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Allergy influences the inflammatory status of the brain and enhances tau-phosphorylation
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2012 (English)In: Journal of Cellular and Molecular Medicine (Print), ISSN 1582-1838, Vol. 16, no 10, 2401-2412 p.Article in journal (Refereed) Published
Abstract [en]

Despite the existing knowledge regarding the neuropathology of Alzheimer's disease (AD), the cause of sporadic forms of the disease is unknown. It has been suggested that systemic inflammation may have a role, but the exact mechanisms through which inflammatory processes influence the pathogenesis and progress of AD are not obvious. Allergy is a chronic inflammatory disease affecting more than 20% of the Western population, but the effects of allergic conditions on brain functions are largely unknown. The aim of this study was to investigate whether or not chronic peripheral inflammation associated with allergy affects the expression of AD-related proteins and inflammatory markers in the brain. On the basis of previously described models for allergy in mice we developed a model of chronic airway allergy in mouse, with ovalbumin as allergen. The validity of the chronic allergy model was confirmed by a consistent and reproducible eosinophilia in the bronchoalveolar lavage (BAL) fluid of allergic animals. Allergic mice were shown to have increased brain levels of both immunoglobulin (Ig) G and IgE with a widespread distribution. Allergy was also found to increase phosphorylation of tau protein in the brain. The present data support the notion that allergy-dependent chronic peripheral inflammation modifies the brain inflammatory status, and influences phosphorylation of an AD-related protein, indicating that allergy may be yet another factor to be considered for the development and/or progression of neurodegenerative diseases such as AD.

Place, publisher, year, edition, pages
2012. Vol. 16, no 10, 2401-2412 p.
Keyword [en]
immunoglobulin, neuroinflammation, tau-phosphorylation, Alzheimer's disease
National Category
Natural Sciences
URN: urn:nbn:se:su:diva-82128DOI: 10.1111/j.1582-4934.2012.01556.xISI: 000309237500017Local ID: P2989OAI: diva2:566745


Available from: 2012-11-09 Created: 2012-11-08 Last updated: 2013-01-30Bibliographically approved

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Lekander, Mats
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Stress Research Institute
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