Parkinson's disease

The Parkinson's disease is the second most common neurodegenerative disorder, characterized by the progressive death of dopamine-producing and other nerve cells. Various molecular mechanisms are associated with the pathophysiology of Parkinson's disease. We investigate the influence of axonal transport, aging, as well as immune cells on the pathology of Parkinson's syndrome.

Axonal Transport:

While the progressive degeneration of nerve cells represents a final stage of pathological changes in neurodegenerative diseases, disturbances in the nerve processes occur early in the course of the disease. We want to find out what influence alpha-synuclein, a protein that determines Parkinson's disease, has on the function of nerve processes and specifically investigate the aspect of axonal transport in connection with alpha-synuclein.

Aging: 

Age is the highest risk factor for developing Parkinson's disease. Therefore, we are interested in the influence of aging on astrocytes and neurons. We treat cells with aging-associated as well as Parkinson-associated stress and investigate the relationship between cell functionality and the occurrence of aging markers, such as senescence markers.

Immune Cells in the Pathophysiology of Parkinson's Disease: 

Although Parkinson's disease is a primary neurodegenerative disorder, it has been found that immune cells are involved in the development of the disease. Much is already known about the harmful influence of the local immune cells of the central nervous system, the microglial cells. The effect of peripheral immune cells, particularly T-lymphocytes, on the pathophysiology of Parkinson's disease is less well understood. Therefore, we are investigating the influence of T-lymphocytes on Parkinson's disease in rodent models and in human (iPSC-based) models.