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2005 Grant - Lahiri
Functional Domains of the BACE Promoter: Implication in Alzheimer's Disease
Debomoy K. Lahiri, Ph.D.
Indiana University School of Medicine
2005 Zenith Fellows Award
A prime suspect in Alzheimer's disease pathology is the beta-amyloid protein fragment, which may disrupt cell-to-cell communication and contribute to cell death. Beta-amyloid is produced in two-stages. The first is the synthesis of APP, or amyloid precursor protein. In the second step, the majority of APP is cut by a protein called BACE, or beta-amyloid cleaving enzyme creating beta-amyloid. High levels of beta-amyloid in Alzheimer's disease may be the result of too much BACE activity.
Debomoy Lahiri, Ph.D., and colleagues are investigating the gene for BACE. Genes are like chemically coded blueprints or instructions for producing a protein. Each gene has a promoter, a kind of switch that turns the gene off and on and initiates the process by which the blueprint is copied and delivered to a cell's protein-making factory.
The researchers aim to characterize the properties of the BACE promoter and delineate the specific regions of genetic code that regulate normal BACE gene expression, or activation. They will also assess factors that may influence BACE gene expression, such as proteins with normal regulatory functions, inflammatory agents of the immune system or molecular factors influenced by diet. An understanding of normal and possible disease-related factors that affect BACE gene expression may identify steps in disease processes and suggest new strategies for therapeutic intervention.