Rehabilitation is difficult since there are no umbrella terms for various neurodegenerative conditions including dementia – memory loss and various forms of cognitive impairment. However, the analysts are registering a careful progress.
A new approach to dementia research may lead us to rehabilitation, but unexpected difficulties can halt this progress.
Dr. Kenneth Kosik, professor of UC Harriman Neuroscience at the University of California, led a team of experts who recently focused on using a drug learned to rehabilitate the toxic accumulation of a protein called ”tau birikim in the brain. </
Generally, tau proteins play a role in stabilizing microtubes. These are axon elements, veren stalks “that connect neurons to brain cells and allow them to communicate.
Someone ini tarot proteins Bir
may think of the ties on the rail tracks that catch the microtube traces. Together, Ber Kosik explains.
However, as a result of a variation, tau proteins sometimes resist false, which means that they become clogged and undersized, by clogging communications between brain cells.
These differences are due to the growth of a form of dementia called aret frontotemporal dementia mas, which affects the temporal and frontal lobes of the brain, causing the deterioration of emotional expression, attitudes and decision-making skills.
Lar Patients initially, if any, do not show too much memory in this course.
New street for dementia rehabilitation
In this study, Kosik team, tau collected cells from individuals who have been collected as well. Then, in the lab, scientists transformed these sampled cells into stem cells and then into neurons, so they could watch what kind of genetic change might affect tau.
Symptoms reported by analysts in the journal Science Translational Medicine, three generations of tac changes in the gene, he said.
Between these three genes, the team focused on a RASD2 – which directs the effectiveness of energy producing molecules called GTPases. .
Muhtemelen I’ve talked about these people because it’s probably accompanied by Huntington’s disease, another neurodegenerative disease, “he said. Kosik added RASD2 and RAS to another female gene. They drag too much attention from analysts because they seem to be sensitive to drugs.
The key to brain wellness: light but often do exercise Exercising the mind of the brain certainly does not require too much physical combat, according to the evidence.Kosik said:
While RASD2 was working, the assayers were interested in a GTPase called RHES that was encoded by this gene. However, although the activity of RHES as a protein was the normal focus of studies, the team was interested in the different routes of this GTPase.
Ik In the end, what we are focusing on is that this protein and all its subscribers are very mysteriously connected to the cell wall of the Family, odak says Kosik.
RHES says it is clinging into the cell walls through a carbon chain learned as a uğ farnesyl group RH. Tedir Scientists refer to the addition process as “farnesilation”.
Work with an existing drug
Transfer We have an enzyme called farnesyl transferase that takes this protein to RHES and added it to the mouse, and we decided to focus on this reaction. ” Kosik, Kos[i] she admitted that it was a little splash itir to leap towards the path.
Past research on fesesesyl transferase focused on disrupt farnesisation and suggested that this action could be a promoter to rehabilitate cancer. galls. In fact, Hak[i] Farnesyltransferase inhibitors have been tested in humans in this category of drugs, f Dr.
Mice with irregular attitudes in 10 weeks were behaving in 20 weeks.
Scientists have found that the drug has stopped the pus and tissue damage in the brain. At the same time, the number of tau expeditions had also been greatly reduced – in fact they were all in the form of accumulated accumulation, but in the hippocampus, the region of the brain that played the most important role in memory resemblance.
“The drug seems to be a very enigmatic course,” Dr. Observations.
Committed to the future but exceeding the limits
To ensure that the Lonafarnib attacked farnesised RHES, the Assayers looked at another dementia model, in which they activated a gene that blocks the construction of RHES.
In this way, the attitude of the mice grew in the same way as Lonafarnib rehabilitation. It proves that this drug is responsible for the fertility of farnesylated RHES.
The post This drug was unable to cure cancer, but it could improve dementia first appeared on Binbon.
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