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

DSpace/Manakin Repository

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

Citable link to this page

 

 
Title: Scara1 deficiency impairs clearance of soluble Amyloid-β by mononuclear phagocytes and accelerates Alzheimer’s-like disease progression
Author: Frenkel, Dan; Wilkinson, Kim; Zhao, Lingzhi; Hickman, Suzanne E.; Means, Terry K.; Puckett, Lindsey; Farfara, Dorit; Kingery, Nathan D.; Weiner, Howard L.; El Khoury, Joseph

Note: Order does not necessarily reflect citation order of authors.

Citation: Frenkel, Dan, Kim Wilkinson, Lingzhi Zhao, Suzanne E. Hickman, Terry K. Means, Lindsey Puckett, Dorit Farfara, Nathan D. Kingery, Howard L. Weiner, and Joseph El Khoury. 2013. “Scara1 deficiency impairs clearance of soluble Amyloid-β by mononuclear phagocytes and accelerates Alzheimer’s-like disease progression.” Nature communications 4 (1): 2030. doi:10.1038/ncomms3030. http://dx.doi.org/10.1038/ncomms3030.
Full Text & Related Files:
Abstract: In Alzheimer’s disease soluble amyloid beta (sAβ) causes synaptic dysfunction and neuronal loss. Receptors involved in clearance of sAβ are not known. Here we use shRNA screening and identify the scavenger receptor Scara1 as a receptor for sAβ expressed on myeloid cells. To determine the role of Scara1 in clearance of sAβ 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.
Published Version: doi:10.1038/ncomms3030
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3702268/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:11879346
Downloads of this work:

Show full Dublin Core record

This item appears in the following Collection(s)

 
 

Search DASH


Advanced Search
 
 

Submitters