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Pexidartinib treatment in Alexander disease model mice reduces macrophage numbers and increases glial fibrillary acidic protein levels, yet has minimal impact on other disease phenotypes.

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Title: Pexidartinib treatment in Alexander disease model mice reduces macrophage numbers and increases glial fibrillary acidic protein levels, yet has minimal impact on other disease phenotypes.
Authors: Boyd MM; Pharmaceutical Sciences Division, School of Pharmacy, University of Wisconsin-Madison, Madison, USA., Litscher SJ; Pharmaceutical Sciences Division, School of Pharmacy, University of Wisconsin-Madison, Madison, USA., Seitz LL; Pharmaceutical Sciences Division, School of Pharmacy, University of Wisconsin-Madison, Madison, USA., Messing A; Waisman Center, University of Wisconsin-Madison, Madison, USA.; Department of Comparative Biosciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, USA., Hagemann TL; Waisman Center, University of Wisconsin-Madison, Madison, USA., Collier LS; Pharmaceutical Sciences Division, School of Pharmacy, University of Wisconsin-Madison, Madison, USA. lcollier@wisc.edu.
Source: Journal of neuroinflammation [J Neuroinflammation] 2021 Mar 08; Vol. 18 (1), pp. 67. Date of Electronic Publication: 2021 Mar 08.
Publication Type: Journal Article
Journal Info: Publisher: BioMed Central Country of Publication: England NLM ID: 101222974 Publication Model: Electronic Cited Medium: Internet ISSN: 1742-2094 (Electronic) Linking ISSN: 17422094 NLM ISO Abbreviation: J Neuroinflammation Subsets: MEDLINE
Database: MEDLINE Ultimate
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  Data: Pexidartinib treatment in Alexander disease model mice reduces macrophage numbers and increases glial fibrillary acidic protein levels, yet has minimal impact on other disease phenotypes.
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  Data: <searchLink fieldCode="AU" term="%22Boyd+MM%22">Boyd MM</searchLink>; Pharmaceutical Sciences Division, School of Pharmacy, University of Wisconsin-Madison, Madison, USA.<br /><searchLink fieldCode="AU" term="%22Litscher+SJ%22">Litscher SJ</searchLink>; Pharmaceutical Sciences Division, School of Pharmacy, University of Wisconsin-Madison, Madison, USA.<br /><searchLink fieldCode="AU" term="%22Seitz+LL%22">Seitz LL</searchLink>; Pharmaceutical Sciences Division, School of Pharmacy, University of Wisconsin-Madison, Madison, USA.<br /><searchLink fieldCode="AU" term="%22Messing+A%22">Messing A</searchLink>; Waisman Center, University of Wisconsin-Madison, Madison, USA.; Department of Comparative Biosciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, USA.<br /><searchLink fieldCode="AU" term="%22Hagemann+TL%22">Hagemann TL</searchLink>; Waisman Center, University of Wisconsin-Madison, Madison, USA.<br /><searchLink fieldCode="AU" term="%22Collier+LS%22">Collier LS</searchLink>; Pharmaceutical Sciences Division, School of Pharmacy, University of Wisconsin-Madison, Madison, USA. lcollier@wisc.edu.
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  Data: <searchLink fieldCode="JN" term="%22101222974%22">Journal of neuroinflammation</searchLink> [J Neuroinflammation] 2021 Mar 08; Vol. 18 (1), pp. 67. <i>Date of Electronic Publication: </i>2021 Mar 08.
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  Data: <i>Publisher: </i><searchLink fieldCode="PB" term="%22BioMed+Central%22">BioMed Central </searchLink><i>Country of Publication: </i>England <i>NLM ID: </i>101222974 <i>Publication Model: </i>Electronic <i>Cited Medium: </i>Internet <i>ISSN: </i>1742-2094 (Electronic) <i>Linking ISSN: </i><searchLink fieldCode="IS" term="%2217422094%22">17422094 </searchLink><i>NLM ISO Abbreviation: </i>J Neuroinflammation <i>Subsets: </i>MEDLINE
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