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Is This Experimental Drug A Promising Alzheimer's Treatment?
Is This Experimental Drug A Promising Alzheimer's Treatment?

Yahoo

time01-04-2025

  • Health
  • Yahoo

Is This Experimental Drug A Promising Alzheimer's Treatment?

If you're someone who is at high risk of developing dementia or Alzheimer's disease, it can be pretty emotionally and mentally draining, especially if you feel like there's very little you can do to delay its onset (aside from following a healthy diet and lifestyle, and getting enough sleep). But new research on an experimental drug suggests that it could potentially help lower the odds of developing Alzheimer's in people who are genetically predisposed to the devastating condition. Of course, Alzheimer's is a complex disease, and there's no silver bullet treatment. The findings, which were published in The Lancet Neurology, are a little complicated and highly specific to a certain group of people. They also raise a lot of questions from experts about the potential impact of this treatment plan in the general population. Here's what you should know, and what doctors think of the drugs. Meet the experts: Clifford Segil, DO, is a neurologist at Providence Saint John's Health Center in Santa Monica, CA; Amit Sachdev, MD, MS, is the medical director in the Department of Neurology at Michigan State University. Randall J. Bateman, MD, is a study co-author and professor of neurology at Washington University in St. Louis For the study, researchers recruited 73 people with rare and inherited genetic mutations that cause the overproduction of a protein called amyloid in the brain. In case you're not familiar, amyloid is found, but in the brain it clumps together to form "plaques" between nerve cells. Too much build-up of these amyloid plaques in the brains can lead to issues with brain function and is linked to Alzheimer's, per the National Institute on Aging (NIA). But we'll get to more of that later. For the study, the researchers gave the study participants an experimental anti-amyloid drug. They found that 22 participants who had no cognitive problems at the study's start and who took the drug the longest (an average of eight years) had a 50 percent lower chance of developing symptoms. The researchers didn't study the impact of the treatment on people who already have Alzheimer's disease. Instead, they looked at people with a very high likelihood of developing it who were within 10 to 15 years before they were expected to develop the disease based on their family history. So, the treatment is more geared towards delaying or halting onset rather than curing an existing disease. Amyloid plaques are areas where amyloid (again, a protein) has built up, explains Amit Sachdev, MD, MS, medical director in the Department of Neurology at Michigan State University. 'You can think of it a lot like a scab on your skin,' he says. 'The scab is rough, it isn't supposed to be there and, if it gets too thick, it causes a problem.' But there is some debate about whether targeting amyloid will help lower the risk of Alzheimer's disease, says Clifford Segil, DO, a neurologist at Providence Saint John's Health Center in Santa Monica, CA. 'Targeting brain amyloid is not a slam dunk for Alzheimer's prevention as we do not have any tests that are in use clinically to predict Alzheimer's onset,' he says. 'Most neurologists liken [amyloid plaques] to skin freckles, which are normal aging phenomena and extremely infrequent[ly] became a skin cancer,' Dr. Segil continues. 'Many Alzheimer's scientists liken them to unexploded land mines which, if left alone, will cause older people to lose the ability to tie their shoes and all but surely get Alzheimer's disease.' The treatment uses anti-amyloid antibodies to break down the plaques, Dr. Sachdev explains. 'The anti-amyloid antibodies attach to amyloid and use the immune system to remove it,' he says. 'This is very effective, because the immune system is excellent at getting rid of things that do not belong.' But Dr. Sachdev also says that the drug relies on inflammation to clear the plaques. (Think of it like this: Inflammation is a natural bodily response to kickstart healing in the body, bringing various cells and biological tools to the site of injury to repair it. The treatment seems to trigger inflammation.) 'More than 50 percent of patients who were exposed in this study had changes to their brain [including potential for swelling and bleeding] that could be related to inflammation,' he says. As such, these medications come with the risk of brain bleeding, brain swelling, and brain shrinkage, making them risky to use, Dr. Segil points out. Not yet, says Randall J. Bateman, MD, study co-author and professor of neurology at Washington University in St. Louis. This is partly because the study was quite niche. "Our trial tested this in rare families with mutations that cause Alzheimer's disease," Dr. Bateman says. This trial originally ended in 2020. Right now, there are ongoing trials that will wrap up in a few years, and if those are successful, the treatment could potentially be made available to the public, per Dr. Bateman. But some doctors aren't convinced these treatments should be used. One of the medications in the treatment (gantenerumab) is no longer made. 'The company developing it has decided to go into go in a different direction,' Dr. Sachdev says. Anti-amyloid medications also come with a high risk of side effects, including death—and that's concerning to many doctors and families, Dr. Segil says. 'Like most neurologists in the U.S. today, we are not using this family of medications,' he says. 'Clinical neurologists like me continue to be skeptical that the benefits outweigh the risks of anti-amyloid medications for dementia.' 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New drug could reduce risk of early-onset Alzheimer's disease
New drug could reduce risk of early-onset Alzheimer's disease

The Independent

time20-03-2025

  • Health
  • The Independent

New drug could reduce risk of early-onset Alzheimer's disease

An experimental drug appears to reduce the risk of Alzheimer's in people 'destined' to develop the disease in middle age. The study, published in the journal The Lancet Neurology, involved 73 people with rare, inherited genetic mutations that cause the overproduction of the protein amyloid in the brain. This all but guarantees they will develop Alzheimer's disease in their 30s, 40s or 50s. For 22 patients who had no cognitive problems at the start of the study, and who received the anti-amyloid drug the longest – an average of eight years – the treatment lowered the risk of developing symptoms by half. The results boost hopes similar treatments being developed to target more common forms of Alzheimer's - that appear when people reach their sixties, seventies and eighties - might also be effective. These findings provide new evidence to support the theory that amyloid leads to Alzheimer's disease. It's thought amyloid forms toxic plaques around brain cells and as the brain becomes affected, there is also a decrease in chemical messengers, called neurotransmitters, involved in sending messages between brain cells. The study suggests removing such plaques or stopping them form forming can prevent symptoms of the memory robbing disease. 'Everyone in this study was destined to develop Alzheimer's disease and some of them haven't yet,' said senior study author Randall Bateman of Washington University in St Louis, Missouri. 'We don't yet know how long they will remain symptom-free – maybe a few years or maybe decades. 'In order to give them the best opportunity to stay cognitively normal, we have continued treatment with another anti-amyloid antibody in hopes they will never develop symptoms at all. 'What we do know is that it's possible at least to delay the onset of the symptoms of Alzheimer's disease and give people more years of healthy life.' The study participants consisted of people who had originally enrolled in the first Alzheimer's prevention trial in the world, launched in 2012, and then continued into an extension of the trial in which they received an anti-amyloid drug. All participants in the trial had no-to-very-mild cognitive decline and were within 15 years before to 10 years after their expected age of Alzheimer's onset, based on family history. When the initial trial concluded in 2020 researchers reported that one of the drugs, gantenerumab, lowered amyloid levels in the brain. But the researchers did not see evidence of cognitive benefit then because the group without symptoms – regardless of whether they were on drug or placebo – hadn't cognitively declined. As a result, the researchers continued to study the drug to determine whether higher doses or longer treatment could prevent or delay cognitive decline, and found it could reduce the risk of developing symptoms from 100 per cent to 50 per cent. Gantenerumab is no longer made by Roch, the company that developed it, because it did not slow symptoms of a more common non-genetic form of Alzheimer's in a trial of 1,900 participants. But there are other anti-amyloid drugs being developed. Although the trial was limited to people with genetic forms of Alzheimer's that lead to early onset, researchers expect that the study's results will inform prevention and treatment efforts for other forms of Alzheimer's disease. Both early-onset and late-onset Alzheimer's disease can start with amyloid slowly collecting in the brain two decades before memory and thinking problems arise. Dr Richard Oakley, associate director of research and innovation at the Alzheimer's Society, and who was not involved in the study, said it showed there is 'hope on the horizon' to beat Alzheimer's. 'These exciting early-stage results hint that long-term anti-amyloid treatments, started before Alzheimer's disease symptoms appear, could potentially delay symptom onset,' he said. 'However, these results need to be treated with caution; this trial focuses on a very small group of individuals with genetic forms of Alzheimer's disease. Longer-term follow up of this group and larger studies will tell us more about the effect of these drugs in these types of Alzheimer's.'

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