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New study is given the opportunity to prevent cell death in Parkinson's disease

In a new study, researchers have identified a way to die and prevent the door for the development of treatments that slow the progression of neurodegenerative diseases such as Parkinson's disease.

The old “cell-suicide” program of our body, apoptosis, is regulated by interactions between members of BC lymphoma 2 (BCL-2) protein family. Some of these proteins promote the survival of the cells, others trigger cell death. Scientists were able to use some of the death facilities of these proteins to treat certain blood cancer.

Now, led by the Walter and the Eliza Hall Institute of Medical Research (Wehi) in Melbourne, Australia, has discovered a new study on how to do the opposite: block cell cell death by focusing on one of these proteins and opening the door for treatments that stop the progression of neurodegenerative diseases such as Parkinson's disease.

“At the moment there are no treatments that prevent neurons from dying to slow Parkinson's progress,” said Professor Grant Dewson, who, with the study of the study, conducted the study and head of the Parkinson's research center in Wehi. “All drugs that could be able to do this could be groundbreaking.”

B-cell lymphoma 2 Antagonist/Killer (BAK) and B cell lymphoma 2-associated X-protein (BAX) are proteins of the BCL-2 family that cause cell death by pushing through the wall of the mitochondria, the energy generator of the cell. If BAK and BAX do not work correctly, this can lead to an impaired apoptosis and contribute to autoimmune and degenerative diseases.

The structure of the BAX protein, which is involved in the cell death process

Wehi

Against this background, the researchers relyed on the ultra-high throughput screening capabilities of the National active ingredient Discovery Center based in Wei, around 106,572 connections to identify one that aimed at a cell protein, bax.

“We were enthusiastic to find a small molecule that aims at a killer protein called Bax and it doesn't work,” said Professor Guillaume Lessverung Professor Guillaume, said the cross-cross author and the head of the new medical and diagnostic department from Wehi. “Although it is not the case in most cells in neurons, the elimination of BAX can be enough to limit cell death.”

Small molecules are organic compounds with a low molecular weight that is often used in drug development because they go through cell membranes and interact with proteins in the cell. The researchers observed that the little molecule they identified they called Weihi-3773 inhibited Bax's ability to break the mitochondria of the cell and prevent his death.

“For the first time we were able to keep Bax away from mitochondria and keep the cells alive with this molecule,” said the main author of the study, Kaiming Li, the main author of the study, and a researcher in the laboratory under the direction of Dewson. “This could pave the way for the next generation of cell death inhibitors to combat degenerative conditions.”

The study was published in the magazine Science progress.

Source: Wehi

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