The 4th Proteostasis and Disease Research Symposium

Michele Vendruscolo is Professor of Biophysics, Co-Director of the Centre for Misfolding Diseases and Director of the Chemistry of Health Laboratory at the Department of Chemistry of the University of Cambridge where he moved over 20 years ago. His work is aimed at establishing the fundamental principles of protein homeostasis and protein aggregation, and at exploiting these principles to develop methods for drug discovery in neurodegenerative diseases. He has published over 450 scientific papers and 20 patents, and given over 500 invited lectures at international meetings. He is founder, director and chief scientific officer of Wren Therapeutics, a drug discovery company that targets protein misfolding diseases. 

Professor Michele Vendruscolo  

University of Cambridge, UK 

Dr. Finley graduated from Harvard College in 1980. He received his PhD from MIT, having worked with Alex Varshavsky and in collaboration with Aaron Ciechanover. His thesis work, identifying a mammalian cell line expressing a temperature-sensitive ubiquitin activating enzyme, showed unexpectedly that the ubiquitin pathway is the major pathway for selective protein degradation. This work also revealed that the pathway is essential and that it is linked to cell cycle control and the stress response. He was appointed in 1988 to the faculty at Harvard Medical School, where he remains today, studying proteasome regulation, function, and assembly as well as global proteome remodeling. 

Professor Daniel Finley  

Harvard Medical School, USA

Doctor Benedetta Bolognesi completed her PhD in the Department of Chemistry at the University of Cambridge (UK) under the supervision of Prof. Chris Dobson. Her work focused on the intrinsic determinants of aggregation and toxicity of the amyloid-beta peptide. Doctor Bolognesi then moved to the Centre for Genomic Regulation (Barcelona, Spain) with an interdisciplinary Marie Curie fellowship to elucidate the mechanisms underlying dosage sensitivity in yeast. She is now a Junior Group Leader at the Institute for Bioengineering of Catalunya in Barcelona, Spain. The central question to her research is understanding how protein self-assembly can cause cellular toxicity - a complex question that individual disciplines failed to exhaustively address. Doctor Bolognesi has tackled this problem by means of several approaches during my career, ranging from biophysics to cell biology and genomics. Her group combines genomics to biophysics to study functional and dysfunctional protein self-assembly. They have developed a deep mutational scanning strategy to quantitatively measure the toxicity of thousands of protein sequences in parallel. They have also recently combined deep mutagenesis to another approach through which we are able to measure the ability of thousands of sequences to nucleate amyloids. 

Doctor Benedetta Bolognesi  

Institute for Bioengineering of Catalonia, Spain 

Michael Heneka studied medicine in Tübingen, Lausanne and London from 1990-1996. He obtained his medical degree at the Institute of Pharmacology for which he received the 1998 Attempto Award of the University of Tübingen. He started his clinical residency in neurology at the Dept. of Neurology of the Univ. of Tübingen in 1996 and joined the Dept. of Neurology at the University of Bonn in 1999. After his clinical board examination (2002) and habilitation (2003) he took the chair as professor for molecular neurology at the University of Münster in 2004. In 2008 he was appointed professor for clinical neurosciences at the University of Bonn heading the DFG Clinical Research Unit 177. Since 2010 Prof. Heneka has served as neurological director of the joint memory clinic of the Departments of Psychiatry and Neurology. Since 2016 acts as director of the Dept. of Neurodegenerative Disease and Geriatric Psychiatry. His scientific interest is focussing on the role of innate and adaptive immune mechanisms for neurological disorders. Beyond his research, Michael Heneka serves as Associate Editor of Neurology: Neuroinflammation and Neuroimmunology and editorial board member of Molecular Neurobiology, Journal of Neurochemistry and Alzheimer Research & Therapy. He is the organizing chair of the biennial conference “Venusberg Meeting on Neuroinflammation”. In 2011 he received the Christa Lorenz Award for ALS Research and in 2013 the Hans und Ilse Breuer Award for Alzheimer Research. 

Professor Michael Heneka  

German Centre for Neurodegenerative Disease, Germany

Professor Ursula Jakob received her Ph.D. in the Department of Physical Biochemistry from the University of Regensburg in 1995 for her work on the identification and characterization of Hsp90 and small heat shock proteins as molecular chaperones. She then moved to Michigan where she conducted a 5-year postdoctoral fellowship in the lab of Dr. James Bardwell. There, she discovered the heat shock protein Hsp33 as the first known redox-regulated chaperone. This work helped establish the field of redox-regulation in biology. In 2000, she received the Burroughs Wellcome Fund Career Award and started her independent research career at the University of Michigan one year later. She is now the Patricia S. Yaeger Collegiate Professor in the Department of Molecular, Cellular and Developmental Biology and Professor in the Department of Biological Chemistry at the University of Michigan Medical School. Her main interest concerns the role of oxidative stress and redox regulation in aging and disease. She has published over 100 peer-reviewed articles and has received awards from the National Institute of Aging (NIA), the National Institute of Allergy and Infectious Disease (NIAID), and the National Institute of General Medical Sciences (NIGMS). In 2014, she was elected to the Bavarian Academy of the Sciences and Humanities. In 2019, she received the Breakthrough in Gerontology Award.  

Professor Ursula Jakob  

University of Michigan, USA 

Professor Yuji Goto obtained a Doctoral Degree (1982) from the Graduate School of Science, Osaka University. He experienced postdoctoral period in 1986-1988 at UC Santa Cruz. His current research interests include protein folding, stability and misfolding. At the Institute for Protein Research (1998-2020), his group developed several key techniques studying amyloid fibrils. These include the H/D exchange of amyloid fibrils monitored by NMR, the real-time and single-fiber monitoring of amyloid growth by total internal reflection fluorescence microscopy, and the calorimetric measurements of amyloid formation. He has shown that ultrasonication is an effective agitation to trigger amyloid formation and invented HANdai Amyloid Burst Inducer (HANABI). Now, he proposes an alternative view of amyloid fibrils as supersaturation-limited crystal-like aggregates formed above solubility. He was the first President of Asian Pacific Protein Association (2010-2011).  

Professor Yuji Goto  

Graduate School of Engineering Microsonochemistry Joint Research Laboratory, Osaka University, Japan 

Kay Double is Professor of Neuroscience at the Brain and Mind Centre at the University of Sydney where she heads the Neurodegeneration Research Laboratory. Kay holds a PhD, and the international degree of the Habilitation, in neurochemistry. Her work focuses on cellular mechanisms for neuronal vulnerability in neurodegenerative disorders of movement and dementia. Her recent work focuses on the roles of altered biometal homeostasis and metalloprotein structure and function in neurodegeneration, particularly in Parkinson disease and amyotrophic lateral sclerosis where her team have identified a shared disease-associated pathway. Her ultimate aim is to develop disease-modifying interventions which can slow or stop these disease processes. Her approach is multidisciplinary and highly collaborative nationally and internationally.  

Professor Kay Double  

University of Sydney, Australia

Associate Professor Mike Griffin is laboratory head in the Department of Biochemistry and Molecular Biology at the Bio21 Molecular Science and Biotechnology Institute, University of Melbourne. He completed his PhD at the University of Canterbury, New Zealand in 2005 and then moved to the Bio21 institute, where studied amyloid formation by serum apolipoproteins. In 2011 he was awarded an ARC Australian Postdoctoral Fellowship, in 2013 the C.R. Roper Fellowship and in 2015 an ARC Future Fellowship. His research focuses on understanding the structural and mechanistic underpinnings of protein-protein interactions, ranging from protein misfolding and aggregation events that lead to the formation of amyloid, through to native interactions that lead to formation of large multimeric complexes. He is particularly interested in the interactions of small heat-shock proteins with soluble amyloid forming proteins and mature amyloid fibrils, and how these interactions modulate fibril formation and the properties of amyloid aggregates. 

Associate Professor Michael Griffin  

University of Melbourne, Australia

Doctor Nadinath Nillegoda is a cell biologist studying cellular repair mechanisms that help maintain protein homeostasis after proteotoxic stress insults. He completed his PhD in Biomedical Sciences at the Mount Sinai School of Medicine of New York University and postdoctoral work at Heidelberg University and the German Cancer Research Center. He is currently working as a Group Leader at the Australian Regenerative Medicine Institute at Monash University. His work combines biochemistry, cell biology and animal models of disease to understand how potentially cytotoxic protein aggregates are solubilized (disaggregated) and cleared in human cells.  His research opens the possibility to reverse, rather than prevent protein aggregation, therefore, is an attractive new direction for future therapeutic interventions for a broad range of protein conformational disorders that have limited or no cures.  

Doctor Nadinath Nillegoda  

Monash University, Australia

Professor Massimo Hilliard received his PhD in Biological Chemistry and Molecular Biology in 2001 from the University of Naples, Italy, working under the supervision of Dr Paolo Bazzicalupo.  He then undertook postdoctoral training with Prof William Schafer at the University of California San Diego, and with Prof Cori Bargmann at the University of California San Francisco and Rockefeller University.   In 2007, he was appointed as a Senior Research Fellow at the Queensland Brain Institute, University of Queensland, where he has established his independent laboratory.  He was subsequently awarded an ARC Future Fellowship, and in 2015 was promoted to Associate Professor and awarded a NHMRC Senior Research Fellowship.  In 2019, he was promoted to Professor.  During his career Prof Hilliard has focused on understanding the molecular mechanisms that regulate neuronal development, maintenance, and repair, using C. elegans as a model system.  His laboratory has identified the molecular mechanisms that regulate axonal fusion, an axonal repair event in which the two separated fragments of an injured axon rejoin and reconstitute the original tract.  His research has been funded by the NIH, NHMRC, and ARC, and his discoveries have been published in top tier journals, including Nature and Science. 

Professor Massimo Hilliard  

University of Queensland, Australia

Doctor Lou Fourriere completed her PhD in September 2016 in the Cell Biology and cancer department at the Institut Curie (Paris, France) after 4 years in the laboratory of Franck Perez. Her research investigated the role of microtubules in intracellular trafficking, particularly membrane trafficking from the Golgi to the cell surface. By using the Retention Using Selective Hooks (RUSH) system, which had been developed by Franck Perez, to synchronize the anterograde trafficking of cargoes in real time, she showed that cargoes are delivered to ‘hot spots’ on the plasma membrane and that microtubules were not strictly essential for cargoes delivery to the surface. After her PhD, Lou joined the team of Paul Gleeson (Bio21 Molecular Science and Biotechnology Institute, University of Melbourne). She is investigating the intracellular trafficking of the b-secretase (BACE1) and amyloid precursor protein (APP) to characterize their trafficking routes and the machinery regulating these trafficking routes, information that could be exploited for future development of novel therapeutics for Alzheimer’s disease. By using a range of optical imaging approaches including the RUSH system, spinning disk, TIRF microscopy, and high resolution imaging she has been able to track the transport pathways of newly synthesized BACE1 and APP in HeLa cells and mouse primary neurons. Her studies have demonstrated the partitioning of BACE1 and APP within the Golgi apparatus, a process which is critical to the regulation of APP processing and amyloid production within the secretory pathway. 

Doctor Lou Fourriere-Chea  

University of Melbourne, Australia

Dr. Julia Pagan performed her postgraduate studies in the laboratory of Professor Kum Kum Khanna at the Queensland Institute of Medical Research.  Her post-doctoral work was performed in the Biochemistry Department at New York University Langone Medical Center under the mentorship of Professor Michele Pagano.  Here, she studied the molecular and biochemical mechanisms by which cullin-RING ligases (CRLs) [particularly, SCF (Skp1-Cul1-F-box protein) ubiquitin ligase complexes also known as CRL1s] regulate cell growth and proliferation. In 2018, she moved to the School of Biomedical Sciences, UQ, to commence a teaching and research position. Her research program at UQ uses interdisciplinary approaches incorporating biochemistry, proteomics, molecular and cell biology to understand how individual ubiquitin ligase subunits specifically target their substrates. We focus particularly on understanding the regulation of centrosomes, microtubules and mitochondria. Corrupting the regulatory pathways that coordinate these organelles can have major health consequences and is the driving force behind many diseases, including cancers and neurodegenerative disorders. 

Doctor Julia Pagan  

University of Queensland, Australia