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2006 Grant - Jucker
Exogenous Induction of Cerebral Amyloidogenesis
Mathias Jucker, Ph.D.
Hertie-Institute for Clinical Brain Research
2006 Zenith Fellows Award
Beta-amyloid is a protein fragment suspected of playing a role in Alzheimer's disease. This fragment is clipped in a two-stage process from a molecule called amyloid precursor protein (APP). Accumulation of beta-amyloid may trigger a series of pathological events that disrupt cell-to-cell communication and destroy cells. However, scientists know little about why beta-amyloid deposits accumulate in the brain.
Studies have shown in that in some neurodegenerative diseases a malformed disease-related protein may induce healthy proteins of the same kind to take on the aberrant properties. In other words, there is something about the properties of the malformed proteins that perpetuate the problem in others.
Mathias Jucker, Ph.D., and colleagues are examining whether beta-amyloid possesses a similar ability to induce additional beta-amyloid accumulation. In recent studies, they injected human beta-amyloid extract into the brains of mice genetically altered to produce human APP. They found that the extract did, indeed, induce beta-amyloid accumulation in the mice brains.
Dr. Jucker's team has proposed to investigate further how beta-amyloid accumulation may be a self-perpetuating phenomenon by (1) identifying and characterizing the inducing properties of beta-amyloid and (2) characterizing the properties of the mice brains that regulate amyloid accumulation. Greater understanding of the mechanisms involved in the accumulation of beta-amyloid in living brains may shed light on the pathological course of Alzheimer's disease and suggest new therapeutic strategies.