Racial disparities in dementia are due to social determinants of health, with genetic ancestry playing no role, according to a new study led by researchers at Washington University School of Medicine in St. Louis.
Washington University Professor of Neurology Dr. Joy Snider joins the show to talk about the new Alzheimer’s drug that was approved by the FDA in July.
The drug, Kisunla, made by Eli Lilly, is the latest in a new class of treatments that could modestly slow cognitive decline in initial stages of the disease but also carry safety risks.
Nearly all adults with Down syndrome will develop evidence of Alzheimer’s disease by late middle age. A new study by researchers at Washington University School of Medicine in St. Louis shows that the disease both starts earlier and moves faster in people with Down syndrome, a finding that may have important implications for the treatment and care of this vulnerable group of patients.
Washington University is known the world over for being a leader in neuroscience research. And the university underscored its commitment to the neurosciences by building an 11-story hub on the Medical Campus that enables researchers to work more collaboratively and creatively. The goal: to accelerate the translation of science into treatments to help those living with neurodegenerative diseases.
A review of dementia research highlights unequal healthcare outcomes for Black and Hispanic people in the US
The medications have not been widely tested in Black people with the disease, underscoring stark — and persistent — disparities
Alzheimer’s disease has plagued one large Colombian family for generations, striking down half of its members in the prime of life. But one member of that family evaded what had seemed would be fate: Despite inheriting the genetic defect that caused her relatives to develop dementia in their 40s, she stayed cognitively healthy into her 70s.
Researchers at Washington University School of Medicine in St. Louis now think they know why. A previous study had reported that, unlike her relatives, the woman carried two copies of a rare variant of the APOE gene known as the Christchurch mutation. In this study, researchers used genetically modified mice to show that the Christchurch mutation severs the link between the early phase of Alzheimer’s disease, when a protein called amyloid beta builds up in the brain, and the late phase, when another protein called tau accumulates and cognitive decline sets in. So the woman stayed mentally sharp for decades, even as her brain filled with massive amounts of amyloid. The findings, published Dec. 11 in the journal Cell, suggest a new approach to preventing Alzheimer’s dementia.
…researchers at Washington University School of Medicine in St. Louis have found — in mice — that Alzheimer’s-like tau deposits in the brain lead to the accumulation of a form of cholesterol known as cholesteryl esters, and that lowering cholesteryl ester levels helps prevent brain damage and behavioral changes.
In search of ways to prevent these destructive tau tangles, researchers at Washington University School of Medicine in St. Louis have identified a key step in their development. Intervening at this step potentially could forestall the destructive cascade of events that results in brain damage, the researchers said. The findings are published Sept. 20 in the journal Molecular Psychiatry.
The Food and Drug Administration (FDA) recently gave full approval to Leqembi (lecanemab) for patients in the early stages of Alzheimer’s disease. Barbara Joy Snider, MD, PhD, answers questions about the drug.
NIH-supported study lays groundwork for Alzheimer’s clinical trials involving people with intellectual disabilities
Patients who live in less affluent neighborhoods and those from underrepresented racial or ethnic groups are less likely than others to receive specialized care for dementia, including Alzheimer’s disease, a new study from Washington University School of Medicine in St. Louis indicates. Further, the research shows that Black people are more likely than white people to be diagnosed with dementia at a later, more advanced stage, which could contribute to inequities in access to new treatments.
Researchers at Washington University School of Medicine in St. Louis and Lund University in Lund, Sweden, have identified a form of tau that could serve as a marker to track Alzheimer’s progression. The marker also could be used by Alzheimer’s drug developers to assess whether investigational tau-based drugs – the next frontier in Alzheimer’s drug development – are effective against the disease. Such drugs theoretically would benefit people in later stages of the disease, when tau tangles play a crucial role.
If researchers could uncover and mimic whatever protects these escapees, they might develop better treatments — even preventive therapies — not only for families plagued by inherited Alzheimer’s but for everyone.
In Alzheimer’s and related neurodegenerative diseases, the brain protein tau is closely linked to brain damage and cognitive decline. A new study from researchers at Washington University School of Medicine in St. Louis indicates that T cells play a key role in tau-related neurodegeneration, a finding that suggests new treatment strategies for Alzheimer’s and related diseases.
Microglia-mediated T cell infiltration drives neurodegeneration in tauopathy
Neurologists discuss the major milestones in identifying biomarkers for detecting early Alzheimer’s disease over the past two decades.
Globalization of ADRD clinical trials has become a pressing need as 68% of the people living with ADRD will reside in low-middle-income countries (LMICs) by 2025.
For 20 years, the Knight Alzheimer Disease Research Center has worked to boost diversity in clinical trials.
“This drug is not a cure. It doesn’t stop people from getting worse, but it does measurably slow the progression of the disease,” said Dr. Joy Snider, a neurologist at Washington University in St. Louis. “That might mean someone could have an extra six months to a year of being able to drive.”
Randall Bateman of Washington University, St. Louis, presented the biomarker evidence, concluding that it indicates the treatment modified underlying biology. “These findings support the ability to change the course of Alzheimer’s disease,” he told Alzforum.
Biogen Inc. and Eisai Co. caused a stir in September when they announced positive results in a late-stage trial for a closely watched Alzheimer’s drug, lecanemab. Doctors tempered their excitement, though, until they could scrutinize the full peer-reviewed data.
That data arrived Tuesday night. And while it is stoking enthusiasm that physicians might soon be able to offer patients a treatment that can slow the progression of the devastating disease, doctors need to carefully balance that optimism with safety concerns and the reality that the drug is far from a cure — and in fact, it’s hard to quantify how meaningful it might be for a given patient.
The second (and third) time was not the charm for Roche’s experimental antibody drug for Alzheimer’s disease. The company last night announced gantenerumab had failed to show a statistically significant benefit in two large, late-stage clinical trials that tested its ability to slow patients’ cognitive decline—echoing a previous failure in another so-called phase 3 trial.
A new diagnostic tool by C2N Diagnostics is an important new tool for physicians in the evaluation of Alzheimer disease. It could pave the way for earlier diagnosis and treatment and greater enrollment in clinical trials.
Researchers at Washington University School of Medicine in St. Louis have found an innovative way to improve waste clearance from the brain, and thereby possibly treat or even prevent neurodegenerative conditions. They showed that immune cells surrounding the brain influence how efficiently waste is swept out of the brain, and that such immune cells are impaired in old mice, and in people and mice with Alzheimer’s disease. Further, they found that treating old mice with an immune-stimulating compound rejuvenates immune cells and improves waste clearance from the brain.
Scientists are launching a study designed to make or break the hypothesis that Alzheimer’s is caused by a sticky substance called beta-amyloid. The study will give an experimental anti-amyloid drug to people as young as 18 who have gene mutations that often cause Alzheimer’s to appear in their 30s or 40s.
A five-year, $9 million grant from the National Institute on Aging of the National Institutes of Health (NIH) will fund research led by several investigators at Washington University School of Medicine in St. Louis and at the University of Texas at San Antonio to answer that question.
The Alzheimer’s disease (AD) drug lecanemab’s recent success in Biogen’s Phase III clinical trials might have more to do with its effect in increasing levels of soluble amyloid-beta than in decreasing amyloid plaques in the brain, the findings of a new study published in the Journal of Alzheimer’s Disease on October 4, 2022, suggests.
Carlos Cruchaga, PhD, the Barbara Burton and Reuben M. Morriss III Professor in psychiatry, is one of three Zenith Fellows selected this year and one of only 146 Alzheimer’s researchers chosen for the honor since it was created in 1991.
Dr. Jorge Llibre is a Washington University neurologist that researches Alzheimer’s. He says research shows the Hispanic community is two times more likely to develop Alzheimer’s or dementia than non-Hispanics.
Researchers at Washington University School of Medicine in St. Louis have found a new druggable pathway that potentially could be used to help prevent Alzheimer’s dementia.
A study by researchers at Washington University School of Medicine in St. Louis has shown that targeting astrocytes — an inflammatory cell in the brain — reduces tau-related brain damage and inflammation in mice.
On today’s show, we’ll focus on the future of biomarkers in Alzheimer’s disease. We know that amyloid beta and tau protein deposit long before patients with Alzheimer’s develop symptoms. If we could use biomarkers to detect this pathology early, and treat patients early, could we prevent the progression to dementia?
Could drugs prevent Alzheimer’s? These trials aim to find out
A research team at Washington University School of Medicine in St. Louis has identified potential new treatment targets for Alzheimer’s disease, as well as existing drugs that have therapeutic potential against these targets.
A research team at Washington University School of Medicine in St. Louis has identified potential new treatment targets for Alzheimer’s disease, as well as existing drugs that have therapeutic potential against these targets.
A research team at Washington University School of Medicine in St. Louis has identified potential new treatment targets for Alzheimer’s disease, as well as existing drugs that have therapeutic potential against these targets.
A new study shows safety and potential benefit for patients with mild disease. Axon’s experimental vaccine AADVac1—currently the most clinically advanced tau therapy in development—aims to do exactly that. Its goal is to activate our bodies’ defense system to clear out free-floating tau proteins in our brains before they can form harmful tangles that accumulate inside nerve […]
When the U.S. government approved the Alzheimer’s disease drug aducanumab last month despite shaky evidence of clinical benefits, Suzanne Schindler saw an immediate consequence: “We’re going to have to do a lot more biomarker testing.” Schindler, a neurologist at the Washington University School of Medicine in St. Louis, expects many patients with memory problems will […]
An investigational Alzheimer’s drug reduced molecular markers of disease and curbed neurodegeneration in the brain, without demonstrating evidence of cognitive benefit, in a phase 2/3 clinical trial led by researchers at Washington University School of Medicine in St. Louis through its Dominantly Inherited Alzheimer Network-Trials Unit (DIAN-TU). These results led the trial leaders to offer the drug, […]