Scara1 deficiency impairs clearance of soluble amyloid-β by mononuclear phagocytes and accelerates Alzheimer’s-like disease progression

Dan Frenkel (), Kim Wilkinson, Lingzhi Zhao, Suzanne E. Hickman, Terry K. Means, Lindsay Puckett, Dorit Farfara, Nathan D. Kingery, Howard L. Weiner and Joseph El Khoury ()
Additional contact information
Dan Frenkel: Sagol School of Neuroscience, George S. Wise Faculty of Life Sciences, Tel Aviv University
Kim Wilkinson: Center for Immunology and Inflammatory Diseases
Lingzhi Zhao: Center for Immunology and Inflammatory Diseases
Suzanne E. Hickman: Center for Immunology and Inflammatory Diseases
Terry K. Means: Center for Immunology and Inflammatory Diseases
Lindsay Puckett: Center for Immunology and Inflammatory Diseases
Dorit Farfara: Sagol School of Neuroscience, George S. Wise Faculty of Life Sciences, Tel Aviv University
Nathan D. Kingery: Center for Immunology and Inflammatory Diseases
Howard L. Weiner: Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
Joseph El Khoury: Center for Immunology and Inflammatory Diseases

Nature Communications, 2013, vol. 4, issue 1, 1-9

Abstract: Abstract In Alzheimer’s disease, soluble amyloid-β causes synaptic dysfunction and neuronal loss. Receptors involved in clearance of soluble amyloid-β are not known. Here we use short hairpin RNA screening and identify the scavenger receptor Scara1 as a receptor for soluble amyloid-β expressed on myeloid cells. To determine the role of Scara1 in clearance of soluble amyloid-β in vivo, we cross Scara1 null mice with PS1-APP mice, a mouse model of Alzheimer’s disease, and generate PS1-APP-Scara1-deficient mice. Scara1 deficiency markedly accelerates Aβ accumulation, leading to increased mortality. In contrast, pharmacological upregulation of Scara1 expression on mononuclear phagocytes increases Aβ clearance. This approach is a potential treatment strategy for Alzheimer’s disease.

Date: 2013
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/ncomms3030 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms3030

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms3030

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().