AgeingRequirement of Notch in adulthood for neurological function and longevityPresente, Asaf1; Andres, Andrew1; Nye, Jeffrey S.1,2, CAAuthor Information Departments of 1Molecular Pharmacology and Biological Chemistry, and 2Pediatrics, Northwestern University School of Medicine, 303 E. Chicago Ave. MC S215, Chicago, IL 60611 USA CA,1Corresponding Author. Current address: CNS Genomics Discovery Research, Pharmacia Corporation, 301 Henrietta Street, Kalamazoo, MC 49007, USA Received 25 June 2001; accepted 8 August 2001 NeuroReport: October 29th, 2001 - Volume 12 - Issue 15 - p 3321-3325 Buy Abstract Although Notch proteins rely upon presenilins for activation and can modulate neuritic architecture, their role in aging adults and Alzheimer's disease is unknown. Here we examine Drosophila in which Notch function was selectively diminished in adulthood. An outcrossing strategy was employed to reduce the effect of recessive modifiers of lifespan, and a temperature-sensitive allele or inducible dominant-negative Notch transgenes were used to reduce Notch function. A progressive neurological syndrome with loss of flight and shortened lifespan was observed in adults with compromised Notch function. Notch protein persists in aging adult Drosophila brains. However, no evidence of neurodegeneration in the central nervous system was detected. We conclude that Notch activity is constitutively required in the adult fly for neurological function. © 2001 Lippincott Williams & Wilkins, Inc.