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Abstract

Previous studies have implicated that Alzheimer�s disease (AD) is likely caused by deposition of amyloid beta peptides in plaques in brain tissue. However, this �amyloid beta hypothesis� has been challenged lately by clinical studies.Amyloid beta peptides are cleavage products of amyloid precursor protein (APP) that plays a key role in the pathogenesis of AD. Besides, APP is ubiquitously expressed in human and has been highly conserved during evolution. However, the physiological functions of APPin development remain largely unknown. To identify additional genes that modulate APP functions in vivo, we ectopically expressed human APP in the Drosophila nervous system and observed a locomotion defect in adult flies. Using this phenotype, we have conducted a genetic screen of P-element insertion lines and founda novel gene that was named as�Chi�. We found that loss of Chi not only suppress APP-induced adult locomotion defect, but also APP-induced cell death in development. However, down regulation of Chi failed to suppress APP-induced NMJ and locomotion defect in larval stage, suggesting Chi is mainly involved in the cell death function of APP in development. Further studies will reveal whether Chi suppresses APPinduced adult locomotion defect by inhibition of cell death in the nervous system, and the molecular mechanism by which Chi modulates the cell death function of APP.

Biography

Pu Ren is a PhD student at School of Life Science and Technology, Tongji University, China. Main field of research interest is molecular genetics.