Alzheimer’s disease (AD) is a devastating neurodegenerative disease that affects more than 15 million people worldwide. The social and economic burden of AD is enormous. There are estimates that by 2040, approximately 500’000 Australians will suffer from AD, with associated health costs of about 3% of the GDP. Unfortunately, until today, there is no effective treatment available.

To assist in the development of a safe treatment of AD, we developed cellular and animal models for AD and related disorders, using tissue culture, transplantation, transgenic and knockout techniques. Specifically, we aim to understand in molecular detail the mechanisms involved in the pathogenesis of AD and related neurodegenerative disorders.

Histopathologically, AD is characterized by β-amyloid (Aβ42)-containing plaques and tau-containing neurofibrillary tangles (NFTs). NFTs are composed of hyperphosphorylated filamentous forms of the microtubule-associated protein tau. They are, in the absence of amyloid plaques, also abundant in additional neuro-degenerative diseases including frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17). How Aβ production and tau dysfunction cause functional impairment of neurons and eventual neurodegeneration is not fully understood.

Previously, we established several transgenic mouse models including FTDP-17 (P301L) tau mutant mice, which develop NFTs. Their numbers can be increased upon intracerebral injection of fibrillar Aβ42. We also established a human SH-SY5Y tissue culture system of tau filament formation.

Reflecting the histopathological and clinical overlap between AD and Parkinson’s disease we have recently started to work on Parkinson’s-related aspects.

With the help of both proteomic and transcriptomic approaches, we have started to identify components of the patho-cascades in AD, to dissect pathogenic mechanisms and to identify exogenous factors with an impact on the AD pathology. As pathogenic mechanisms are likely shared between a whole range of neurodegenerative disorders, potential drugs targeting Aβ or tau might benefit a broader spectrum of neurodegenerative disorders than previously anticipated. Eventually we hope that our efforts will assist in the development of therapeutic treatment strategies.



  1. My name is Yesica, i am university student Lic. nutrition. I study about Choline and Alzheimer. Where can i get information?

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