Prof Lars Ittner

TEAM LEADER PROFILE

Principal Senior Research Fellow, NeuRA Professor, School of Medical Sciences, UNSW
NHMRC Senior Research Fellow

+612 9385 0016


Lars Ittner graduated in medicine from the University of Ulm in Germany in 2001, and was awarded with the Doctor of Medicine from the University of Zurich in Switzerland in 2002. In 2002 Lars was selected into the highly competitive Postgraduate (PG) Course for Experimental Biology and Medicine, held at the University of Zurich. After completing the PG course, he became a Postdoctoral Research Fellow in the laboratory of Prof Fischer till June 2005. In July 2005, he joined Prof Jürgen Götz as a Postdoctoral Research Fellow to establish the Alzheimer’s and Parkinson’s Disease Laboratory at the Brain & Mind Research Institute of the University of Sydney, focusing his work on neurodegenerative disorders. In April 2011, he was promoted to Associate Professor and has led the Alzheimer’s and Parkinson’s Disease Laboratory since early 2012. In July 2013, Lars joined the School of Medical Sciences at the University of New South Wales and Neuroscience Research Australia to head the Dementia Research and Transgenic Animal Units. In January 2014 Lars became a full Professor in the Department of Anatomy at the University of New South Wales.

Projects Prof Lars Ittner is currently involved with

CURRENT PROJECTS

Alzheimer’s disease

This project focuses on how pathology spreads during disease progression, the link between amyloid-β (Aβ) and tau pathology, and down-stream mechanisms of Aβ- and tau toxicity.

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Alzheimer’s disease

Healthy brain ageing

This project aims at understanding the physiological functions of tau, in particular in the post-synapse, and how these functions change during aging.

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Healthy brain ageing

Drug development

The focus of this project is on advancing tau-targeted immunotherapy and compounds that interfere with pathological processes mediated by tau.

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Drug development

Frontotemporal dementia and motor neurone disease

This project’s objective is to develop cell culture and mouse models to study underlying pathomechanisms and develop/test new treatments.

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Frontotemporal dementia and motor neurone disease

Stroke

This new line of our research aims at revealing the role of the cytoskeleton in brain damage after stroke.

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Stroke

RESEARCH TEAM

YAZI KE Lecturer : yazi.ke@unsw.edu.au

Fabien Delerue

FABIEN DELERUE Lecturer : fabien.delerue@unsw.edu.au

JANET VAN EERSEL Lecturer : j.vaneersel@unsw.edu.au

ARNE ITTNER Postdoctoral Research Fellow : a.ittner@unsw.edu.au

Sook Wern Chua

SOOK WERN CHUA Postdoctoral Research Fellow : sook.chua@unsw.edu.au

ANNIKA VAN HUMMEL Postdoctoral Research Fellow : a.vanhummel@unsw.edu.au

ADAM MARTIN Postdoctoral Research Fellow : adam.martin2@unsw.edu.au

Josefine Bertz

JOSEFINE BERTZ Research Assistant : j.bertz@unsw.edu.au

YIJUN LIN Research Assistant : yijun.lin@unsw.edu.au

TROY BUTLER Research Assistant : troy.butler@unsw.edu.au

Claire Stevens

CLAIRE STEVENS PhD student

Mian Bi

MIAN BI PhD Student : m.bi@student.unsw.edu.au

STEFANIA IPPATI PhD Student : s.ippati@student.unsw.edu.au

Lisa Suh

LISA SUH PhD Student : lisa.suh@unsw.edu.au

JULIA VAN DER HOVEN PhD Student : j.vanderhoven@student.unsw.edu.au

ALEXANDER VOLKERLING PhD Student : a.volkerling@student.unsw.edu.au

MAGDALENA PRZYBYLA PhD Student : m.przybyla@unsw.edu.au

WEI LEE PhD Student : wei.lee@student.unsw.edu.au

PRITA ASIH PhD Student : p.asih@student.unsw.edu.au

KRISTIE STEFANOSKA PhD Student : k.stefanoska@unsw.edu.au

MERRYN BRETTLE PhD Student : m.brettle@unsw.edu.au

SHERILYN YAO Student Assistant : sherilyn.yao@student.unsw.edu.au

PUBLICATIONS

FTD and ALS--translating mouse studies into clinical trials.

Ittner LM, Halliday GM, Kril JJ, Götz J, Hodges JR, Kiernan MC

Frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) are related neurodegenerative disorders, which are characterized by a rapid decline in cognitive and motor functions, and short survival. Although the clinical and neuropathological characterization of these diseases has progressed–in part–through animal studies of pathogenetic mechanisms, the translation of findings from rodent models to clinical practice has generally not been successful. This article discusses the gap between preclinical animal studies in mice and clinical trials in patients with FTD or ALS. We outline how to better design preclinical studies, and present strategies to improve mouse models to overcome the translational shortfall. This new approach could help identify drugs that are more likely to achieve a therapeutic benefit for patients.

Early-onset axonal pathology in a novel P301S-Tau transgenic mouse model of frontotemporal lobar degeneration.

van Eersel J, Stevens CH, Przybyla M, Gladbach A, Stefanoska K, Chan CK, Ong WY, Hodges JR, Sutherland GT, Kril JJ, Abramowski D, Staufenbiel M, Halliday GM, Ittner LM

In TAU58/2 mice, early tau pathology induces functional deficits of neurones associated with NF pathology. This appears to be specific to tau, as similar changes are observed in FTLD-tau, but not in FTLD with TDP-43 inclusions. Therefore, TAU58/2 mice recapitulate aspects of human FTLD-tau and AD pathology, and will become instrumental in studying disease mechanisms and therapeutics in the future.

Amyotrophic lateral sclerosis and frontotemporal dementia: distinct and overlapping changes in eating behaviour and metabolism.

Ahmed RM, Irish M, Piguet O, Halliday GM, Ittner LM, Farooqi S, Hodges JR, Kiernan MC

Metabolic changes incorporating fluctuations in weight, insulin resistance, and cholesterol concentrations have been identified in several neurodegenerative disorders. Whether these changes result from the neurodegenerative process affecting brain regions necessary for metabolic regulation or whether they drive the degenerative process is unknown. Emerging evidence from epidemiological, clinical, pathological, and experimental studies emphasises a range of changes in eating behaviours and metabolism in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). In ALS, metabolic changes have been linked to disease progression and prognosis. Furthermore, changes in eating behaviour that affect metabolism have been incorporated into the diagnostic criteria for FTD, which has some clinical and pathological overlap with ALS. Whether the distinct and shared metabolic and eating changes represent a component of the proposed spectrum of the two diseases is an intriguing possibility. Moreover, future research should aim to unravel the complex connections between eating, metabolism, and neurodegeneration in ALS and FTD, and aim to understand the potential for targeting modifiable risk factors in disease development and progression.

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