We generated a genetically conditional expression model of TAU protein in adult zebrafish brain


Alzheimer‘s disease is the most common neurodegenerative disease, and one of the cellular hallmarks is toxicity caused by a protein called TAU. In humans, mutations in TAU leads to disruption of the microtubules, the major transport routes in our neurons. When we lose the integrity of our microtubules, neurons die. A big question is: “Can we stop the death of neurons by preventing the toxicity of TAU protein, and can we cure neurodegeneration?”

Today, we are glad to announce our recent publication that works in small steps towards this big question:

We are excited to have a clue that zebrafish may show us the way how to prevent TAU-dependent neurodegenerative disorders such as #Alzheimer’s disease or FrontotemporalDementia. In our study, we made the zebrafish brain produce the most aggressive and disease-associated mutated version of human TAU protein. As a result, we found that zebrafish brain may have a molecular program that prevents TAU-mediated toxicity, and keeps the neurons alive. This finding is significant and may help us to find out how we can cure TAU-dependent neurodegenerative diseases in humans. Combined with our previous findings in Kizil Lab at DZNE Helmholtz Association, we are stepping towards a better understanding how we can regenerate after neurodegeneration – a fascinating question for clinical studies.

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