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Alzheimer’s disease (AD) is a neurodegenerative disease identified by two major neuropathological hallmarks namely extracellular plaques containing Aβ protein and neurofibrillary tangles (NFT’s) made up of hyperphosporylated tau protein. AD neuropsychological symptoms include a gradual onset and progressive decline of cognitive functions such as episodic memory, language and attention. Additionally, non-cognitive changes such as behavioural and psychological symptoms are prominent in patients with AD. For the examination and understanding of the neuropathological mechanisms and neuropsychological symptoms of AD, mouse models and animal behavioural read-outs respectively, have proved to be essential. In this research we aim to establish a better understanding of AD pathogenesis and its related cognitive and non-cognitive symptoms through the use of behavioural read-outs involving mouse models. We made use of two mouse models with the C57BL/6J background: 1) the biAT mouse model (Tau.P301L x APP.V717I) expressing both major hallmarks of human AD and 2) the TLPH mouse model (Tau.P301L) expressing tau pathology only. The biAT and TLPH mouse models were tested at 5 to 6 months of age over a period of 2 months. They were exposed to a large test battery including a variety of behavioural experiments. Spatial memory performance was studied in the mouse models using the Morris water maze as the most established paradigm for the investigation of hippocampus-dependent learning. In addition, paradigms such as contextual and cued fear conditioning and sociability/preference for social novelty were included for the investigation of cognitive-related symptoms. Other behavioural tests including the elevated plus maze, open field, marble burying, tail suspension and 24h assessment were used for the investigation of non-cognitive symptoms. As opposed to WT mice, we expected transgenic mouse models to display neuropathological related cognitive and non-cognitive symptoms of AD. Contrary to our expectations, the results did not demonstrate major, consistent cognitive, social nor neuropsychological AD-like symptoms in the biAT or TLPH mouse models compared to WT controls. Besides several environmental and genetic factors that could have contributed to this, another possibility is that the AD-related neuropathology has a later onset in these C57BL/6J-backcrossed mouse models. Moreover, although C57BL/6 mice were described to perform well in these tasks and previously have been successfully used in our lab with the same equipment, the WT controls in this research overall seemed to display abnormal behaviour. For future experiments, mice at a more advanced age could be tested and the breeding schemes may need to be redesigned so that littermate wildtype control mice are available.