Work

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

Year: 2013

Type: article

Source: Nature Communications

DOI: 10.1038/ncomms3030

Authors: Dan Frenkel, Kim Wilkinson, Lingzhi Zhao, Suzanne E. Hickman, Terry K. Means, Lindsay Puckett, Dorit Farfara, Nathan D. Kingery, Howard L. Weiner, Joseph El Khoury

Institutions: Tel Aviv University, Brigham and Women's Hospital, Harvard University, Massachusetts General Hospital

Language: English

Topic: Alzheimer's disease research and treatments

Subfield: Cellular and Molecular Neuroscience

Field: Neuroscience

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: bronze

Funders: Alzheimer's Association, Dana Foundation, Israel Science Foundation, National Institutes of Health, National Institute on Aging, National Institute of Allergy and Infectious Diseases, National Institute of Diabetes and Digestive and Kidney Diseases, National Institute of Neurological Disorders and Stroke

Awards: Role of the Innate Immune System in Aging and Development of Alzheimer's Disease, Mechanisms of anti-fungal immunity mediated by SCARF1 and CD36, CD36 in Alzheimer's Disease, Toll-Like Receptor Signaling in Alzheimer's Disease, Generation of a comprehensive panel of reagents for research on scavenger recepto, Center for the Study of Inflammatory Bowel Disease at Massachusetts General Hospital

OpenAlex ID: W2132663452

FWCI: 5.052

Cites: 40

Cited by: 217

Related to: 10