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• W2025868035 abstract "Cholesterol metabolic disturbance has been shown to promote the formation and deposition of beta-amyloid (Aβ) in Alzheimer's disease (AD). Several lines of evidences suggest the involvement of cholesterol-rich microdomains (lipid rafts) in the γ– and β-cleavage of the amyloid precursor protein (APP) and low cellular cholesterol levels or disruption of lipid rafts stimulates the non-pathogenic processing by α-secretase. Previous studies from our laboratory have revealed that cholesterol, besides enhancing Aβ production, increases the susceptibility to Aβ-induced oxidative stress, by modulating the mitochondrial pool of glutathione (mGSH), a major defence against ROS generated from mitochondria.Thus, the aim of this work was to examine in vivo the correlation between elevated levels of brain mitochondrial cholesterol and the severity of AD-like neuroinflammation and neuronal damage. Transgenic mice that overexpress SREBP-2 (tgSREBP2), a transcription factor that controls cholesterol synthesis, and wild-type mice (WT) were exposed to a continuous intracerebroventricular infusion of oligomeric human Aβ 1–42 for 28 days (1.2 μg/ day), and determined the degree of glial activation, oxidative stress, synaptic degeneration, and amyloid deposition in the hippocampus. Brain mitochondria from tgSREBP2 mice exhibited 1.8–2 fold increase of cholesterol levels and decreased mGSH content (2.3±0.7 vs. 4.5±0.8 nmols/mg prot). Although plaque number and overall Aβ load were similar between WT and tgSREBP2 mice following Aβ 1–42 infusion, F4/80 immunostaining indicative of activated microglia was significantly increased in Aβ-infused tgSREBP2 mice with respect to WT and this was accompanied by the upregulation of TNF levels. Markers of oxidative stress such as protein carbonyl and 8-hydroxyguanosine residues were only detected in CA1/CA2 hippocampal regions of Aβ-infused tgSREBP2. Furthermore, determination of the levels of the pre-synaptic protein synaptophysin by western blot showed that Aβ infusion led to a significant synaptic degeneration in tgSREBP2 mice. Overall, our data suggest that increased mitochondrial cholesterol could play a critical role in the development of AD pathology by potentiating the Aβ-induced oxidative stress and neuroinflammatory processes." @default.
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• W2025868035 date "2008-07-01" @default.
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• W2025868035 title "P4-184: Increased mitochondrial cholesterol enhances glial activation and neuronal oxidative stress induced by intracerebroventricular infusion of human beta-amyloid" @default.
• W2025868035 doi "https://doi.org/10.1016/j.jalz.2008.05.2251" @default.
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