Research in our laboratory is now focused primarily on Alzheimer’s disease (AD). The histopathological hallmark of AD is the presence in brain of extracellular plaques of ß-amyloid peptide fibrils, and intraneuronal neurofibrillary tangles, which are filaments composed of the protein, tau. Despite the conspicuous appearance of plaques and tangles, a growing body of evidence points to their building blocks, ß-amyloid and tau oligomers, as being the toxic molecular species that cause AD. For example, we have found that tau expression is required for several adverse effects of ß-amyloid oligomers on neurons, including microtubules loss, ectopic re-rentry into the cell cycle and cytotoxicity. The goals of our work are to decipher the metabolic links that connect ß-amyloid and tau to damage neurons, to define the structures and pathological properties of various types of ß-amyloid and tau oligomers, and to develop effective therapeutic and diagnostic tools for AD.