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For example, the European Union’s Drugs Regulator refused to approve the first to come to its desk in the last summer, although it has partially reversed that decision. And in England, despite the regulatory approval, the National Health Service does not yet introduce them. Many researchers suspect that they can do better when given earlier, perhaps prevention. This is the easiest way to find out, they say, clinical tests on those for which Alzheimer’s start is almost guaranteed: people with Down syndrome.
As the life expectancy of people with down has increased, it is clear that most will eventually develop Alzheimer’s. Studies show that 70-88% will do so till the age of 65 years. The comparable figure in the normal population is 8–10%. So far, however, the tests of Alzheimer’s drugs have excluded those, meaning that doctors feel that they cannot safely write them to those individuals. Including the people of the down in future tests can not only offer treatment to them, it can also increase the future of Alzheimer’s prevention for all.
The link between situations is a genetic hiccup. Down people have an additional copy of chromosome 21 in their cells. It brings an additional copy of the gene encoding amyloid protein (APP), which is an molecule involved in the development and development of neurons. Unfortunately, there is also an app-like its name mentions-a small protein, the forearm in some circumstances of the beta-amyloid, which forms a clump called plaque in the brain of people with Alzheimer’s. Additional gene copy means that people with down have a high level of app and, therefore, more beta-amyloid. As a result, all of them have all of them as long as they are 40 years old. After about 15 years, most of the dementia occur.
A waterfall of problems
Although there is rarely a clear genetic cause without a down without Alzheimer’s, the contains between the app, the beta-amyloid and the dementia (which emerged in the 1980s) suggest an inherent mechanism. In 1991, John Hardy, now a neurocientist at University College, London, and his late colleague David Alsop (then in Queen’s University, Belfast) proposed the amylaid cascade hypothesis. It produced beta-amyloid in the brain, which is the driving force behind the Alzheimer, which is affected by it, whether it is down or not. Other signs of Alzheimer’s, such as brain shrinkage and tangles of another unusual protein called tau, are thought to come later.
The amyloid cascade hypothesis remains the most effective explanation for the development of Alzheimer’s. Thus a discovery is now for drugs that get rid of beta-amyloid. The test has failed after the test. But two substances have been found to work. These are artificial antibodies called lechanmabs and dononmabs which are particularly connected to beta-amyloid, giving it a green signal for disposal. Although both drugs slow down cognitive decline, they do not do so. After 18 months, the dementia score for people receiving lechanmabs was reduced by 27% compared to those receiving a placebo. For Dononmab, it was 35%. Ideally the drugs will stop the decline completely – or also reverse it. Given that 20% of the people receive lekainmabs and 24% of those receiving Dononmabs (although most harmless) brain inflammation and brain bleeding, suspicion that new drugs are worth it, it makes sense.
Critics of amyloid cascade hypothesis have considered the lack of antibodies as beta-amyloid is wrong target. They feel that tau, or even app can be more important. Others, who still support the Hardy-Allasop explanation, suspect that two drugs can do better when given in life. They suggest that as long as most of the patients take them, the disease is prevented from removing amyloids far away. If this is true, anti-amyloid drugs may be better suited to prevention than treatment.
A clear way of testing it would be to run a clinical test on a cohort, for which Alzheimer’s is finally close to a certainty, but before the symptoms determined in earlier symptoms, people with down syndromes. Clear, but radical. Companies are careful to include people with confused conditions in their tests, for fear of affecting their results. And in fact, additional efforts are required to obtain informed consent, so that they and their families can be understood to be risk.
He is starting to change. A test of Dononmab with a down by researchers at the University of Southern California, Aladdin, will begin later this year. And an existing test, Abate, which is already testing a separate anti-ammunotherapy in the US, Britain and Spain, already incorporates them. This is too much for the turnaround down and their families to advocate by people.
A notable moment was a speech by Frank Stephens to hear an US Congress in 2017, a board member of the Global Down syndrome Foundation, who is himself, Down. In three years after this speech, which received a permanent ovation from the Congressfolk assembled, from the National Institute of Health, the National Institute of Research for Down Dout $ 35M to $ 35M to $ 35M to $ 35M. By 2023, the figure increased to $ 133m. Mr. Stephens says that it changed the vision of scientists to study the syndrome.
These tests will require care that they take into account to ensure any risk associated with high beta-amyloid in people’s brain with downs. Last year, post -mortem studies of brain tissue from 15 people with this situation found that lechanmabs are bound by amyloids stuck in the walls of blood vessels in all analyzed tissue. That binding is believed to be responsible for inflammation and bleeding of the brain observed in general-population tests. People with down may thus be at high risk of those side effects and may require low doses.
However, if drugs prove safe and effective, when symptoms are administered before the onset of the symptoms-or even before amyloid build-up-it can offer people with many additional years of hope below, perhaps without Alzheimer’s, even without Alzheimer’s. For others, in which it is difficult to predict the onset of Alzheimer’s, researchers will still need to improve early diagnosis to fully achieve benefits. The work published in Nature Azing in 2024, in which blood protein was used to help predict ten years before the traditional diagnosis, it may be possible soon to help. In addition, the performance of drugs will show whether the prevailing understanding of Alzheimer’s is correct. After thirty years after amyloid cascade hypothesis, such a test is well overdose.
© 2025, The Economist Newspaper Limited. All rights reserved. From The Economist, published under license. The original material can be found on www.economist.com
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