Atorvastatin Improves Mitochondrial Function and Prevents Oxidative Stress in Hippocampus Following Amyloid-β1-40 Intracerebroventricular Administration in Mice.

Molecular Neurobiology
Gianni ManciniCarla I Tasca

Abstract

Amyloid-β (Aβ) peptides play a significant role in the pathogenesis of Alzheimer's disease (AD). Neurotoxic effects promoted by Aβ peptides involve glutamate transmission impairment, decrease of neurotrophic factors, mitochondrial dysfunction, oxidative stress, synaptotoxicity, and neuronal degeneration. Here, we assessed the early events evoked by Aβ1-40 on the hippocampus. Additionally, we sought to unravel the molecular mechanisms of atorvastatin preventive effect on Aβ-induced hippocampal damage. Mice were treated orally (p.o.) with atorvastatin 10 mg/kg/day during 7 consecutive days before the intracerebroventricular (i.c.v.) infusion of Aβ1-40 (400 pmol/site). Twenty-four hours after Aβ1-40 infusion, a reduced content of mature BDNF/proBDNF ratio was observed in Aβ-treated mice. However, there is no alteration in synaptophysin, PSD-95, and doublecortin immunocontent in the hippocampus. Aβ1-40 promoted an increase in reactive oxygen species (ROS) and nitric oxide (NO) generation in hippocampal slices, and atorvastatin prevented this oxidative burst. Mitochondrial OXPHOS was measured by high-resolution respirometry. At this time point, Aβ1-40 did not alter the O2 consumption rates (OCR) related to phosphorylating state asso...Continue Reading

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Methods Mentioned

BETA
pharmacotherapies
the
transgenic
transmission electronic microscopy
dissection

Software Mentioned

Statistica®
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