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The University of Southampton
Biological Sciences

CANCELLED - Tau Protein and Neurodegeneration Event

Dr Michel Goedert
26 March 2020
Building 29│Room 1101 L/T | Highfield Campus

For more information regarding this event, please email Professor Vincent O’connor at .

Event details

SoBS Distinguished Lecturer Seminar Series Programme 2019-20

Abundant inclusions made of hyperphosphorylated filamentous tau protein are characteristic of many human neurodegenerative diseases, including Alzheimer’s disease, tangle-only dementia, chronic traumatic encephalopathy, Pick’s disease, argyrophilic grain disease, progressive supranuclear palsy, corticobasal degeneration, as well as dominantly inherited frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17T). The identification of mutations in MAPT, the tau gene, in FTDP- 17T established that dysfunction of tau protein is sufficient to cause neurodegeneration and dementia. Tau inclusions appear to exist as multiple conformers that propagate through the brain, suggesting a conceptual link between tauopathies and prion diseases. The structures of amyloid filaments can be determined using electron cryo-microscopy. We have reported the structures of tau filaments from Alzheimer’s disease, Pick’s disease, chronic traumatic encephalopathy and corticobasal degeneration. Evidence so far indicates inter-disease, but not inter-subject, variability of tau filament structures.

Different tau isoforms play a role in giving rise to distinct filament structures. In addition, cofactors and/or post-translational modifications may be involved. It seems clear that filamentous tau adopts distinct folds in different human neurodegenerative diseases, establishing the existence of conformers of assembled tau.

Speaker information

Dr Michel Goedert, University of Cambridge, Current work is aimed at developing experimental animal models of tauopathies and alpha-synucleinopathies and at identifying disease modifiers.

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