Matches in SemOpenAlex for { <https://semopenalex.org/work/W1569688440> ?p ?o ?g. }
Showing items 1 to 65 of
65
with 100 items per page.
- W1569688440 abstract "Alzheimer’s disease (AD) is the most common form of dementia. It ischaracterized by the accumulation of amyloid plaques in the brain, made of β-amyloid (Aβ) fragments which activate NADPH oxidase expressed in astrocytesand microglia, increasing the rate of production of reactive oxygen species(ROS) ultimately leading to neuronal dysfunction and degeneration responsiblefor the cognitive deficits observed in AD. However, the mechanisms by which Aβinduces toxicity remain elusive. In this thesis I explored the mechanisms bywhich oxidative stress leads to Aβ-induced neuronal death.Ca2+ signalling is intimately involved in the regulation of glial responses, andcan have both protective and detrimental effects on the nervous tissue.Therefore, I have explored the effects of Aβ on cell signalling in primary cultureof cortical astrocytes, looking at the interplay between Ca2+ and ROS. My resultsshow that Aβ induces toxicity by causing depletion of the Ca2+ stores (ER)through ROS production.While increased ROS generation may have dramatic consequences on brainphysiology, techniques to measure ROS generation remain unsatisfactory andcontroversial. I therefore began by investigating new probes to measure ROS,such as HSP-FRET and rxYFPgrp1.A complicate cascade of inflammatory events take place in astrocytes duringAβ toxicity, but the cell death that follows is neuronal. Neurons can be protectedby antioxidants or inhibitors of NADPH oxidase. Accordingly, I aimed to clarifyhow the activation of the astrocytic NADPH oxidase results in neuronal death. Ifound evidence that activation of NADPH oxidase by Aβ causes the upregulationof Poly (ADP-ribose) polymerase 1 (PARP-1) in astrocytes. Under conditions ofoxidative stress PARP-1 overactivation depletes NAD+ which causes a loss ofmitochondrial oxidative phosphorylation, loss of mitochondrial membranepotential and ultimately ATP depletion, leading to cell death.In summary, the work presented investigates Aβ actions on astrocytessignalling and describes a novel mechanism by which Aβ causes neuronaldeath." @default.
- W1569688440 created "2016-06-24" @default.
- W1569688440 creator A5008545868 @default.
- W1569688440 date "2011-06-28" @default.
- W1569688440 modified "2023-09-24" @default.
- W1569688440 title "β-amyloid induced oxidative stress and its effects onastrocytes and neurons" @default.
- W1569688440 hasPublicationYear "2011" @default.
- W1569688440 type Work @default.
- W1569688440 sameAs 1569688440 @default.
- W1569688440 citedByCount "0" @default.
- W1569688440 crossrefType "dissertation" @default.
- W1569688440 hasAuthorship W1569688440A5008545868 @default.
- W1569688440 hasConcept C169760540 @default.
- W1569688440 hasConcept C185592680 @default.
- W1569688440 hasConcept C190283241 @default.
- W1569688440 hasConcept C203014093 @default.
- W1569688440 hasConcept C2776151105 @default.
- W1569688440 hasConcept C2776914184 @default.
- W1569688440 hasConcept C2779719074 @default.
- W1569688440 hasConcept C2779830541 @default.
- W1569688440 hasConcept C31573885 @default.
- W1569688440 hasConcept C48349386 @default.
- W1569688440 hasConcept C55493867 @default.
- W1569688440 hasConcept C86803240 @default.
- W1569688440 hasConcept C95444343 @default.
- W1569688440 hasConceptScore W1569688440C169760540 @default.
- W1569688440 hasConceptScore W1569688440C185592680 @default.
- W1569688440 hasConceptScore W1569688440C190283241 @default.
- W1569688440 hasConceptScore W1569688440C203014093 @default.
- W1569688440 hasConceptScore W1569688440C2776151105 @default.
- W1569688440 hasConceptScore W1569688440C2776914184 @default.
- W1569688440 hasConceptScore W1569688440C2779719074 @default.
- W1569688440 hasConceptScore W1569688440C2779830541 @default.
- W1569688440 hasConceptScore W1569688440C31573885 @default.
- W1569688440 hasConceptScore W1569688440C48349386 @default.
- W1569688440 hasConceptScore W1569688440C55493867 @default.
- W1569688440 hasConceptScore W1569688440C86803240 @default.
- W1569688440 hasConceptScore W1569688440C95444343 @default.
- W1569688440 hasLocation W15696884401 @default.
- W1569688440 hasOpenAccess W1569688440 @default.
- W1569688440 hasPrimaryLocation W15696884401 @default.
- W1569688440 hasRelatedWork W1598539018 @default.
- W1569688440 hasRelatedWork W1964539405 @default.
- W1569688440 hasRelatedWork W1974800178 @default.
- W1569688440 hasRelatedWork W2013096139 @default.
- W1569688440 hasRelatedWork W2015811991 @default.
- W1569688440 hasRelatedWork W2037801678 @default.
- W1569688440 hasRelatedWork W2050392023 @default.
- W1569688440 hasRelatedWork W2065714966 @default.
- W1569688440 hasRelatedWork W2075798709 @default.
- W1569688440 hasRelatedWork W2083355844 @default.
- W1569688440 hasRelatedWork W2085278496 @default.
- W1569688440 hasRelatedWork W2086562792 @default.
- W1569688440 hasRelatedWork W2140616438 @default.
- W1569688440 hasRelatedWork W2149709906 @default.
- W1569688440 hasRelatedWork W2162690000 @default.
- W1569688440 hasRelatedWork W2167983401 @default.
- W1569688440 hasRelatedWork W2983366658 @default.
- W1569688440 hasRelatedWork W3056264410 @default.
- W1569688440 hasRelatedWork W3167252487 @default.
- W1569688440 hasRelatedWork W44743453 @default.
- W1569688440 isParatext "false" @default.
- W1569688440 isRetracted "false" @default.
- W1569688440 magId "1569688440" @default.
- W1569688440 workType "dissertation" @default.