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Title: Effect of β-Amyloid on synaptic plasticity and learning processes
Author: Gengler, Simon Marcel
ISNI:       0000 0004 2720 1638
Awarding Body: University of Ulster
Current Institution: Ulster University
Date of Award: 2010
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Alzheimer's disease (AD) is characterised by memory impairments and the occurrence of neuronal depositions of β-Amyloid. Transgenic mouse models expressing mutated genes found in inherited forms of AD have been engineered as tool to test AD medication. Therefore it is crucial to characterise the onset and nature of memory impairments and underlying synaptic dysfunction in AD mouse models. In this study, memory and synaptic function of the APPPSI-21 mouse model was analysed with behavioural tests and field potential recordings from CA3-CAl-synapses in vivo. In the water maze, APPPSI-21 mice showed impairments in spatial reference memory at the age of 6, 12 and 15 months, revealed decreased alternations in the T-Maze at 8 and 15 months of age and showed perseveration at 14 to 15 months of age in a habit reversal task. It was concluded that APPPSI-21 mice have impaired short term spatial memory at least from 6 months of age onwards, and impaired mental flexibility starting between 5 and 8 months of age. Synaptic function of APPPSI-21 mice was tested at the ages of 4.5, 6, 8, and 15 months. Potentiation of the field potential was found to be increased at 6 months and decreased at 15 months of age, suggesting altered synaptic function in APPPSI-21 mice starting between 4.5 and 6 months of age. The potential beneficial effects of Val(8)GLP-l-treatment on AD pathology was tested in 17 month old wild type and APPPSI-21 mice, that were injected daily with 25 nmol Val(8)GLP- l/kg for 21 days. This treatment resulted in improved potentiation of the field potential in wild type, but not in APPPSI-21 mice. Val(8)GLP-l-treatment decreased fibrillar β-Amyloid in the cortex of APPPSI-21 mice, when stained with Congo red. These results suggest that Val(8)GLP-l-treatment may be able to inhibit depositioning of β- Amyloid in brains that suffer from amyloidosis.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available