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New Class of Highly Effective Inhibitors Protects against Neurodegeneration

Heidelberg neurobiologists decode central mechanism of degenerative processes in the brains of mouse models and develop new principle for therapeutic agents

Neurobiologists at Heidelberg University have discovered how a special receptor at neuronal junctions that normally activates a protective genetic programme can lead to nerve cell death when located outside synapses. Their fundamental findings on neurodegenerative processes simultaneously led the researchers at the Interdisciplinary Center for Neurosciences (IZN) to a completely new principle for therapeutic agents. In their experiments on mouse models, they discovered a new class of highly effective inhibitors for protecting nerve cells. As Prof. Dr Hilmar Bading points out, this novel class of drugs opens up – for the first time – perspectives to combat currently untreatable diseases of the nervous system. The results of this research were published in “Science”.

The research by Prof. Bading and his team is focused on the so-called NMDA receptor. This receptor is an ion channel protein that is activated by a biochemical messenger: the neurotransmitter glutamate. It allows calcium to flow into the cell. The calcium signal sets in motion plasticity processes in the synapse but also propagates into the cell nucleus, where it activates a protective genetic programme. Glutamate-activated NMDA receptors located in the junctions of the nerve cells have a key function in the brain, contributing to learning and memory processes as well as neuroprotection. But the same receptors are also found outside of synapses. These extra-synaptic NMDA receptors pose a threat because their activation can lead to cell death. Normally, however, efficient cellular uptake systems for glutamate make sure that these receptors are not activated and nerve cells remain undamaged. More...

Gene defect influences tumor development in childhood brain tumors

Medulloblastoma are the most common malignant brain tumors affecting children. The greatest danger is that the cancer cells can quickly spread to the surrounding tissues. Two genetic defects play a key role in the onset of these tumors, as scientists at the Hopp Children's Cancer Center Heidelberg (KiTZ), the German Cancer Research Center (DKFZ) and the National Institute of Neuroscience in Tokyo have discovered. The aim is for the findings to help scientists develop personalized treatment strategies for young patients.

At the Hopp Children's Cancer Center Heidelberg (KiTZ), scientists are conducting intensive research into the onset of medulloblastoma in order to develop new therapy options. "The onset of malignant medulloblastoma cells has genetic causes and follows several stages," explains Lena Kutscher, a Junior Group Leader at the KiTZ and the DKFZ. "First, genetic mutations cause excessive proliferation of certain precursor nerve cells, and growths develop. If more mutations occur, they can turn into malignant tumor cells that spread into the surrounding tissue."

Together with colleagues from the National Institute of Neuroscience in Tokyo and from St. Jude Children's Hospital in the USA, the research team came across two key genetic drivers for the onset of medulloblastoma in the Sonic Hedgehog medulloblastoma subgroup (SHH). The BCOR gene is regarded as a tumor suppressor gene, and its protein product normally suppresses the uncontrolled division of cells with genetic defects, thereby preventing the onset of tumors. Earlier studies have shown that in eight percent of young SHH patients, BCOR is mutated or has been partially deleted from the genome. Boys are particularly affected by this mutation. More...

The Chica and Heinz Schaller Foundation is proud to announce a CHS Research Awards winner 2020: Dr. Ana Oliveira

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...