Studies on zebrafish
However, until now little was known about the function of TDP-43. What are the consequences when this protein becomes non-functional? In order to answer this question, the team led by Bettina Schmid cooperated with the research group of Prof. Christian Haass to investigate the larvae of specially bred zebrafish. Their genetic code had been modified in such a way that no TDP-43 was produced in the organism of the fish. The result: the young fish showed massive muscle wasting and died a few days after hatching. Moreover, the extensions of the nerve cells which control the muscles were abnormal.
"To some extent, these are symptoms typical of ALS and FTD. Therefore, a loss of function of TDP-43 does seem to play a critical role in the disease," says Haass, Site Speaker of the DZNE Munich Site and chair of Metabolic Biochemistry at LMU.
The study revealed one more finding which surprised the researchers: the blood flow of the fish was massively disturbed. "It is well known that circulatory disorders play a part in other forms of dementia, notably in the case of Alzheimer's," says Haass. "We now want to investigate whether such problems with blood flow may be a general problem of neurodegenerative diseases and whether such problems occur particularly in patients with ALS and FTD."
|Contact: Dirk Frger|
Helmholtz Association of German Research Centres