Meeting Abstract
29.7 Saturday, Jan. 4 15:00 Examining Temporal Relationships Between Amyloid β Accumulation, Reactive Oxygen Species Accumulation, and Loss of Neurological Function in a C. elegans Model of Alzheimer’s Disease LAGARDE, M.T.*; RIVERA, G.; O’LEARY, F.A.; St. Edward’s University; St. Edward’s University; St. Edward’s University mlagard@stedwards.edu
Alzheimer’s disease (AD) is characterized by a gradual loss of cognitive function accompanied by numerous neuropathologies. These include the accumulation of neurofibrillary tangles, amyloid plaques, a rise in oxidative stress levels, and neuronal death. Current AD research seeks to understand the causal relationship between amyloid accumulation and oxidative stress and whether either one acts as the primary driver of the pathological process (Zhang, et al., 2012). The nematode C. elegans is a useful model for neurodegenerative disease due to its short life span, simple nervous system, and the availability of a variety of disease models. In this project we examined the temporal relationship between the progression of cognitive decline, the level of reactive oxygen species (ROS), and amyloid plaque formation in an AD model expressing neuronal amyloid beta. C. elegans AD strain, AD control and wild type control were cultured at 20°C on solid agar medium seeded with E. coli OP-50. Populations were synchronized by dissolution in sodium hypochlorite bleach solution to which eggs are resistant (Stiernagle, 2006). ROS species were assayed at five ages across the lifespan using 2’,7’-dichlorfluorescein-diacetate (DCFH-DA) fluorescent measurement (Wu, et al., 2006). Associative learning was assessed by training worms to associate food with a specific temperature. Trained worms were then tested for learning on a foodless temperature gradient. Data indicates that the AD model exhibits an associative learning deficit on days 7 and 9 which precedes abnormal oxidative stress levels on day 9. This may suggest that oxidative stress does not directly contribute to cognitive dysfunction.
