CONICET | Buscador de Institutos y Recursos Humanos

Alzheimer?s disease (AD) was first described over a century ago; however at the present its precise etiology remains unknown. Several hypotheses have been postulated to explain the pathogenesis of sporadic AD. Among these, the ?amyloid cascade hypothesis? (ACH) has gained enormous relevance based on genetic and biochemical evidences. One of its major predictions is that interference with Aβ aggregation may be therapeutically useful. Interestingly, the outcome of recent clinical trials including vaccination and targeted therapy aimed at reducing Aβ levels suggests that such strategy may not have the expected impact on AD progression and, in some cases, it may even cause life-threatening side effects. Thus, we think it is timely and highly relevant to the AD research community to revisit this subject in a thorough, objective and open-minded way.