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A laboratory study is developing a drug for the treatment of Alzheimer's disease from an anticancer drug called lonafarnib.
According to "Newsweek", the drug might be able to get rid of unnatural Tao proteins, called entanglements, ie tangles, which along with other abnormal proteins called senile plaques, are characteristics of Alzheimer's disease.
These plaques and entanglements form observable structures in the brain of deceased Alzheimer's patients under a microscope.
Kenneth Cossick, a neurologist at the University of California at Santa Barbara, explained that mice were used to develop tao tangles, and laboratory results showed that lonafarnib formation was inhibited.
This approach, called repositioning, involves the use of a drug originally invented for the treatment of another disease, but its effectiveness is unexpected in another disease.
Because Tao in entanglement of nerve fibers is an important feature of Alzheimer's disease and as the disease has reached epidemic levels around the world, it is thought that the drug should be a top priority for the clinical trial testing.
The main component of nerve fibrosis is the Tau protein, a normal brain protein that accumulates during the disease in the form of long, cord-like structures, leading to the suffocation of nerve endings in the brain.
An impressive thing in changing the location of an anticancer drug is that the test has fully demonstrated its safety in humans. There is currently no medication that can modify or prevent Alzheimer's disease, which confirms the importance of monitoring results and the transfer of experience from the mouse to the larynx. man, but it is necessary to specify many details before proceeding.
The study collected skin cells from patients with a form of dementia called temporal frontal dementia, which presents only fibrous neuralgia and no plaque.
The study also identified the cause of patient dementia, a genome mutagenesis, abnormally activated in cells, from a protein called Rhes, a protein belonging to a family of proteins targeted by the anticancer drug lonafarnib.
When the mice were fed, this drug prevented the formation of tau tangles in the brain; the result of the disturbance remained normal brain activity.
Mice that did not take this drug all developed advanced dementia.
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