Dornan, Faculty Advisor, Dr. Wayne

Tinkler, Greg

Digital Commons @ Illinois Wesleyan University

Illinois Wesleyan UniversityDigital Commons @ IWUJohn Wesley Powell Student ResearchConference 1994, 5th Annual JWP ConferenceApr 23rd, 9:00 AM - 4:00 PMβ-Amyloid (1-42) and Its Role in Developing anAnimal Model of Alzheimer's DiseaseGreg TinklerIllinois Wesleyan UniversityDr. Wayne Dornan, Faculty AdvisorIllinois Wesleyan UniversityFollow this and additional works at: http://digitalcommons.iwu.edu/jwprcThis Event is brought to you for free and open access by The Ames Library, the Andrew W. Mellon Center for Curricular and FacultyDevelopment, the Office of the Provost and the Office of the President. It has been accepted for inclusion in Digital Commons @ IWU bythe faculty at Illinois Wesleyan University. For more information, please contact digitalcommons@iwu.edu.©Copyright is owned by the author of this document.Greg Tinkler and Dr. Wayne Dornan, Faculty Advisor, "β-Amyloid (1-42) and Its Role in Developing an Animal Model ofAlzheimer's Disease" (April 23, 1994). John Wesley Powell Student Research Conference. Paper 56.http://digitalcommons.iwu.edu/jwprc/1994/posters/56J3-AMYLOID (1-42) AND ITS ROLE IN DEVELOPING AN ANIMAL MODEL OF ALZHEIMER'S DISEASE Greg Tinkler, and Dr. Wayne Dornan"', Department of Psychology, IWU. Alzheimer's disease is a neurodegenerative disorder characterized by neurofibrillary tangles and neuritic plaques. The major component of neuritic plaques is J3-amyloid. In humans, J3-amyloid is a chain of amino acids varying in length from 39 to 43. Current studies have shown that J3-amyloid (1-40) is toxic to cells in vitro , with the 25-35 chain of amino acids supposedly being responsible for the cell death. However, the ability of the protein to cause cell death in vivo is still being questioned. One problem is that the (1-40) form has been found to aggregate very rapidly in most solvents, which could prevent a successful injection of J3A into a rat. Recently. the (1-42) form has been purified and synthesized. As opposed to the (1-40) form, the new 42 amino acid sequence has a slower rate of sedimentation, which increases the likelihood of an effective injection. In order to determine the effect of J3A (1-42) on spatial tasks, 0.5 microliters of the peptide were injected bilaterally into the dorsal hippocampus of male Long Evans rats. Control groups were also utilized. The first control group consisted of injections of a scrambled version of the peptide, the second group being the vehicle (DMSO) alone. The animals, which had been pretrained on a radial arm maze, were allowed to recuperate from surgery and were then tested on the maze again. The maze consisted of eight arms, five of which were always baited for a particular animal. Session latency, latency to first choice, number of correct choices, number of reference memory errors, number of correct and incorrect errors, and the total number of choices were recorded for each animal. Items that were then calculated included the percent of correct choices, the average choice latency, and the total number of errors. Testing continued for two weeks, after which the reinforcers from three of the arms were removed and shifted them to the three arms which had previously been unbaited. Three days later, all reinforcers were removed except for the two arms which had been baited for both of the previous configurations. These two reconfiguration procedures were done in an attempt to differentiate between animals using procedural memory and those relying on declarative memory, which is controlled by the hippocampus. The data was analyzed using ANOV A. The rats were perfused after testing, and the histologies are currently being completed. There was no significant difference between the three groups. These results suggest that injections of J3A do not affect the retention of previously learned spatial tasks in the rat. Further studies will assess the affects of bilateral injections of J3A (1-42) into the hippocampus on the acquisition of a spatial learning task. 

β-Amyloid (1-42) and Its Role in Developing an Animal Model of Alzheimer\u27s Disease

http://digitalcommons.iwu.edu/cgi/viewcontent.cgi?article=1327&context=jwprc

β-Amyloid (1-42) and Its Role in Developing an Animal Model of Alzheimer\u27s Disease

Abstract

Similar works

Full text

Available Versions

Digital Commons @ Illinois Wesleyan University