Animal models mimicking human diseases are necessary tools to translate knowledge from basic science to applications for patients. Since cause and development of a disease involve multiple factors (i.e. internal-genetic, external-toxic), several different models and, if appropriate, different species (i.e. mouse, primate) need to be examined. For this reason we have worked on or with the following mouse models:
Parkinsonian phenotype:

  • 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)
  • Transgenic ([A30P]α-synuclein)
  • Transgenic WT α-synuclein
  • Conditional (time- and/or tissue-specific) gene inactivation
  • Cre/LoxP-recombinase system
  • work in progress, in cooperation with S. Göbbels and K.-A. Nave (MPI Exp. Med., Göttingen)

Drosophila

Drosophila melanogaster as animal model for neurodegenerative processes.

The molecular principles underlying neurodegenerative processes are still not fully understood. The histological hallmark of Parkinson’s disease is the presence of intracellular aggregates, of which the protein α-synuclein is one of the major constitutive. In the case of Alzheimer’s disease one finds aggregates of the tubulin associated protein tau. We are using the fruitfly Drosophila melanogaster as an animal model to study the processes within a cell leading to the formation of aggregates and/or cell death.

In this context, our main focus is to produce and analyze highly toxic variants of α-synuclein in its relation to neurodegenerative processes.