While over 170 Alzheimer s mouse models have been in use since the 1990s, those models mimic early-onset AD, also known as familial AD, which accounts for less than 5 percent of total AD cases. Until recently, scientists introduced mutations found in familial risk human genes, such as the amyloid precursor protein and presenilin 1, into the mouse genome to generate the mouse models. The UCI team decided to take a new approach by developing a mouse model better positioned to analyze causes of late-onset AD. Also called sporadic AD, this new model encompasses the remaining 95 percent of cases. We believed models developed on the rare familial type might be a reason therapies have worked in the lab but haven t translated into clinical trial success, said Frank LaFerla, professor of neurobiology & behavior and the study s co-senior author; he is also dean of the UCI School of Biological Sciences and director of the UCI Alzheimer s Disease Research Center. We decided it was time t
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