Christina Unger Lithner, Monika M. Hedberg and Agneta Nordberg Pages 818 - 831 ( 14 )
During the last few decades, numerous stable transgenic mouse strains have been developed in order to mimic a range of Alzheimers disease (AD)-related pathologies. Although none of the models fully replicates the human disease, the models have been a key feature in translational research, providing significant insights into the pathophysiology of AD. They have also been widely used in the preclinical testing of potential therapies. The choice of transgenic mouse model, as well as the stage of Aβ pathology, significantly contributes to the outcome of the studies. Therefore, it is important to combine studies in different transgenic mouse models and detailed in vitro experiments to obtain a complete understanding of the origin of the disease, the actual sequences of early pathological events as well as being able to evaluate the effects of new drugs in the treatment of AD.
Amyloid precursor protein, alzheimer's disease, β-amyloid, neurodegeneration, neuropathology, transgenic mice, amyloid cascade hypothesis, hippocampus, hereditary disorder, memory deficits, APP Mutations
Karolinska Institutet, NVS, Division of Alzheimer Neurobiology, Novum Floor 4, Karolinska University Hospital, Huddinge, S-141 86 Stockholm, Sweden.