| First Author | Frenkel D | Year | 2013 |
| Journal | Nat Commun | Volume | 4 |
| Pages | 2030 | PubMed ID | 23799536 |
| Mgi Jnum | J:221229 | Mgi Id | MGI:5638515 |
| Doi | 10.1038/ncomms3030 | Citation | Frenkel D, et al. (2013) Scara1 deficiency impairs clearance of soluble amyloid-beta by mononuclear phagocytes and accelerates Alzheimer's-like disease progression. Nat Commun 4:2030 |
| abstractText | In Alzheimer's disease, soluble amyloid-beta causes synaptic dysfunction and neuronal loss. Receptors involved in clearance of soluble amyloid-beta are not known. Here we use short hairpin RNA screening and identify the scavenger receptor Scara1 as a receptor for soluble amyloid-beta expressed on myeloid cells. To determine the role of Scara1 in clearance of soluble amyloid-beta 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 Abeta accumulation, leading to increased mortality. In contrast, pharmacological upregulation of Scara1 expression on mononuclear phagocytes increases Abeta clearance. This approach is a potential treatment strategy for Alzheimer's disease. |
