Prof. Dr. Estifanos Ghebremedhin, Institut für klinische Neuroanatomie
am 7. Mai 2018
Parkinson’s disease is the most common movement disorder and the second most common neurodegenerative disease after Alzheimer’s disease. The main neuropathological features of Parkinson’s disease are harmful protein deposits called Lewy bodies and Lewy neurites. They consist mainly of insoluble lumps of the protein alpha-synuclein. At present, however, the causes and development of the neurodegenerative process in Parkinson’s disease are only known to a limited extent.
In contrast to many other neurodegenerative diseases, the changes occur not only in the central but also in the peripheral nervous system. It is currently assumed that the altered protein spreads within the nervous system in a similar way to the prion protein – for example in Creutzfeldt-Jakob disease. The process of protein folding is essential. This means the development of the three-dimensional structure that is a prerequisite for the faultless function of the protein. It is assumed that the altered or misfolded alpha-synuclein can be transferred between nerve cells and that other alpha-synucleins also misfold. This leads to a chain of interconnected nerve cells with incorrectly folded proteins that could be responsible for neurodegeneration. Whether the pathological process spreads from the central to the peripheral nervous system or vice versa is still an open question.