Loss (Beta-Amyloid Fibril, Osaka Mutation)
(In the collection of Lab Central - Kendall Square, Cambridge)
24" h x 34" w
Is DNA (or RNA) essential to life? In 1997, Stanley Prusiner received the Nobel Prize for work on "prions," proteins apparently capable of self-replication. Are these proteins "alive?"
Prion-like proteins are found in the body (e.g., the brain) properly folded into their normal shapes. They normally behave like proteins. The "prion version" of the same protein has a different fold, and acts as a mold, causing the normal versions to "copy" the abnormal shape. As these abnormally folded proteins accumulate, they stick together to form fibrils - structures with potentially lethal consequences to the cell.
Beta-amyloid is such a protein. The abnormal forms aggregate into fibrils which are associated with plaques found in the brains of those with Alzheimer's and certain other neurological conditions. The Osaka mutation (deletion of glu22) of beta-amyloid [2mvx.pdb], the basis of this stained glass piece, is associated with early onset Alzheimer's. The piece shows 10 beta-amyloid proteins, 5 on top, 5 below, which have aggregated to form a fibril. The colors are chosen so the proteins seem to "fade" as they recede in space. This color change symbolizes both dissolution of the fibril, a potential therapeutic goal for Alzheimer's, and the loss of memory associated with this disease - a possible consequence of the presence of these fibrils.