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Scientists For The First Time Synthesize Deadly Artificial Prions

For the first time in the science history, scientists at Case Western Reserve University of Medicine (CWRU) have created artificial human prions with the aim to develop a cure for common brain disorders.

Prions are deadly brain proteins that cause devastating infections in the brain. When they bind to normal proteins, they can create a terrifying domino effect that prods millions of minuscule holes in the brain resulting in genetic brain disorders and fatal damage.

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Microscopic image of synthetic human prions accumulating in the brain of a mouse that was genetically altered to produce a certain human protein. Image: Case Western Reserve School of Medicine

A common brain disorder associated with prions is the Creutzfeldt-Jakob disease (CJD) which generally affects at least one in a million people around the globe.

According to Jiri G. Safar, a neurologist at CWRU, the clones were formed through a series of test tube processes and using more advanced biophysical tools. Dr. Safar is hopeful that through this breakthrough, scientists will understand the replication of human prions and develop a certain drug that can inhibit their activity in the brain.

During the experimentation process, the synthetic human prions were tested to transgenic mice and resulted in neurological dysfunction. The first deaths occurred after 459 and the second occurred after 224 days.

There were already previous studies before using animal prions. However, they were not as conclusive and effective as compared to using human prions. The animal prions generally have a different structure and their replication process does not apply to humans.

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“With the production of synthetic human prions, researchers can finally engage in a feature-for-feature comparison”, says Dr. Safar. “The discovery will also open the door to a higher possibility of discovering a cure for Alzheimer’s disease and Parkinson’s disease considering that they spread through the brain in a similar way as CJD.”

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