Vanillic acid attenuates Aβ_1-42-induced oxidative stress and cognitive impairment in mice.

ABSTRACT: Increasing evidence demonstrates that β-amyloid (Aβ) elicits oxidative stress, which contributes to the pathogenesis and disease progression of Alzheimer's disease (AD). The aims of the present study were to determine and explore the antioxidant nature and potential mechanism of vanillic acid (VA) in Aβ_1-42-induced oxidative stress and neuroinflammation mediated cognitive impairment in mice. An intracerebroventricular (i.c.v.) injection of Aβ_1-42 into the mouse brain triggered increased reactive oxygen species (ROS) levels, neuroinflammation, synaptic deficits, memory impairment, and neurodegeneration. In contrast, the i.p. (intraperitoneal) administration of VA (30 mg/kg, for 3 weeks) after Aβ_1-42-injection enhanced glutathione levels (GSH) and abrogated R

SUBMITTER: Amin FU 

PROVIDER: S-EPMC5241654 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature