Matches in SemOpenAlex for { <https://semopenalex.org/work/W2023271373> ?p ?o ?g. }
Showing items 1 to 82 of
82
with 100 items per page.
- W2023271373 endingPage "A18" @default.
- W2023271373 startingPage "A18" @default.
- W2023271373 abstract "<h3>Background</h3> Circulating or dietary cholesterol is not able to cross the blood-brain barrier (BBB) and cholesterol homeostasis in brain is thought to depend largely on endogenous biosynthesis. Cholesterol biosynthesis and content are reduced in the brain of several models of Huntington’s disease (HD) (Valenza <i>et al</i>., 2005; 2007; 2010). This cerebral dysfunction is measurable also in HD patients starting from early disease stages (Leoni <i>et al</i>., 2008; Leoni <i>et al</i>., 2013). <h3>Aims</h3> In the adult brain cholesterol-dependent neuronal activities, such as neurite outgrowth and synaptic properties, mainly rely on the transport of cholesterol from astrocytes on ApoE-containing particles (Mauch <i>et al</i>., 2001). Cholesterol supply to neurons might be reduced in HD astrocytes by contributing to neuronal dysfunction in HD neurons. <h3>Methods and results</h3> Here we show that primary astrocytes obtained from R6/2 HD mice and from mouse knock-in Neural Stem (NS) cell lines expressing mutant huntingtin produce and release less cholesterol bound to ApoE-containing lipoproteins into the medium, compared to control astrocytes. Accordingly, conditioned medium from wild-type astrocytes (GCMwt), but not from R6/2 astrocytes (GCMHD) or from wt astrocytes depleted of lipoproteins (GCMwt-delip), is able to compensate the defect in neurite outgrowth and to ameliorate synaptic-related properties in HD neurons. In parallel we established a dose-response relationship between cholesterol application and these parameters. Furthermore, results from gain and loss of function experiments in wt and HD primary astrocytes reinforce the notion of an altered cross-talk between astrocytes and neurons which can be rescued experimentally. <h3>Conclusions</h3> In conclusion, our results suggest that astrocytes carrying the HD mutation are the major responsible of the cholesterol dysfunction in HD as they contribute to supply less cholesterol to the surrounding neurons." @default.
- W2023271373 created "2016-06-24" @default.
- W2023271373 creator A5005647434 @default.
- W2023271373 creator A5006877403 @default.
- W2023271373 creator A5019870236 @default.
- W2023271373 creator A5020172277 @default.
- W2023271373 creator A5064191727 @default.
- W2023271373 creator A5087588860 @default.
- W2023271373 creator A5089345009 @default.
- W2023271373 date "2014-09-01" @default.
- W2023271373 modified "2023-09-27" @default.
- W2023271373 title "B27 Disruption Of Astrocyte-neuron Cholesterol Cross-talk Affects Neuronal Function In Huntington's Disease" @default.
- W2023271373 doi "https://doi.org/10.1136/jnnp-2014-309032.55" @default.
- W2023271373 hasPublicationYear "2014" @default.
- W2023271373 type Work @default.
- W2023271373 sameAs 2023271373 @default.
- W2023271373 citedByCount "0" @default.
- W2023271373 crossrefType "journal-article" @default.
- W2023271373 hasAuthorship W2023271373A5005647434 @default.
- W2023271373 hasAuthorship W2023271373A5006877403 @default.
- W2023271373 hasAuthorship W2023271373A5019870236 @default.
- W2023271373 hasAuthorship W2023271373A5020172277 @default.
- W2023271373 hasAuthorship W2023271373A5064191727 @default.
- W2023271373 hasAuthorship W2023271373A5087588860 @default.
- W2023271373 hasAuthorship W2023271373A5089345009 @default.
- W2023271373 hasConcept C113246987 @default.
- W2023271373 hasConcept C126322002 @default.
- W2023271373 hasConcept C134018914 @default.
- W2023271373 hasConcept C169760540 @default.
- W2023271373 hasConcept C202751555 @default.
- W2023271373 hasConcept C2776925932 @default.
- W2023271373 hasConcept C2777542381 @default.
- W2023271373 hasConcept C2778163477 @default.
- W2023271373 hasConcept C2778794669 @default.
- W2023271373 hasConcept C2779134260 @default.
- W2023271373 hasConcept C2780647506 @default.
- W2023271373 hasConcept C2781427258 @default.
- W2023271373 hasConcept C529278444 @default.
- W2023271373 hasConcept C55493867 @default.
- W2023271373 hasConcept C57089818 @default.
- W2023271373 hasConcept C71924100 @default.
- W2023271373 hasConcept C86803240 @default.
- W2023271373 hasConcept C95444343 @default.
- W2023271373 hasConceptScore W2023271373C113246987 @default.
- W2023271373 hasConceptScore W2023271373C126322002 @default.
- W2023271373 hasConceptScore W2023271373C134018914 @default.
- W2023271373 hasConceptScore W2023271373C169760540 @default.
- W2023271373 hasConceptScore W2023271373C202751555 @default.
- W2023271373 hasConceptScore W2023271373C2776925932 @default.
- W2023271373 hasConceptScore W2023271373C2777542381 @default.
- W2023271373 hasConceptScore W2023271373C2778163477 @default.
- W2023271373 hasConceptScore W2023271373C2778794669 @default.
- W2023271373 hasConceptScore W2023271373C2779134260 @default.
- W2023271373 hasConceptScore W2023271373C2780647506 @default.
- W2023271373 hasConceptScore W2023271373C2781427258 @default.
- W2023271373 hasConceptScore W2023271373C529278444 @default.
- W2023271373 hasConceptScore W2023271373C55493867 @default.
- W2023271373 hasConceptScore W2023271373C57089818 @default.
- W2023271373 hasConceptScore W2023271373C71924100 @default.
- W2023271373 hasConceptScore W2023271373C86803240 @default.
- W2023271373 hasConceptScore W2023271373C95444343 @default.
- W2023271373 hasIssue "Suppl 1" @default.
- W2023271373 hasLocation W20232713731 @default.
- W2023271373 hasOpenAccess W2023271373 @default.
- W2023271373 hasPrimaryLocation W20232713731 @default.
- W2023271373 hasRelatedWork W1709163017 @default.
- W2023271373 hasRelatedWork W1985474993 @default.
- W2023271373 hasRelatedWork W1994447059 @default.
- W2023271373 hasRelatedWork W2008488809 @default.
- W2023271373 hasRelatedWork W2010404670 @default.
- W2023271373 hasRelatedWork W2023271373 @default.
- W2023271373 hasRelatedWork W2062454002 @default.
- W2023271373 hasRelatedWork W2071004203 @default.
- W2023271373 hasRelatedWork W2478182096 @default.
- W2023271373 hasRelatedWork W2784139684 @default.
- W2023271373 hasVolume "85" @default.
- W2023271373 isParatext "false" @default.
- W2023271373 isRetracted "false" @default.
- W2023271373 magId "2023271373" @default.
- W2023271373 workType "article" @default.