New drug may prevent Alzheimer's decline
The first drug capable of preventing Alzheimer's disease is finally being worked out. That's because scientists have discovered that they can cleanse the sticky plaques in the brain that cause dementia.
This was chosen by scientists as the best news in the last 25 years and the breakthrough, if confirmed, could change the lives of thousands of people with Alzheimer's disease.
Aducanumab is the antibody being studied for the treatment of Alzheimer's. Scientists were surprised to find that patients treated with high doses of the antibody had a decrease in amyloid plaques, which prevented brain cells from communicating leading to irreversible memory loss and cognitive decline. six months of treatment, patients stopped having deterioration in the brain compared to people taking placebo alone, suggesting that dementia had been discontinued. "These results could be watersheds if the effects on memory decline are confirmed in more extensive studies, "said David Allsop, professor of neuroscience at the University of Lancaster.
The first drug to prevent dementia may be available in just a few years. "The results of this clinical study make us optimistic that we can potentially make a breakthrough in the treatment of Alzheimer's disease," said Professor Roger Nitsch at the Institute of Regenerative Medicine at the University of Zurich, Switzerland. Although it is a small sample, the fact that there is a deceleration of cognitive decline and functional decline is important. "The group with a high degree of amyloid removal was basically stable. If we could reproduce this would be fantastic," says Roger Nitsch.
Currently 850,000 people live with dementia in Britain, a figure that is expected to rise to one million 2025 and two million by 2050. The most common type of dementia is Alzheimer's disease, but scientists have been unable to reach consensus on the cause of the condition. Current treatments may reduce symptoms to some extent , but there is still nothing that can stop or slow the progression of the disease. This new study indicates a potential treatment for the problem and further shows that amyloid plaque buildup may be blamed by Alzheimer's. P>
Scientists tested several human immune cells with amyloid in a laboratory until they found one capable of producing an antibody which was separated from the plates. The study published in the journal Nature showed that scientists tested different levels of the drug over a year, as well as giving a placebo group. They found that as the dose was increased, more amyloids were removed from the brain.
The drug is most effective for patients in the early stages of Alzheimer's disease or among those who have not yet begun to show symptoms. Several universities are working on early blood tests for dementia that could identify the disease for up to a decade or more before the first physical signs appear.
Two large clinical trials will be conducted to evaluate the safety and efficacy of the drug. A total of 2,700 early-stage Alzheimer's patients will be screened, but researchers are still recruiting British participants. "The results suggest that aducanumab may slow memory and mental decline in people with Alzheimer's disease. is only exploratory in this initial trial, it shows a positive picture for ongoing studies with the drug, "said Dr. David Reynolds, chief scientific officer of Alzheimer Research in the UK.Professor David Allsop of the University of Lancaster, UK, comments: "This study shows that it is possible to have a dose-response test, to reduce the extent of amyloid plaque formation in the brains of people with very early signs of dementia Although there have been suggestions that there could be an effect on the symptoms of the disease, we need to see more results. "Richard Morris, a professor of neuroscience at the University of Edinburgh in the UK, reports:" We still can not say that we have a cure for Alzheimer's disease, as this is only a first step. for success in the next steps. "
It does not hurt, but the feeling is horrible. From nowhere, the person stops seeing or even has the agonizing sensation of being with pets in their field of vision. All this because the retina, one of the inner layers of the eye, has left the place and therefore the name of the clinical picture of retinal detachment.
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