Pathophysiological mechanisms in amyloidosis mouse models.

Alzheimer's disease (AD) is the most frequent form of neurodegenerative disease resulting in progressive loss of memory and cognitive abilities. AD is vastly becoming a major medical and social-economical problem in our ageing society. In Europe alone, approximately 7 million people suffer from AD. Despite intense research, pathophysiological mechanisms underlying AD and related disorders are still insufficiently documented. Valid animal models are essential in research ensuing elucidation of humandisease processes and testing of potential therapeutic strategies. The valid APP23 transgenic mouse model will be used to further study underlying pathophysiological mechanisms related to soluble aggregates of the amyloid-beta peptide and reactivation of the cell cycle in neurons, with presumed effects at the neurochemical, electrophysiological, morphological and behavioural level. In addition, a model for vascular dementia will be developed by crossing APP23 mice with atherogenic ApoE knockout mice.Based on parallel genetic and environmental risk factors, pathophysiological aspects, and response to therapeutic interventions, it is assumed that convergent disease processes are the basis of AD and atherosclerosis. Behavioural, biochemical and pathological assessments will shed more light onto the link between AD and atherosclerosis, as well as the role of the amyloid precursor protein in atherosclerosis.

Keywords:MOUSE MODELS, PATHOPHYSIOLOGY, AMYLOIDOSIS

Disciplines:Laboratory medicine, Neurosciences, Biological and physiological psychology, Cognitive science and intelligent systems, Developmental psychology and ageing