Scara1 deficiency impairs clearance of soluble Amyloid-β by mononuclear phagocytes and accelerates Alzheimer’s-like disease progression
Hickman, Suzanne E.
Kingery, Nathan D.
El Khoury, Joseph
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CitationFrenkel, 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.
AbstractIn 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.
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