Aβ Star is Born? Memory Loss in APP Mice Blamed on Oligomer | ALZFORUM
In a clever bit of sleuthing, Karen Ashe and colleagues appear to have solved the case of the mysterious memory loss in young mice engineered to express a mutated form of the human amyloid precursor protein (APP). Mysterious because the mice display memory problems as early as 6 months of age, in the absence of any neuronal loss and long before amyloid deposits appear in their brains. From Ashe’s previous work, and work from other labs (see review by Walsh and Selkoe, 2004, and Barghorn et al., 2005), all signs pointed toward a soluble oligomeric form of Aβ as the culprit, but no one knew exactly what that form might be in vivo. Now, Ashe and colleagues at University of Minnesota in Minneapolis, along with collaborators from several other U.S. institutions, report the identification of a soluble, extracellular Aβ12-mer that appears responsible for erasing memory in their mice. The oligomer, which they call Aβ*56 (Aβstar56), appears in the brain precisely when memory impairment commence
In a clever bit of sleuthing, Karen Ashe and colleagues appear to have solved the case of the mysterious memory loss in young mice engineered to express a mutated form of the human amyloid precursor protein (APP). Mysterious because the mice display memory problems as early as 6 months of age, in the absence of any neuronal loss and long before amyloid deposits appear in their brains. From Ashe’s previous work, and work from other labs (see review by Walsh and Selkoe, 2004, and Barghorn et al., 2005), all signs pointed toward a soluble oligomeric form of Aβ as the culprit, but no one knew exac
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