Alzheimer's disease is a public health crisis that will grow to devastating proportions over the next several decades unless effective therapies are found. Two hallmark pathologies in the brain have characterized the disease since it was first described over 100 years ago by Alois Alzheimer. The first is the neuritic plaque, a fibrillar structure composed largely of the beta-amyloid peptide (or BAP) surrounded by dystrophic neurites, activated macrophages, and reactive astrocytes. The second is the neurofibrillary tangle, consisting of neuronal inclusions of the microtubule-associated protein tau in a highly fibrillar form. For most of the history of Alzheimer's research, these structures and their associated biologies have been studied in relative isolation. Vigorous debates as to which pathology is more relevant to disease has in addition led to what has been referred to as the "BAP-tist/Tau-ist" wars, further isolating these biologies. As many of the front-line therapies designed to test 'the amyloid hypothesis' are reaching the clinic and failing to show efficacy, the research community is reconsidering some of the prevailing dogmas and seeking to better integrate our understanding of Alzheimer's disease biology and how it unfolds during aging. The goal of this symposium is to revisit the old BAP-tist/Tau-ist schism and ask whether two fields of research on one disease can offer each other mechanistic clues in the quest to find effective therapies.