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.
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 (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.
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.
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.