What are the causes of synapse failure in Alzheimer's disease?

The degeneration of synapses – the contact sites between nerve cells – is considered to be the main cause of neurodegenerative diseases like Alzheimer's, Parkinson's or prion diseases. As head of a new research group at the German Center for Neurodegenerative Diseases (DZNE), Professor Jochen Herms investigates why synapses degenerate and what can be done to impede the process. Herms also holds the chair “Translational Research in the Field of Neurodegeneration” at the Ludwig-Maximilians-Universität in Munich.

What are the proteins involved in the degradation of synapses? Which cellular changes take place and which drugs may counteract the degenerative process? To answer these questions Herms and his colleagues have specialized on long-term in vivo two-photon microscopy. This method makes it possible to monitor structural changes at synapses in the mouse brain for a period of weeks or months. “This is much more sensitive than observing the behavior of animals. In addition, drawing a parallel to the human diseases is far more straight forward, at least if one assumes synaptic failure as primary cause of neurodegenerative diseases,” says Herms.

Recently Herms made the headlines with an approach to developing a new method for early detection and therapy control of Alzheimer's disease. This method aims to detect tau aggregates – protein structures that accumulate in the central nervous system in Alzheimer's disease – in the retina of the eye. Currently, the researchers are still testing the method in animal models. But if the process turns out to be applicable to humans it would be possible to develop new diagnostic tools for Alzheimer’s disease. “Early diagnosis of Alzheimer's is very important because the disease begins long before the first symptoms appear. An effective therapy against Alzheimer's disease has not yet been established and this can most likely be attributed to the fact that in previous clinical studies, therapy started too late,” Herms explains.

Herms is very enthusiastic about his appointment with DZNE. “We will only advance in Alzheimer research if we critically bring into question common assumptions and develop new hypotheses. The strong support we receive at DZNE and the critical mass of scientists at DZNE provide us with the right environment required to achieve this goal,” he says. At the DZNE, Herms will focus entirely on doing basic research. In this undertaking, he will strongly profit from his medical background and profound knowledge in neuropathology: “Having a clear picture of the disease in humans helps a lot to better assess the relevance of certain observations in animal models,” says Herms.

Jochen Herms studied medicine, received his MD from the University Medical Center Hamburg-Eppendorf and then worked at the Max Planck Institute for Biophysical Chemistry in Göttingen in the lab of Otto Creutzfeldt. Afterwards he specialized in neuropathology at the University Göttingen and completed his habilitation on the function of the prion protein in neurons in 1999. Since 2001 he has been professor of neuropathology at the Ludwig-Maximilians-Universität in Munich (LMU), where he was appointed Chair of Translational Research in the Field of Neurodegeneration and joined DZNE in 2011.

Contact information:
Prof. Dr. Jochen Herms
German Center for Neurodegenerative Diseases (DZNE)
Ludwig-Maximilians-Universität Munich
Centre for Neuropathology
Feodor-Lynen Str. 23
81377 Munich
Email: jochen.herms(at)dzne.de
Tel.: +49 (0) 89 / 2180-78010
Daniel Bayer
German Center for Neurodegenerative Diseases (DZNE)
Press- and Public Relations
Email: daniel.bayer(at)dzne.de
Tel: +49 (0) 228 43302 /261

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