| dc.description.abstract | Alzheimer's disease (AD) is a neurodegenerative disease which involves the atrophy of parts of the brain such as the hippocampus and cortex. The presence of two trademarks, neurofibrillary tangles (NFTs) and amyloid plaques (A-beta), inhibit cell signaling properties which lead to learning and memory deficits and eventually cellular death. Inflammation has been linked to the progression of AD pathologies. Our lab has shown that peripheral injections of both bacterial and viral mimetics lead to an elevated level of A-beta levels in the hippocampus of mice. Previous studies have shown hippocampus-dependent learning deficits in those injected with the bacterial mimetic, LPS; however, those injected with polyinosinic: polycytidylic acid (Poly I:C) have not shown hippocampus dependent learning deficits. The current study is aimed at investigating if there is a minimum A-beta level needed in order to induce these cognitive learning deficits. By first conducting a pilot study to normalize the potency of LPS to obtain similar A-beta levels to that of Poly I:C, we were able to set up the control group, the Poly I:C group, the original LPS dose and the new normalized LPS dose. Mice were then give seven consecutive days of intraperitoneal injections of one of the four groups followed by contextual fear conditioning in order to test for hippocampus learning deficits. The lower dose of LPS produced a lower more comparable amount of A-beta to Poly I:C, however their learning behaviors were different. Both the original higher dose LPS and Poly I:C groups failed to learn whereas the lower dose LPS group displayed much less cognitive learning deficits. We believe that A-beta levels are not the only factor impacting learning but that external factors such as cytokine levels may also be involved in the learning deficits normally observed with AD. | |
