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On the other hand, anti-inflammatory cytokines have been suggested to be neuroprotective by reducing neuroinflammation and clearing A\u03b2. To test this hypothesis, we used adeno-associated virus serotype 1 (AAV2\/1) to express an anti-inflammatory cytokine, murine Interleukin-4 (mIL-4), in the hippocampus of APP transgenic TgCRND8 mice with pre-existing plaques.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>mIL-4 expression resulted in establishment of an \u201cM2-like\u201d phenotype in the brain and was accompanied by exacerbated A\u03b2 deposition in TgCRND8 mice brains. No change in holo APP or APP C terminal fragment or phosphorylated tau levels were detected in mIL-4 expressing CRND8 cohorts. Biochemical analysis shows increases in both SDS soluble and insoluble A\u03b2. mIL-4 treatment attenuates soluble A\u03b240 uptake by microglia but does not affect aggregated A\u03b242 internalization by microglia or soluble A\u03b240 internalization by astrocytes.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p>Short term focal mIL-4 expression in the hippocampus leads to exacerbation of amyloid deposition in vivo, possibly mediated by acute suppression of glial clearance mechanisms. Given that recent preclinical data from independent groups indicate engagement of the innate immune system early on during disease pathogenesis may be beneficial, our present study strongly argues for a cautious re-examination of unwarranted side\u2013effects of anti-inflammatory therapies for neurodegenerative diseases, including AD.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/1750-1326-7-36","type":"journal-article","created":{"date-parts":[[2012,7,29]],"date-time":"2012-07-29T12:16:05Z","timestamp":1343564165000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":107,"title":["Hippocampal expression of murine IL-4 results in exacerbation of amyloid deposition"],"prefix":"10.1186","volume":"7","author":[{"given":"Paramita","family":"Chakrabarty","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Li","family":"Tianbai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amanda","family":"Herring","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carolina","family":"Ceballos-Diaz","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pritam","family":"Das","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Todd E","family":"Golde","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2012,7,29]]},"reference":[{"key":"344_CR1","doi-asserted-by":"publisher","first-page":"503","DOI":"10.1016\/j.nbd.2009.10.006","volume":"37","author":"B Cameron","year":"2010","unstructured":"Cameron B, Landreth GE: Inflammation, microglia, and Alzheimer's disease. 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