Alzheimer's disease (AD) is the most common form of dementia with nearly 44 million people affected worldwide. Characteristic neuropathological hallmarks of the disease are β-amyloid plaques which result from abnormal protein aggregation and deposition of β-amyloid peptide (Aβ). Aβ is produced by cleavage of the amyloid precursor protein. The amyloid-cascade-hypothesis postulates, based on strong genetic evidences, that Aβ accumulation is the central event in the etiology of AD. Here we use long-term in vivo two-photon imaging to investigate the dynamics of β-amyloid plaque genesis and growth in transgenic mouse models of Alzheimer's disease. A fluorescent dye is used to stain β-amyloid plaques in vivo and repeated injections enable us to follow plaque formation as well as their growth kinetics. In order to assess the size of β-amyloid plaques over time we established image analysis protocols to extract quantitative data from the high resolution four dimensional datasets. The results from our study in mice showed sigmoid-shaped growth kinetics similar to those found in humans with a familiar record of Alzheimer's disease by applying a β-amyloid radioactive tracer in combination with positron emission tomography imaging. We hope this work will help testing therapeutic strategies for Alzheimer's disease in animal models and translating them to the human situation.
Who Should Attend? - Everybody interested in recent developments in Alzheimer's disease therapy - Researchers working in the field of β-amyloid plaque genesis and growth - Scientists interested in new methods of testing efficacy of Alzheimer's therapies in preclinical studies
Key Learning Objectives: - Methods to investigate the efficacy of therapeutic strategies to treat Alzheimer's disease.