Perturbation of 3R/4R tau ratio impairs app axonal transport in neurons derived from human embryonic stem cells (HESC)

LACOVICH, VALENTINA; ALLOATTI, MATÍAS; ESPINDOLA, SONIA LORENA

Chicago

Congreso; SfN's 45th annual meeting; 2015

Society for Neuroscience

Alzheimer?s disease is characterized by the abnormal abundance of two hallmark proteins, APP and tau. In the last two decades several studies have tried to propose a molecular cascade of events leading to the pathology. One of the approaches to study the mechanisms leading to disease is to use transgenic mice bearing mutations that have been described in familiar cases of AD. The triple-transgenic model (3xTg-AD; PS1M146V, APPSWE and tauP301L) developed an age-related and progressive neuropathological phenotype that included both plaques and tangles, providing evidence of amyloid cascade hypothesis, by which Aβ deposits precede tau alterations. However it was later shown that if tau is knocked out, there are no amyloid related changes, thus leaving an open question about how APP and tau are interlinked.