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β-Amyloid-Induced Inflammation and Cholinergic Hypofunction in the Rat Brain in Vivo: Involvement of the p38MAPK Pathway

Giovannini, Maria Grazia, Scali, Carla, Prosperi, Costanza, Bellucci, Arianna, Vannucchi, Maria Giuliana, Rosi, Susanna, Pepeu, Giancarlo, Casamenti, Fiorella·2002·Neurobiology of Disease
DOI 10.1006/nbdi.2002.0538
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Abstract

Injection into the nucleus basalis of the rat of preaggregated Abeta(1-42) produced a congophylic deposit and microglial and astrocyte activation and infiltration and caused a strong inflammatory reaction characterized by IL-1beta production, increased inducible cyclooxygenase (COX-2), and inducible nitric oxide synthase (iNOS) expression. Many phospho-p38MAPK-positive cells were observed around the deposit at 7 days after Abeta injection. Phospho-p38MAPK colocalized with activated microglial cells, but not astrocytes. The inflammatory reaction was accompanied by cholinergic hypofunction. We investigated the protective effect of the selective COX-2 inhibitor rofecoxib in attenuating the inflammatory response and neurodegeneration evoked by Abeta(1-42). Rofecoxib (3 mg/kg/day, 7 days) reduced microglia and astrocyte activation, iNOS induction, and p38MAPK activation to control levels. Cholinergic hypofunction was also significantly attenuated by treatment with rofecoxib. We show here for the first time in vivo the pivotal role played by the p38MAPK microglial signal transduction pathway in the inflammatory response to the Abeta(1-42) deposit.

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Metadata

Authors
Giovannini, M. G., Scali, C., Prosperi, C., Bellucci, A., Vannucchi, M. G., Rosi, S., Pepeu, G., & Casamenti, F.
Venue
Neurobiology of Disease
Publisher
Elsevier BV
Published
2002-11
Volume
11
Issue
2
Pages
257-274
ISSN
0969-9961
DOI
10.1006/nbdi.2002.0538
Cited by
190
References
7
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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