See also http://alzheimerlab.wordpress.com.

Lab profile

Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the two most common neurodegenerative disorders in humans. They are characterised by insoluble protein deposits; beta-amyloid plaques and tau-containing neurofibrillary lesions in AD, and alpha-synuclein-containing Lewy bodies in PD. As a significant percentage of patients have clinical and pathological features of both diseases, the patho-cascades of the two diseases might overlap.

Professor Jürgen Götz and his team address key questions in the field by combining transgenic and knockout techniques with a particularly wide array of analytical tools including functional genomics. With the recent establishment of the tiny roundworm C. elegans as a novel model organism in the lab, a further step is made towards a treatment of these debilitating diseases.

Animal models have become indispensable in basic and biomedical research. The identification of pathogenic mutations in familial forms of Alzheimer’s disease (AD) and frontotemporal dementia (FTD) greatly assisted in establishing transgenic animals that model key aspects of the human disease. In AD, mutations have been identified in the APP, PSEN1 and PSEN2 genes (n indicating current numbers of mutations), whereas in FTD with Parkinsonism linked to chromosome 17 (FTDP-17), mutations have been identified in the MAPT gene encoding tau. AD is characterised by amyloid plaques and neurofibrillary tangles (NFTs), while in FTDP-17, NFTs occur in the absence of overt plaques. The formation of these two lesions has been faithfully reproduced in vivo. Of the clinical features that characterize AD and FTD some have been reproduced in model organisms. Other aspects such as the distinct spreading that characterizes the NFT pathology in AD or the distinct age of onset and disease duration that discriminates, e.g., carriers of mutations in the tau-encoding MAPT gene and the progranulin-encoding PGRN gene have not been reproduced.

Animal models have become indispensable in basic and biomedical research. (A) The identification of pathogenic mutations in familial forms of Alzheimer's disease (AD) and Frontotemporal dementia (FTD) greatly assisted in establishing transgenic animals that model key aspects of the human disease. In AD, mutations have been identified in the APP, PSEN1 and PSEN2 genes (n indicating current numbers of mutations), whereas in FTD with Parkinsonism linked to chromosome 17 (FTDP-17), mutations have been identified in the MAPT gene encoding tau. AD is characterized by amyloid plaques and NFTS, while in FTDP-17, NFTs occur in the absence of overt plaques. The formation of these two lesions has been faithfully reproduced in vivo. (B) Of the clinical features that characterize AD and FTD some have been reproduced in model organisms. (C) Other aspects such as the distinct spreading that characterizes the NFT pathology in AD or (D) the distinct age of onset and disease duration that discriminates, e.g., carriers of mutations in the tau-encoding MAPT gene and the progranulin-encoding PGRN gene have not been reproduced.