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| Home > Publications Database > Replacement of brain-resident myeloid cells does not alter cerebral amyloid-β deposition in mouse models of Alzheimer's disease. > print |
| 001 | 138286 | ||
| 005 | 20240321220416.0 | ||
| 024 | 7 | _ | |a 10.1084/jem.20150478 |2 doi |
| 024 | 7 | _ | |a pmid:26458770 |2 pmid |
| 024 | 7 | _ | |a pmc:PMC4612086 |2 pmc |
| 024 | 7 | _ | |a 0022-1007 |2 ISSN |
| 024 | 7 | _ | |a 1540-9358 |2 ISSN |
| 024 | 7 | _ | |a 1540-9538 |2 ISSN |
| 024 | 7 | _ | |a altmetric:4619585 |2 altmetric |
| 037 | _ | _ | |a DZNE-2020-04608 |
| 041 | _ | _ | |a English |
| 082 | _ | _ | |a 610 |
| 100 | 1 | _ | |a Varvel, Nicholas H |0 P:(DE-2719)2810540 |b 0 |e First author |u dzne |
| 245 | _ | _ | |a Replacement of brain-resident myeloid cells does not alter cerebral amyloid-β deposition in mouse models of Alzheimer's disease. |
| 260 | _ | _ | |a New York, NY |c 2015 |b Rockefeller Univ. Press |
| 264 | _ | 1 | |3 online |2 Crossref |b Rockefeller University Press |c 2015-10-12 |
| 264 | _ | 1 | |3 print |2 Crossref |b Rockefeller University Press |c 2015-10-19 |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1593002562_30277 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
| 336 | 7 | _ | |a JOURNAL_ARTICLE |2 ORCID |
| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 520 | _ | _ | |a Immune cells of myeloid lineage are encountered in the Alzheimer's disease (AD) brain, where they cluster around amyloid-β plaques. However, assigning functional roles to myeloid cell subtypes has been problematic, and the potential for peripheral myeloid cells to alleviate AD pathology remains unclear. Therefore, we asked whether replacement of brain-resident myeloid cells with peripheral monocytes alters amyloid deposition in two mouse models of cerebral β-amyloidosis (APP23 and APPPS1). Interestingly, early after repopulation, infiltrating monocytes neither clustered around plaques nor showed Trem2 expression. However, with increasing time in the brain, infiltrating monocytes became plaque associated and also Trem2 positive. Strikingly, however, monocyte repopulation for up to 6 mo did not modify amyloid load in either model, independent of the stage of pathology at the time of repopulation. Our results argue against a long-term role of peripheral monocytes that is sufficiently distinct from microglial function to modify cerebral β-amyloidosis. Therefore, myeloid replacement by itself is not likely to be effective as a therapeutic approach for AD. |
| 536 | _ | _ | |a 342 - Disease Mechanisms and Model Systems (POF3-342) |0 G:(DE-HGF)POF3-342 |c POF3-342 |f POF III |x 0 |
| 588 | _ | _ | |a Dataset connected to CrossRef, PubMed, |
| 650 | _ | 7 | |a Amyloid beta-Peptides |2 NLM Chemicals |
| 650 | _ | 7 | |a Membrane Glycoproteins |2 NLM Chemicals |
| 650 | _ | 7 | |a Receptors, Immunologic |2 NLM Chemicals |
| 650 | _ | 7 | |a Trem2 protein, mouse |2 NLM Chemicals |
| 650 | _ | 2 | |a Alzheimer Disease: metabolism |2 MeSH |
| 650 | _ | 2 | |a Alzheimer Disease: pathology |2 MeSH |
| 650 | _ | 2 | |a Alzheimer Disease: therapy |2 MeSH |
| 650 | _ | 2 | |a Amyloid beta-Peptides: metabolism |2 MeSH |
| 650 | _ | 2 | |a Animals |2 MeSH |
| 650 | _ | 2 | |a Brain: metabolism |2 MeSH |
| 650 | _ | 2 | |a Brain: pathology |2 MeSH |
| 650 | _ | 2 | |a Disease Models, Animal |2 MeSH |
| 650 | _ | 2 | |a Female |2 MeSH |
| 650 | _ | 2 | |a Male |2 MeSH |
| 650 | _ | 2 | |a Membrane Glycoproteins: analysis |2 MeSH |
| 650 | _ | 2 | |a Mice |2 MeSH |
| 650 | _ | 2 | |a Mice, Inbred C57BL |2 MeSH |
| 650 | _ | 2 | |a Monocytes: physiology |2 MeSH |
| 650 | _ | 2 | |a Myeloid Cells: physiology |2 MeSH |
| 650 | _ | 2 | |a Receptors, Immunologic: analysis |2 MeSH |
| 700 | 1 | _ | |a Grathwohl, Stefan A |0 P:(DE-HGF)0 |b 1 |
| 700 | 1 | _ | |a Degenhardt, Karoline |0 P:(DE-2719)2810939 |b 2 |u dzne |
| 700 | 1 | _ | |a Resch, Claudia |0 P:(DE-2719)9000263 |b 3 |u dzne |
| 700 | 1 | _ | |a Bosch, Andrea |0 P:(DE-2719)2380523 |b 4 |u dzne |
| 700 | 1 | _ | |a Jucker, Mathias |0 P:(DE-2719)2000010 |b 5 |u dzne |
| 700 | 1 | _ | |a Neher, Jonas J |0 P:(DE-2719)2811021 |b 6 |e Last author |u dzne |
| 773 | 1 | 8 | |a 10.1084/jem.20150478 |b : Rockefeller University Press, 2015-10-12 |n 11 |p 1803-1809 |3 journal-article |2 Crossref |t Journal of Experimental Medicine |v 212 |y 2015 |x 1540-9538 |
| 773 | _ | _ | |a 10.1084/jem.20150478 |g Vol. 212, no. 11, p. 1803 - 1809 |0 PERI:(DE-600)1477240-1 |n 11 |q 212:11<1803 - 1809 |p 1803-1809 |t Journal of experimental medicine |v 212 |y 2015 |x 1540-9538 |
| 856 | 7 | _ | |2 Pubmed Central |u http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4612086 |
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