Jürgen Götz, PhD
Primary tabs
JAD profile
Associate Editor
Term Expiration:
12/31/2025
Affiliation(s):
Queensland Brain Institute (QBI); The University of Queensland (St Lucia Campus)
ORCID URL:
Areas of Interest:
Alzheimer's disease, amyloid, frontotemporal dementia, mitochondria, phosphorylation, tau, transgenic
Biography & Research:
Jürgen Götz studied biochemistry at the University of Basel, and earned his PhD in immunology in the laboratory of Nobel Laureate Georges Köhler at the Max-Planck-Institute in Freiburg, Germany (1989). After postdoctoral work at UCSF and the Preclinical Research Division at Novartis Ltd in Basel, he established his reputation in the Alzheimer’s field as a research group leader at the University of Zürich (1994–2005). From 2005 - 2011, he has been Chair of Molecular Biology and Director of the Alzheimer’s and Parkinson’s Laboratory at the Brain and Mind Research Institute of the University of Sydney. In February 2012 he took up the position as Foundation Chair of Dementia Research at The University of Queensland and inaugural director of the Clem Jones Centre for Ageing Dementia Research (CJCADR) at the Queensland Brain Institute (QBI).
Research: Jürgen Götz uses transgenic mouse models to dissect pathomechanisms in Alzheimer’s disease (AD). He generated the first tau transgenic mouse model with an early AD phenotype (EMBO J 1995). Together with Dr. Hutton, Götz published the first mouse model with NFT formation (JBC 2001a). He provided long-sought evidence for the amyloid cascade hypo-thesis by combining a transgenic and a transplantation approach (Science 2001). This highly cited work was accompanied by an Editorial in the same issue of Science, and selected as Milestone Paper by the Alzforum (alzforum.org). Jürgen Götz further provided a role for FGF5 in the hair growth cycle (Cell 1994), worked on prions (Cell 1998), and showed that the catalytic subunit of PP2A is essential for development (PNAS 1998) and that PP2A is a key enzyme in tau phosphorylation (JBC 2001b, AmJPathol 2003). He established the first in vitro model of Aβ-induced tau filament formation (JBC 2003). By functional genomics, he provided evidence for mitochondrial dysfunction and a role for glyoxalase in AD (PNAS 2003, JBC 2005, Proteomics 2006, PNAS 2009). He identified a novel dendritic function of tau (Cell 2010). He developed a novel ultrasound-based treatment of amyloid-depositing mice that he intends to develop for clinical application in AD patients (Science Transl Med 2015). In addition, he authored several well-cited reviews (e.g. BRR 2001, MolPsych 2004, NatRevNeurosci 2008, NatRevNeurosci 2011).
