Researchers have discovered brakes that can stop the death of nerve cells, which gives hope to reach a new treatment for a Parkinson’s disease.
The study dealt with a form of Parkinson’s forms caused by a single genetic mutation that causes an increase in a protein that impedes the brain’s ability to protect itself, and the researchers found that inhibiting this protein can stop damage and allow nerve cells recovery.
The study was conducted by researchers from Stanford University in California, USA, and its results were published in the magazine “Science Signaling”, on July 1st, and wrote about the American Journal of Newsweek.
“These results indicate that it may be possible to improve the condition of Parkinson’s patients, not just its stability.”
Parkinson is known as tremors in the limbs during rest, and although this most famous offer, some early signs of the disease usually appear about 15 years ago, and Dr. Susan explained that these first signs include constipation, loss of sense of smell and rapid eye movement disorder in which the activity of the brain in which the awakening person acts without moving the muscles, and experts believe that most dreams occur during the sleep of rapid eye movement.
Dr. Susan explains that about a quarter of cases are caused by genetic mutations, one of which is the most common of mutations that increase an enzyme activity called Kinaz, rich in lalysin “LRRK2” (LRRK2).
The high level of Kinaz rich in liliin 2 in the brain changes the cell structure by losing their antennas (or initial cilia) that allow them to send and receive chemical messages.
The signals are going back and forth between the neuromamine cells in the proper brain in two regions of the brain known as the stritum and black substance.
And when dopamine neurons are exposed to tension, they release a protein signal in the planned body, and this causes supported neurons and cells to produce the so -called neurological protection factors that protect other cells from death.
When you lose the ability to receive messages
When the Kinaz activity, rich in liliin, exceeds 2 specific limits, the loss of initial cilia in the planned body cells prevents them from receiving the signal, and as a result of which neurological protection factors do not produce.
The researchers believe that when the cells lose their cilia, they are also on their way to death because they need cilia to receive the signals that keep them alive.
It is possible to combat excess Kinaz enzyme, rich in lalysin 2, using the so -called Kinaz inhibitor, a molecule associated with the enzyme and reduces its activity.
The researchers began testing whether this inhibitory was also able to unlike the effects of the excess -rich kinase of the Kinaz 2, as well as whether it is possible for the completely mature nerve cells and supported glial cells to re -grow lost cilia and restore their ability to communicate.
Initially, the results were not promising, and the inhibitory team gave two weeks to mice bearing the kinaz mutation rich in LLINENS 2 (and showers appear compatible with Parkinson’s early disease) to no avail.
However, researchers were inspired by recent studies on sleep and waking courses, which found that the initial cilia on the mature cells concerned has grown and shrinking every 12 hours.
“The results indicating that other unpopular cells develop the cilia, we realize that it is theoretically possible that the fastening works,” says Dr. Susan.
The team decided to experience giving fastening to mice for a longer period, and the results were 3 months later.
The mice – which received treatment for a longer period – witnessed an increase in the percentage of neurons and glial cells in the planned body with the initial cilia, returning to the same level in the healthy mice.
This had an effect in restoring communication between dopamine neurons and the planned body, which led to a natural secretion of neurological protection factors.
The researchers also found that the level of protein signals from the dopamine neurons decreased, indicating that they were under less pressure, and they found that the density of the neuromamine ends of dopamine in the scheme in the mice doubled, indicating that the neurons that were in the stage of death were recovered.