Ethanolamine plasmalogen (PlsEtn), a major phospholipid in neuronal membranes [60-90 mol% of ethanolamine glycerophospholipid (EtnGpl)], is specifically decreased in brains from patients with Alzheimer's disease (AD). The present study investigated how PlsEtn administration affects cognitive deficits and lipid composition in an animal model of AD. AD model rats were infused with amyloid-β (Aβ) into the cerebral ventricle and divided into three groups.
View Article and Find Full Text PDFDeposition of amyloid β peptide (Aβ) into the brain causes cognitive impairment. We investigated whether prescription pre-administration of n-3 fatty acids improves cognitive learning ability in young rats and whether it protects against learning ability impairments in an animal model of Alzheimer's disease that was prepared by infusion of Aβ(1-40) into the cerebral ventricles of rats. Pre-administration of TAK-085 (highly purified and concentrated n-3 fatty acids containing eicosapentaenoic acid ethyl ester and docosahexaenoic acid ethyl ester) at 300 mg kg(-1) day(-1) for 12 weeks significantly reduced the number of reference memory errors in an 8-arm radial maze, suggesting that long-term administration of TAK-085 improves cognitive leaning ability in rats.
View Article and Find Full Text PDFAlzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive and memory deterioration. Production and accumulation of beta-amyloid peptide (Abeta) is central to the pathogenesis of AD. Recent studies have demonstrated that PKA/CREB-dependent signaling pathway and long-term potentiation are inhibited by sublethal concentrations of Abeta(1-42) in cultured hippocampus neurons.
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