Latest news with #RandallBateman
Yahoo
31-03-2025
- Health
- Yahoo
An Alzheimer's Blood Test Might Predict Advanced Disease
Credit - Getty Images With two new treatments for Alzheimer's disease approved in recent years, there's growing hope for people at risk of the memory-robbing condition. But tests to detect the condition still lag behind. Earlier diagnosis would mean that people could take advantage of the drugs sooner, when the medicines are most effective. Detection is currently tricky. Brain scans like PET can pick up amyloid plaques, the clumps of protein that are the hallmark of the disease, but by the time these form, people's brain function is already declining. The scans are also expensive and not available at all hospitals. More sensitive ways to detect amyloid and tau, another protein related to the disease, are possible by analyzing spinal fluid, but that requires a painful and potentially dangerous spinal tap. Blood tests for the two proteins have not yet been approved by the U.S. Food and Drug Administration—although they have received breakthrough designation from the agency, which means they are getting expedited review as studies of the tests are completed. In a new study published in Nature Medicine, researchers led by a group at Washington University in St. Louis report promising results of a blood test they developed to detect a different from of tau than the one that existing tests target. This form, they say, is a better indicator of how much of the damaging protein has built up in patients' brains—and those levels correlate with the severity of a person's disease. By comparing the results from the blood test to those from brain scans, the team determined that the blood test was 92% accurate in its readings of tau. Read More: 5 Ways to Keep Your Brain Sharp As You Age Dr. Randall Bateman, professor of neurology at Washington University and senior author of the paper, says that the presence of both amyloid and tau proteins in patients' brains is essential to diagnosing Alzheimer's. Amyloid plaques take years to develop, and it's not until sufficient clusters of the protein have formed that symptoms like memory loss, confusion, and disorientation occur. Once amyloid aggregates form, then tau starts to develop abnormally both inside and outside of brain neurons. Outside of the cell, tau forms what scientists call phosphorylated tau—what current tests can detect. But inside of brain neurons, tau in Alzheimer's patients breaks down further, and instead of adopting neat, linear forms as it does in people without Alzheimer's, it becomes crystalized and forms a mess of protein resembling tangled yarn. 'Tau tangles are most associated with a person's dementia symptoms,' says Bateman. 'Plaques are like the fuel driving a lot of changes that we observe [in patients] over time. But not until the fire ignites, with the spread of tau tangles, does the brain really fall apart.' He says that the crystalized form of tau is more strongly linked to cognitive decline associated with Alzheimer's, so detecting the first signs of this form of tau would help doctors to identify patients on the brink of developing more severe memory and cognitive problems. 'This is the first report of a tau tangle marker in the blood," he says. Read More: Changing Your Diet and Lifestyle May Slow Down Alzheimer's In 2023, Bateman and his team developed the first test for this crystalized form of tau, but in the spinal fluid. Because of the inconvenience and risk of spinal taps, the team then focused on looking for the same telltale signs of crystalized tau in the blood. After tediously screening a variety of blood markers, they finally found it. 'We went through molecule by molecule, atom by atom, looking for the exact structure of the forms of tau that [we knew] existed, and then discovered the form that was uniquely identified with the presence of tangles.' Bateman founded a company, C2N Diagnostics, to manufacture and provide the test to researchers for use in clinical trials. The blood-based test could speed development of anti-tau treatments for Alzheimer's, since drug developers can fairly quickly determine whether a compound they are testing is having any effect on the amount of tau building up in a patient's brain from a vial of blood. 'A lot of us think that if we can slow down or reverse the formation of tau tangles, then it's a good strategy to slow down or reverse Alzheimer's,' says Bateman. '[The test] can accelerate how quickly new treatments are developed.' Having a relatively easy way to track tau levels in Alzheimer's could also provide new clues about how the disease progresses, and potentially provide new targets for drugs. It's not clear yet how the phosphorylated forms of tau that exist outside of neurons are related to the crystalized forms that cells generally harbor inside, but it's possible that at some point, the buildup of phosphorylated tau triggers the formation of destructive crystalized tau inside neurons. Another unanswered question is why some fragments of the crystalized tau make their way outside of the nerve cells. Understanding that process could lead to new strategies for controlling tau and perhaps slowing the progression of the disease. 'If we want better treatments for patients," says Bateman, "then we have to understand what causes the disease." Contact us at letters@
The Independent
20-03-2025
- 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.'
