cites W2047719279 @default.
- W3028471102 cites W2050323317 @default.
- W3028471102 cites W2050347556 @default.
- W3028471102 cites W2055079309 @default.
- W3028471102 cites W2055361873 @default.
- W3028471102 cites W2055749053 @default.
- W3028471102 cites W2057886219 @default.
- W3028471102 cites W2060458492 @default.
- W3028471102 cites W2063921446 @default.
- W3028471102 cites W2064913654 @default.
- W3028471102 cites W2066011396 @default.
- W3028471102 cites W2066575706 @default.
- W3028471102 cites W2066918975 @default.
- W3028471102 cites W2070895853 @default.
- W3028471102 cites W2071152612 @default.
- W3028471102 cites W2072480165 @default.
- W3028471102 cites W2074800090 @default.
- W3028471102 cites W2075421841 @default.
- W3028471102 cites W2075791440 @default.
- W3028471102 cites W2081768153 @default.
- W3028471102 cites W2082973248 @default.
- W3028471102 cites W2086843814 @default.
- W3028471102 cites W2089141103 @default.
- W3028471102 cites W2098718365 @default.
- W3028471102 cites W2099347739 @default.
- W3028471102 cites W2100026237 @default.
- W3028471102 cites W2103163836 @default.
- W3028471102 cites W2104227586 @default.
- W3028471102 cites W2104838343 @default.
- W3028471102 cites W2105442740 @default.
- W3028471102 cites W2107366065 @default.
- W3028471102 cites W2110171555 @default.
- W3028471102 cites W2112169034 @default.
- W3028471102 cites W2112884278 @default.
- W3028471102 cites W2113808242 @default.
- W3028471102 cites W2113917457 @default.
- W3028471102 cites W2114358785 @default.
- W3028471102 cites W2115995998 @default.
- W3028471102 cites W2118040247 @default.