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Researchers Discover Brain Cancer Mechanism Responsible For Neuron Death


Researchers Discover Brain Cancer Mechanism Responsible For Neuron Death

Scientists from the Virginia Commonwealth University and Institute of Molecular Medicine  discovered the way through which the most common type of brain cancer leads to neuron cell death also known as neuron degradation.

The research results can help scientists further, to find new treatment options to halt neuron degradation and new treatments for other nervous system disorders.

Paul B Fisher recently published study in the Cancer Research journal, revealed that a certain gene also known as oncogene ( gene that can determine cancer onset) astrocyte elevated gene AEG-1 determines neuron degradation by increasing the toxicity effects of glutamate on neurons. Glutamates are essential for neuronal transmission thus for memory and learning skills. Glutamates can acumulate in the sinaptic spaces (the spaces between two neurons) and determine neuron exhaustion by overstimulation them, process also named exicitoxicity.

Neuron Death

Neuron Death

Paul’s B Fisher Study is the first study that provides a theory on how brain cancer leads to neurodegeneration, and provides a link between AEG-1 oncogene and neuron cell death. The AEG-1 onocogene was found present in over 90% of patients with brain cancer.

Glioma is the most common type of brain cancer and statistically the second cause of death due to cancer in adults aged between 20 and 39 according to Paul.

The study also targeted possible therapeutic aproaches for inhibiting AEG-1 oncogene and neuron degradation due to glutamates. Fisher’s scientists team also found that AEG-1 onocgene negatively corelates with a glutamate transporter (EEAT2) in cells that feed and support the neurons also known as glial cells. The transporter was found responsible for regulating glutamate leves in synapses spaces. Altered transport and regulation leads to neuron cell death. The study also showed that during the transcription process the AEG-1 onocgene can interfere with  EEAT2 transporter, leading to neurotoxicity due to excessive glutamate. The theory was demonstrated in practice using samples from patients suffering from glioma.

Unreavelling the mysteries of EEAT2 transporter is a very useful descovery as researchers can now focus on finding better treatments of other neurodegenerative disease such as Lou Ghering’s Disease also know as amyotrophic lateral sclerosis, Alzheimer, epilepsy and many more.

Paul’s B Fisher laboratory was the pioneer of EEAT2 cloning, and now has turned its attention for screening for certain drugs that can be used to regulate EEAT2 transport thus preventing the process of neuron degeneration.