Abstract
Address: 1Department of Ophthalmology, The Ohio State University, College of Medicine, Columbus, OH 43210, USA, 2Department of Biomedical Engineering Center, The Ohio State University, College of Medicine, Columbus, OH 43210, USA, 3Division of Neuropathology, Dept. of Pathology, Rhode Island Hospital and the Warren Alpert Medical School of Brown University, Providence, RI 02903, USA and 4Clinical Neuroscience, Brown Medical School, Providence, RI 02903, USA
Highlights
Alzheimer's disease is characterized by an increase in cerebral deposition of the neurotoxic peptide, amyloid-beta (Aβ)
A suggested mechanism of Aβ accumulation in the central nervous system is an age-related decrease in clearance of Aβ, due to diminished cerebrospinal fluid (CSF) outflow or decrease in transport of Aβ via membrane transporters located within the arachnoid membrane (AM) or arachnoid granulation (AG) cells
The receptor for advanced glycation endproducts (RAGE) and low-density lipoprotein receptor-related protein 1 (LRP1) have been previously identified in the choroid plexus and cerebral microvasculature, where they are utilized for Aβ import (RAGE) and export (LRP-1)
Summary
Deborah M Grzybowski*1,2, Amy C Long, Clint W Allred, David W Holman, John E Donahue, Shelley A Glimcher, Conrad Johanson, Edward Stopa and Martin Lubow. Address: 1Department of Ophthalmology, The Ohio State University, College of Medicine, Columbus, OH 43210, USA, 2Department of Biomedical Engineering Center, The Ohio State University, College of Medicine, Columbus, OH 43210, USA, 3Division of Neuropathology, Dept. Published: 3 February 2009 Cerebrospinal Fluid Research 2009, 6(Suppl 1):S27 doi:10.1186/1743-8454-6-S1-S27. 52nd Annual Meeting of the Society for Research into Hydrocephalus and Spina Bifida Meeting abstracts – A single PDF containing all abstracts in this Supplement is available here.
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