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A British medical team tested Parkinson's disease to transfer the drug directly to the brain.
The patients gave the patients the new drug, which can be controlled by a hole or "outlet" on the side of the patient's head, and gave another placebo group.
The experiment showed an improvement in the symptoms of the disease in both groups, which means that it is not clear if the drug is entirely responsible for the improvement of the symptoms.
However, radiation tests showed improved evidence in affected brain areas in patients who administered the drug through this hole in the head.
The authors of the study say that this suggests a "re-stimulation" of brain cells damaged by the disease.
Other experts have stated that it was too early to say whether this result would improve the symptoms.
Scientists believe that this "port" located on the patient's head can also be used to administer chemotherapy to patients with brain tumors or to test new drugs to treat Alzheimer's disease and stroke. brain.
Parkinson's disease causes progressive brain damage, resulting in a variety of symptoms, such as involuntary tremors, stiffness and muscle stiffness.
In Great Britain, about 145,000 people are infected each year with a disease that can not be reduced or transformed.
In this new study, scientists gave an experimental treatment called neurotransmitter derived from GGF to try to regenerate dead cells in the brain and change their state.
Participants underwent robot-assisted surgery to place four tubes in their brains, allowing the neurotransmitter derived from glial cells to be injected with great precision into the affected areas through a hole located on the side of the brain. the patient's head.
After a preliminary study involving six people to confirm the safety component, 35 patients participated in an "undeclared" trial of a duration of nine months, which showed that half of the patients had been randomly assigned to a neurotransmitter derived from glial cells, while imaginary.
Patients with this condition were diagnosed eight years ago on average, but brain scans of these patients showed images that may appear two years after diagnosis, said Alan Hoon, chief investigator.
"It has been shown by examining positron emission tomography that the drug interacts with its target, the nerve endings of dopamine, and appears to help damaged cells to regenerate or to have a biological response."
After the first nine months of treating patients with a glomerular neurotransmitter or placebo, all participants were able to administer the diet factor for another nine months.
The study showed that all participants, from both groups taking the neurotransmitter derived from glial cells over a period of 18 months, had improved their morbidity rates by moderate to large variance compared with those recorded at the beginning of the study.
The results suggest that the results should be treated with caution because of the potential effect of placebo, a condition in which the patient feels better despite a drug that contains no effective ingredients.
The researchers hope to do more tests to increase neurotransmitter doses derived from glial cells or the duration of treatment.
"A glimmer of hope"
"Although the results are unclear, the study still has a lot of success," said Arthur Roach, research director at the British Parkinson Institute.
"The study has shed light on the potential effects of the glomerular neurotransmitter on damaged brain cells and has shown that treatment is possible and that the drug can also be precisely administered in the brain."
"It's a disappointment," said K-Ray Chaudhry of the Institute of Psychiatry, Psychology and Neurology at King's College London, who is not involved in the study.
But he added that the study is still "very important and suggests a new horizon and a new direction for cell repair-based treatment".
The test results were published in both the Breen and Parkinson medical journals.
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