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- W2126202461 abstract "It has been well established that neuroinflammation is involved in Alzheimer disease (AD) pathogenesis. Accumulation and aggregation of beta-amyloid (Abeta) peptide in the brains of patients with AD result in activation of glial cells which, in turn, initiates neuroinflammatory responses that involve reactive oxygen intermediates and release of inflammatory cytokines. In this study, bilateral intracerebroventricular (i.c.v.) injections of Abeta (25-35) in the rat resulted in impairment in learning and spatial memory and increased immunoreactive staining of AD-related neuropathological markers (Abeta, APP) and inflammatory mediators (OX-6, COX-2) in CA1 and dentate gyrus regions of the hippocampus. Pyrrolidine dithiocarbamate (PDTC) given intraperitoneally 30 min before Abeta injection and daily for 7 days postsurgery significantly prevented Abeta-induced neuropathological and neuroinflammatory responses, as well as the learning and spatial memory deficits. The potential of PDTC for reducing cognitive and neuropathological deficits may provide preliminary evidence for a new approach of AD treatment." @default.
- W2126202461 created "2016-06-24" @default.
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- W2126202461 creator A5066465053 @default.
- W2126202461 creator A5082852366 @default.
- W2126202461 date "2006-07-01" @default.
- W2126202461 modified "2023-09-26" @default.
- W2126202461 title "Effects of pyrrolidine dithiocarbamate on beta-amyloid (25–35)-induced inflammatory responses and memory deficits in the rat" @default.
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- W2126202461 doi "https://doi.org/10.1016/j.nbd.2006.02.008" @default.
- W2126202461 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16624564" @default.
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