Although a considerable amount is known of the biology and later-stage pathobiology of tau across the primary tauopathies, its role in Alzheimer’s disease as an induced pathology is poorly understood. Key questions remain: How does amyloid pathology induce tau pathology in AD? Why does AD tau arise and propagate in the observed neuron types and brain areas? How does tau pathology spread from one neuron and one area to another? An international, cross-institutional consortium of investigators with deep expertise in tau biology, amyloid precursor protein/amyloid beta biology and AD will together address the big questions that have not been convincingly answered, if answered at all. Given that tau is such a strong mediator of neurodegeneration and cognitive impairment in AD, deeper understanding is necessary to enable improved diagnostic and prognostic biomarkers, as well as to identify new opportunities for effective therapeutic intervention.



Marc Diamond, University of Texas Southwestern Medical Center
Role of VCP/p97 in Tau Prion Replication

Karen Duff, University College London
Consortium Chair, Impact of tau mutations and Aβ on tau post-translational modifications and conformation

Bradley Hyman, Massachusetts General Hospital
How do soluble tau species replicate?

Katherine Sadleir & Robert Vassar, Northwestern University
The role of Aβ-induced membrane damage in tau pathology

Henrik Zetterberg and Gunnar Brinkmalm, University of Gothenburg, Sweden
Deep mass spectrometry profiling of tau aggregates in Alzheimer’s disease and other tauopathies