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Issue title: Mini-Forum: Roles of Amyloid-β and Tau Phosphorylation in Neuronal Repair and Protection
Article type: Research Article
Authors: Ramírez-Lugo, Leticia; * | Jensen, Morten S. | Søderman, Andreas | West, Mark J.
Affiliations: Institute of Anatomy, University of Aarhus, Wilhelm Meyers Allé, Arhus C, Denmark | Department of Psychiatry and Human Behavior, University of Mississippi Medical Center, Jackson, MS, USA
Correspondence: [*] Corresponding author: Dr. Leticia Ramírez-Lugo, Institute of Anatomy, Building 1234, University Park, 8000 Aarhus C, Denmark. Tel.: +45 8942 3011; Fax +45 8942 3060; E-mail: letyrlugo@gmail.com or LERALU@ana.au.dk.
Abstract: Age-related changes in taste memory were evaluated in APPswe/PS1dE9 transgenic (Tg) mice and age-matched wild type littermate controls (Wt). These Tg mice produce increasing amounts of amyloid-β in the brain with age, develop significant amounts of plaques by 9 months of age, and provide an opportunity to study the effects of Alzheimer's disease-like amyloidosis on different aspects of taste memory. In groups of mice ranging from 15–16 months of age, the neophobic response and its attenuation were similar in Tg and Wt mice. However, conditioned taste aversion (CTA), which resulted from the association between a new taste and an artificially induced gastric malaise, was significantly reduced in the 15–16 month old Tg mice compared to the Wt mice, but not in the 34 –or 7–8 month old mice. The extinction of CTA was normal in 34 –month old Tg mice, but occurred more rapidly in the 7–8 and 15–16 months old Tg mice than in the age-matched controls. These results provide evidence of differences in the neuronal systems involved in the attenuation of neophobia and CTA and suggest that the progressive amyloidosis that takes place in APPswe/PS1dE9 mice selectively affects the aversion component of taste memory.
Keywords: Alzheimer's disease, conditioned taste aversion, learning, safe taste memory, transgenic mice
DOI: 10.3233/JAD-2009-1141
Journal: Journal of Alzheimer's Disease, vol. 18, no. 2, pp. 281-293, 2009
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