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Amyloid-β and Tau: the Trigger and Bullet in Alzheimer’s Disease Pathogenesis, George Bloom, PhD
October 5, 2016 @ 3:35 pm - 4:00 pm
George Bloom, PhD, Professor of Biology and of Cell Biology, University of Virginia —
The well known behavioral symptoms of Alzheimer’s disease (AD) result from two processes that compromise brain function: synaptic dysfunction and loss among neurons that mediate memory and cognition, and the death of those neurons. It follows naturally that defining the causes of synapse failure and neuron death at the molecular and cellular levels will lead to improved early diagnosis and the development of disease-modifying therapies for AD. A growing body of evidence indicates that soluble forms of amyloid-β (Aβ) and tau, the respective building blocks of the insoluble plaques and tangles that characteristically accumulate in AD brain, work together to cause synapse failure and neuron death. An overview of data that support this pathogenic Aβ-tau connection will be presented, along with a more detailed description of a cellular signaling network that is triggered by soluble Aβ and requires tau to drive neuronal death in AD.