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Heidelberg researchers investigate new approaches to treating neurodegenerative diseases

Protecting nerve cells from losing their characteristic extensions, the dendrites, can reduce brain damage after a stroke. Neurobiologists from Heidelberg University have demonstrated this by means of research on a mouse model. The team, led by Prof.Dr. Hilmar Bading in cooperation with Junior Professor Dr. Daniela Mauceri, is investigating the protection of neuronal architecture to develop new approaches to treating neurodegenerative diseases. The current research findings were published in the journal “Proceedings of the National Academy of Sciences”.

Brain nerve cells possess many arborised dendrites, which can make connections with other neurons. The highly complex, ramified structure of neurons is an important precondition for their ability to connect with other nerve cells, in order to enable the brain to function normally. In earlier studies, the Heidelberg researchers identified the signal molecule VEGFD – Vascular Endothelial Growth Factor D – as a central regulator for maintaining and restoring neuronal structures. “Our current research results demonstrate that a stroke as a consequence of an interruption of the blood supply to the brain leads to a reduction of VEGFD levels. That causes the nerve cells to lose part of their dendrites. They shrink and this leads to impairments of the cognitive and motor abilities,” explains Prof. Bading.

Based on these findings, the researchers at the Interdisciplinary Centre for Neurosciences explored the question of whether the reduction of neuronal structures after a stroke can be prevented by restoring the VEGFD levels. More...

Zum Tod von Günther Schütz, IZN Alumnus

Das Deutsche Krebsforschungszentrum trauert um Günther Schütz, einen großen Wissenschaftler und hoch angesehen ehemaligen Kollegen, der am 28. Mai im Alter von 80 Jahren verstorben ist. Mehr...

What determines the identity of cells?

Scientists from the Hector Institute for Translational Brain Research and Stanford University showed in mice how so-called pioneer factors determine the identity of nerve and muscle cells. During embryonic development, these factors ensure that the various body cells can form. In laboratory experiments, pioneer factors can even be used to transform cell types, for example skin cells into nerve cells. This allows scientists to obtain specific cell types for their research.

Moritz Mall at the German Cancer Research Center (DKFZ, HITBR) and Qian Yi Lee at Stanford University compared two transcription factors that are structurally similar but induce completely different cell types. The factor Ascl1 can program skin cells into nerve cells, while Myod1 can convert skin cells into muscle cells.

Since transcription factors normally exert their effect by binding certain gene switches, the researchers first investigated the DNA binding sites of both factors. Although Ascl1 and Myod1 induce very different cell types, both surprisingly bind to largely overlapping recognition sequences in the mouse genome. This is true both during reprogramming and during normal cell differentiation. "For us, this was an indication that other mechanisms must be involved to ensure that only the desired genes are regulated," explains Mall. In fact, further analyses showed that despite the overlap, Ascl1 and Myod1 each attached to specific regions of the genome with stronger binding power. More...

An epigenetic factor in memory-encoding neurons improves the ability to remember

It is currently thought that memories are represented within the neurons that are activated when we acquire new information and that the retrieval of a memory requires the reactivation of this subset of neuons. The group led by Dr. Ana Oliveira now found that, increasing a protein called Dnmt3a2, that is responsible for establishing chemical marks on the DNA, specifically in hippocampal memory-encoding cells is sufficient to boost memory in mice and to modulate the precision of the reactivation of the memory-encoding cells.

The scientists trained laboratory mice in a Pavlovian-conditioning task, and labelled the cells of the hippocampus that encode the memory for that experience (around 5% of the whole hippocampus). When they increased Dnmt3a2 levels selectively in these memory-encoding cells, they observed that the mice had improved memory performance. This was associated with better reactivation of the “correct” memory-encoding cells during memory recall. Remarkably, the same protein was previously shown to restore aging-related cognitive dysfunctions, and to facilitate the erasure of traumatic memories in mice. Therefore, this study opens a new gate for future studies aimed at designing new therapeutic approaches based on targeting memory-encoding cells, to modulate the duration of memories.

Related article: Neuronal ensemble-specific DNA methylation strengthens engram stability