Dr. George Bloom, a Professor of Biology, Cell Biology and Neuroscience, and Chair of the Department of Biology at the University of Virginia (UVA), speaks about Amyloid-β and Tau, the Trigger and Bullet in Alzheimer’s Disease Pathogenesis.
The defining features of Alzheimer's disease (AD) include conspicuous changes in both brain histology and behavior. AD brain is characterized microscopically by the combined presence of two classes of abnormal structures, extracellular amyloid plaques and intra-neuronal neurofibrillary tangles, both of which comprise insoluble, densely packed filaments. The soluble building blocks of these structures are amyloid-β (Aβ) peptides for plaques and tau for tangles. Aβ peptides are proteolytic fragments of the transmembrane amyloid precursor protein (APP), whereas tau is a brain-specific, axon-enriched microtubule-associated protein.
The behavioral symptoms of AD correlate with the accumulation of plaques and tangles, and are a direct consequence of the damage and destruction of synapses that mediate memory and cognition. Synapse loss can be caused by the failure of live neurons to maintain functional axons and dendrites, or by neuron death. During the past dozen years, a steadily accumulating body of evidence has indicated that soluble forms of Aβ and tau work together, independently of their accumulation into plaques and tangles, to drive healthy neurons into the diseased state, and that hallmark toxic properties of Aβ require tau.
Dr. George Bloom's seminar will highlight his lab's work aimed at unraveling the Aβ-induced, tau-dependent signaling pathways that cause AD.
