Sickness and death are inevitable, but many of us will never get the chance to know exactly when our worst health ailments will strike. Someday soon, though, that might not be true for people with Alzheimer’s disease, research out today shows.
Scientists say they’ve devised a model that can narrow down the onset of Alzheimer’s, the most common form of dementia. Based on simple blood test results, they were able to predict the age, within several years, that someone would develop symptoms. In the short term, this work could improve clinical trials for Alzheimer’s, the researchers say, and down the road, it may help people at higher risk make crucial decisions about their future.
“Given the speed of progress in Alzheimer’s research, blood biomarkers, and modeling, we are hopeful that these kinds of models will be available for clinical care within the next couple of years,” study author Suzanne Schindler, an associate professor of neurology at the Washington University School of Medicine in St. Louis, told Gizmodo.
The Alzheimer’s clock
There have been important advances in Alzheimer’s research lately, including diagnosis.
Though the foolproof test for Alzheimer’s still relies on examining the brain after death, doctors now employ several methods to diagnose the condition in living people with high accuracy, even before symptoms like memory loss appear. Last year, the Food and Drug Administration formally approved the first blood tests for diagnosing or ruling out Alzheimer’s, and still more are on the way.
These tests look for biomarkers closely linked to Alzheimer’s, such as the proteins tau and amyloid beta. In Alzheimer’s, abnormal versions of these proteins build up in the brain. One particular form of abnormal tau, called phosphorylated tau 217 (ptau217), seems to be an especially great biomarker. Since its levels in the blood track so closely with the progression of Alzheimer’s, the WashU researchers believe that ptau217 can act as a clock to predict the visible onset of the disease.
To create their model, the researchers analyzed data from two existing Alzheimer’s research projects, involving roughly 600 older people. These volunteers, who started out in good cognitive health, were given one of several blood tests measuring ptau217, including PrecivityAD2, a commercially available test developed by WashU researchers that’s in the final steps of being reviewed for FDA approval.
“In our study, we found that blood p-tau217 levels increased relatively consistently across individuals, allowing us to estimate the age that individuals became positive on the p-tau217 test,” co-author Kellen Petersen, an instructor in neurology at WashU Medicine, told Gizmodo. “This age at p-tau217 positivity was strongly associated with the age that individuals developed symptoms of Alzheimer’s.”
All in all, the team’s model could predict when someone’s p-tau217 levels would likely soon lead to visible symptoms, though within an average time window of three to four years. Notably, the gap between high p-tau217 levels and Alzheimer’s symptoms was shorter in older volunteers, suggesting that younger people can better fend off brain deterioration. The team’s model also worked with blood tests besides PrecivityAD2, indicating its potential wide usability. Their results were published Thursday in Nature Medicine.
The future of predicting Alzheimer’s
Given the current time frame of three to four years, their clock model is best used in clinical trials for now, the researchers say. But that amount of advance notice could still provide valuable insights.
“Our models will help trials select individuals who are still cognitively unimpaired but more likely to develop symptoms during the clinical trial, which would make trials more efficient,” Petersen said.
The researchers are also optimistic that incorporating data from other blood, imaging, and cognitive tests can further refine their predictions. And eventually, these models should become accurate enough that doctors and patients can use them to guide their next steps.
“For example, individuals who are far from symptom onset might choose to focus on lifestyle modification, while those close to symptom onset might be more proactive and consider participating in clinical trials,” Petersen said. The researchers are already working to improve their models, and they’ve released their code online and created a web-based app so that other research teams can try to do the same.
Right now, Alzheimer’s and other forms of dementia are incurable. But innovations like this could help us one day turn back the clock.
Many moms feel scatterbrained, so it might seem counterintuitive that new research has found a link between pregnancy and breastfeeding and higher cognitive function later in life.
The findings, published by the Alzheimer’s Association, take on a special significance considering that women are disproportionately affected by dementia. Nearlytwo-thirdsof Americans with Alzheimer’s are women, the reasons for which are not fully understood.
To explore the link between female reproduction and dementia, researchers analyzed data from more than 7,000 women who each were around age 70. The women gave information about their reproductive histories and underwent annual cognitive assessments for 13 years.
More cumulative time spent breastfeeding and pregnant was associated with greater cognition, verbal memory and visual memory, the researchers found.
More specifically, women who had been pregnant scored higher on cognitive ability tests than those who had never been pregnant. Women who had breastfed had higher cognitive ability scores and verbal memory scores than those who had never breastfed. These benefits were similar in scale to the impact that being physically active and avoiding smoking have on improved cognition, the researchers said.
The researchers said they now are delving further into the way certain reproductive histories may offer protection against cognitive decline.
“If we can figure out, as a next step, why those reproductive patterns lead to better cognitive outcomes in old age, then we can work toward figuring out how to craft therapies — for example, new drugs, repurposed drugs or social programs — that mimic the naturally-occurring effect we observed,” said the study’s lead author, Molly Fox, an anthropology professor at the University of California Los Angeles.
Boston University researchers in a groundbreaking study found that those with CTE have a much higher chance of being diagnosed with dementia.
The largest study of its kind from the Boston University CTE Center reveals that the progressive brain disease chronic traumatic encephalopathy should be recognized as a new cause of dementia.
The BU researchers discovered that those with advanced CTE — who had been exposed to repetitive head impacts — had four times higher odds of having dementia.
“This study provides evidence of a robust association between CTE and dementia as well as cognitive symptoms, supporting our suspicions of CTE being a possible cause of dementia,” said Michael Alosco, associate professor of neurology at Boston University Chobanian and Avedisian School of Medicine.
“Establishing that cognitive symptoms and dementia are outcomes of CTE moves us closer to being able to accurately detect and diagnose CTE during life, which is urgently needed,” added Alosco, who’s the co-director of clinical research at the BU CTE Center.
The researchers studied 614 brain donors who had been exposed to repetitive head impacts, primarily contact sport athletes.
By isolating 366 brain donors who had CTE alone, compared to 248 donors without CTE, researchers found that those with the most advanced form of CTE had four times increased odds of having dementia.
The four times odds are similar to the strength of the relationship between dementia and advanced Alzheimer’s disease pathology, which is the leading cause of dementia.
Dementia is a clinical syndrome that refers to impairments in thinking and memory, in addition to trouble with performing tasks of daily living like driving and managing finances. Alzheimer’s disease is the leading cause, but there are several other progressive brain diseases listed as causes of dementia that are collectively referred to as Alzheimer’s disease related dementias (ADRD).
With this new study, the authors argue that CTE should now also be formally considered an ADRD.
The study also reveals that dementia due to CTE is often misdiagnosed during life as Alzheimer’s disease, or not diagnosed at all. Among those who received a dementia diagnosis during life, 40% were told they had Alzheimer’s disease despite showing no evidence of Alzheimer’s disease at autopsy. An additional 38% were told the causes of their loved one’s dementia was “unknown” or could not be specified.
In addition, this study addressed the controversial viewpoint expressed by some clinicians and researchers that CTE has no clinical symptoms. As recently as 2022, clinicians and researchers affiliated with the Concussion in Sport Group meeting, which was underwritten by international professional sports organizations, claimed, “It is not known whether CTE causes specific neurological or psychiatric problems.”
Alosco said, “There is a viewpoint out there that CTE is a benign brain disease; this is the opposite of the experience of most patients and families. Evidence from this study shows CTE has a significant impact on people’s lives, and now we need to accelerate efforts to distinguish CTE from Alzheimer’s disease and other causes of dementia during life.”
As expected, the study did not find associations with dementia or cognition for low-stage CTE.
The BU CTE Center is an independent academic research center at the Boston University Avedisian and Chobanian School of Medicine. It conducts pathological, clinical and molecular research on CTE and other long-term consequences of repetitive brain trauma in athletes and military personnel.
Congratulations, you’ve reached the final day of the Brain Health Challenge! Today, we’re asking you to do a few things that might feel a bit out of left field — like getting your blood pressure checked.
No, it isn’t as fun as playing Pips, but experts say it’s one of the most important things you can do for your brain. That’s because heart health and brain health are intrinsically linked.
High blood pressure, in particular, can damage brain cells, and it’s a significant risk factor for stroke and dementia. When blood pressure is too high, it places stress on the walls of arteries in the brain. Over time, that added stress can cause the blood vessel walls to thicken, obstructing blood flow. In other cases, the increased pressure causes the artery walls to thin and leak blood into the brain.
These changes to the blood vessels can sometimes cause a large stroke to occur. More commonly, the damage leads to micro-strokes and micro-hemorrhages, which cause fewer immediate problems and often go unnoticed. But if someone has hypertension for years or decades, these injuries can build up, and the person may start to experience cognitive impairment.
High blood pressure “is known as a silent killer for lots of reasons,” said Dr. Shyam Prabhakaran, the chair of neurology at the University of Chicago. “It doesn’t cause you any symptoms until it does.”
Because the damage accumulates over many years, experts say that managing blood pressure in midlife matters most for brain health. Hypertension can be addressed with medication or lifestyle changes, as directed by your doctor. But the first thing you need to do is know your numbers. If your blood pressure comes back higher than 120/80, it’s important to take it seriously, Dr. Prabhakaran said.
While you’re at it, there are a few other aspects of your physical health that you should check on.
Your eyes and ears are two of them. Hearing and vision loss have both been shown to increase the risk of dementia. Experts think that with less sensory information coming in to stimulate the brain, the regions that process hearing and vision can start to atrophy. What’s more, people with sensory loss often withdraw or are left out of social interactions, further depriving them of cognitive stimulation.
Oral health can also affect your brain health. Research has found a connection between regular flossing and reduced odds of having a stroke. That may be because good oral health can help to reduce inflammation in the body. The bacteria that cause gum disease have also been tied to an increased risk of Alzheimer’s.
And have you gotten your shingles vaccine? There is mounting evidence that it’s a powerful weapon for protecting against dementia. One study found that it lowered people’s odds of developing the condition by as much as 20 percent.
To wrap up this challenge, we want you to schedule a few medical appointments that benefit your brain, as well as your body.
After five days of feeding, exercising and challenging your brain, you are well on your way to better cognitive health. Thanks for joining me this week, and keep up the good habits!
Today, you’re going to do perhaps the single best thing for your brain.
When I asked neurologists about their top behaviors for brain health, they all stressed the importance of physical activity.
“Exercise is top, No. 1, when we’re thinking about the biggest bang for your buck,” said Dr. Gregg Day, a neurologist at the Mayo Clinic.
Numerous studies have shown that people who exercise regularly tend to perform better on attention, memory and executive functioning tests. There can be a small cognitive boost immediately after a workout, and the effects are sustained if people exercise consistently. And while staying active can’t guarantee you won’t develop dementia, over the long term, it is associated with a lower risk of it.
Researchers think that moving your muscles benefits your brain in part because of special signaling molecules called exerkines. During and after a workout, your muscles, fat and other organs release these molecules into the bloodstream, some of which make their way up to the brain. There, those exerkines go to work, helping to facilitate the growth of new connections between neurons, the repair of brain cells and, possibly, the birth of new neurons.
Exercise also appears to improve blood flow in the brain. That ramps up the delivery of good things to brain cells, like oxygen, glucose and those amazing exerkines. And it helps remove more bad things, namely toxic proteins, like amyloid, that can build up and damage brain cells, increasing the risk for Alzheimer’s.
All of the changes brought on by exercise are “essentially allowing your brain to age more slowly than if you’re physically inactive,” said Kirk Erickson, the chair of neuroscience at the AdventHealth Research Institute.
The benefits are particularly pronounced in the hippocampus, a region critical for learning and memory. In older adults, the hippocampus shrinks 1 to 2 percent a year, and it is one of the main areas affected by Alzheimer’s. Researchers think physical activity helps to offset some of that loss.
The best exercise you can do for your brain is the one you’ll do consistently, so find something that you enjoy and that fits easily into your life.
Walking is one option; two neurologists I spoke to said they got their exercise in by walking at least part of the way to their offices. Recent research suggests that just a few thousand steps a day can reduce the risk of dementia. It’s important to get your heart rate up, though, so “walk as though you’re trying to get somewhere on time,” said Dr. Linda Selwa, a clinical professor of neurology at the University of Michigan Medical School.
Or you could try swimming, cycling, Pilates, weight lifting, yoga, pickleball, dancing, gardening — any type of physical exertion can be beneficial.
If the thought of working out feels like a drag, try pairing it with something else you enjoy doing, like listening to an audiobook. This is a trick that Katherine Milkman, a professor who studies habits at The Wharton School of the University of Pennsylvania, calls “temptation bundling.”
For Day 3, we’re asking you to spend at least 20 minutes exercising for your brain. Go for a walk with your accountability partner if they’re nearby. (If not, call them and do a walk-and-talk.) Or let us find you a new workout to try, using the tool below. As usual, we can all meet in the comments to catch up and check in.
Welcome to Day 2 of the Brain Health Challenge. Today, we’re talking about food.
Your brain is an energy hog. Despite comprising about 2 percent of the average person’s body mass, it consumes roughly 20 percent of the body’s energy. In other words, what you use to fuel yourself matters for brain health.
So what foods are best for your brain?
In a nine-year study of nearly 1,000 older adults, researchers at Rush University in Chicago found that people who ate more of nine particular types of food — berries, leafy greens, other vegetables, whole grains, beans, nuts, fish, poultry and olive oil — and who ate less red meat, butter and margarine, cheese, sweet treats and fried food had slower cognitive decline.
Based on these findings, the researchers developed the MIND diet.
Experts think the foods included in the MIND diet are especially good for the brain because they contain certain macro and micronutrients.
Berries and leafy greens, for example, are rich in polyphenols and other antioxidants, said Jennifer Ventrelle, a dietitian at Rush and a co-author of “The Official Mind Diet.” Many of these compounds can cross the blood-brain barrier and help to fight inflammation and oxidative stress, both of which can damage cells and are linked to dementia.
Nuts and fatty fishes, like salmon and sardines, contain omega-3 fatty acids, which are important for building the insulating sheaths that surround the nerve fibers that carry information from one brain cell to another.
Whole grains and beans both contain a hefty dose of fiber, which feeds the good microbes in the gut. Those microbes produce byproducts called short-chain fatty acids that experts think can influence brain health via the gut-brain axis.
You don’t have to revamp your whole diet to get these nutrients. Instead, think about “MIND-ifying” whatever you already tend to eat, said Dr. Joel Salinas, a neurologist at NYU Langone Health and the founder and chief medical officer of the telehealth platform Isaac Health. For instance, add a handful of nuts or berries to your breakfast.
Today’s activity will help you MIND-ify your own meals. Share your choices with your accountability partner and in the comments, and I’ll discuss the ways I’m adjusting my diet, too. For added inspiration, check out these MIND-approved recipes from New York Times Cooking.
Welcome to the Brain Health Challenge! I’m Dana Smith, a reporter at The New York Times, and I’ll be your guide.
To live a healthy life, it’s crucial to have a healthy brain. In the short term, it keeps you sharp and firing on all cylinders. In the long term, it can reduce your risk of cognitive decline, dementia and stroke.
Practicing basic healthy behaviors, like eating nutritious food and getting regular exercise, is the best way to enhance your brain power and protect the longevity of your neurons. These types of lifestyle habits can benefit the brain at any age. And while they won’t guarantee that you’ll never develop dementia or another brain disease, severalclinicaltrials have shown that they can improve cognition or slow decline.
Every day this week, you’ll do an activity that’s good for your brain, and we’ll dig into the science behind why it works. Some of these activities can provide a small immediate cognitive benefit, but the bigger reward comes from engaging in them consistently over time. So along with the neuroscience lessons, we’ll include a few tips to help you turn these actions into lasting habits.
To keep you accountable, we’re encouraging you to complete this challenge with a friend. If you don’t have a challenge buddy, no problem: We’re also turning the comments section into one big support group.
There are so many fascinating ways your daily behaviors affect your brain. Take sleep, for example.
Lots ofstudies have shown that getting a good night’s rest (seven to eight hours) is associated with better memory and other cognitive abilities. That’s because sleep, especially REM sleep, is when your brain transfers short-term memories — things you learned or experienced during the day — into long-term storage.
Sleep is also when your brain does its daily housekeeping. While you rest, the brain’s glymphatic system kicks into high gear, clearing out abnormal proteins and other molecular garbage, including the protein amyloid, which is a major contributor to Alzheimer’s disease. A buildup of amyloid is one reason experts think that people who routinely get less sleep have a higher risk of dementia.
What other behaviors play a big role in brain health? For today’s activity, we’re going to test your knowledge with a quiz. Share your score with your accountability partner and in the comments below — I’ll be in there too, cheering you on.
If the microbiome of those eating plant-based diets protects against the toxic effects of TMAO, what about swapping gut flora?
“Almost 2,500 years ago, Hippocrates stated that ‘All disease begins in the gut.’” When we feed our gut bacteria right with whole plant foods, they feed us right back with beneficial compounds like butyrate, which our gut bugs make from fiber. On the other hand, if we feed them wrong, they can produce detrimental compounds like TMAO, which they make from cheese, eggs, seafood, and other meat.
We used to think that TMAO only contributed to cardiovascular diseases, like heart disease and stroke, but, more recently, it has been linked to psoriatic arthritis, associated with polycystic ovary syndrome, and everything in between. I’m most concerned about our leading killers, though. Of the top ten causes of death in the United States, we’ve known about its association with increased risk of heart disease and stroke, killers number one and five, but recently, an association has also been found between blood levels of TMAO and the risks of various cancers, which are our killer number two. The link between TMAO and cancer could be attributed to the inflammation caused by TMAO, but it could also be oxidative stress (free radicals), DNA damage, or a disruption in protein folding.
What about our fourth leading killer, chronic obstructive pulmonary disease (COPD), like emphysema? TMAO is associated with premature death in patients with exacerbated COPD, though it’s suspected that it’s due to them dying from more cardiovascular disease.
The link to stroke is a no-brainer—no pun intended. It is due to the higher blood pressure associated with higher TMAO levels, as well as the greater likelihood of clots forming in those with atrial fibrillation. Those with higher TMAO levels also appear to have worse strokes and four times the odds of death.
Killer number six is Alzheimer’s disease. Can TMAO even get up into our brains? Yes, TMAO is present in human cerebrospinal fluid, which bathes the brain, and TMAO levels are higher in those with mild cognitive dysfunction and those with Alzheimer’s disease dementia. “In the brain, TMAO has been shown to induce neuronal senescence [meaning, deterioration with age], increase oxidative stress, impair mitochondrial function, and inhibit mTOR signaling, all of which contribute to brain aging and cognitive impairment.”
Killer number seven is diabetes, and people with higher TMAO levels are about 50% more likely to have diabetes. Killer number eight is pneumonia, and TMAO predicts fatal outcomes in pneumonia patients even without evident heart disease. Kidney disease is killer number nine, and TMAO is strongly related to kidney function and predicts fatal outcomes there as well. Over a period of five years, more than half of chronic kidney disease patients who started out with average or higher TMAO levels were dead, whereas among those in the lowest third of levels, nearly 90% remained alive.
How can we lower the TMAO levels in our blood? Because TMAO originates from dietary sources, we could limit our intake of choline- and carnitine-rich foods. They’re so widespread in foods,” though we’re talking about meat, eggs, and dairy. “Therefore, restriction of foods rich in TMA-containing nutrients may not be practical.” Can we just get a vegan fecal transplant? “Vegan donors provided the investigators with a fresh morning fecal sample…”
If you remember, if you give a vegan a steak, despite all that carnitine, they make almost no TMAO compared to a meat-eater, presumably because the vegan hasn’t been fostering steak-eating bugs in their gut. See below and at 3:40 in my video Can Vegan Fecal Transplants Lower TMAO Levels?.
Remarkably, even if you give plant-based eaters the equivalent of a 20-ounce steak every day for two months, only about half start ramping up production of TMAO, showing just how far their gut flora has to change. The capacity of veggie feces to churn out TMAO is almost nonexistent. Instead of eating healthier, what about getting some vegan poop?
In a double-blind, randomized, controlled trial, research subjects either got vegan poop or their own poop back through a hose snaked down their nose, and it didn’t work.
First of all, the vegans recruited for the study started out making TMAO themselves, in contrast to the other study, where they didn’t make any at all. This may be because the earlier study required the vegans to have been vegan for at least a year, and this study didn’t. So, there wasn’t much of a change in TMAO running through their bodies two weeks after getting the vegan poop, but the vegan poop they got seemed to start out with some capacity to produce TMAO in the first place.
So, the failure to improve after the vegan fecal transplant “could be related to limited baseline microbiome differences and continuation of an omnivorous diet” after the vegan-donor transplant. What’s the point of trying to reset your microbiome if you’re just going to eat meat? Well, the researchers didn’t want to switch people to a plant-based diet since they knew that alone can change our microbiome, and they didn’t want to introduce any extra factors. The bottom line is that it seems there may not be any shortcuts. We may just have to eat a healthier diet.
NEW YORK — Federal prison officials say the former CEO of Abercrombie & Fitch is fit to stand trial on federal sex trafficking charges after he was hospitalized with Alzheimer’s disease, Lewy body dementia and a traumatic brain injury.
Michael Jeffries had been ordered to be hospitalized in May. But in a letter filed in federal court in New York on Wednesday, Blake Lott, the acting warden at the Federal Medical Center in Butner, North Carolina said the 81-year-old is “now competent to stand trial.”
Lott didn’t provide further details in the letter but said the center has provided a report to the judge handling the case. Jeffries had been discharged from FMC-Butner on Nov. 21, according to previous filings in the case.
Brian Bieber, an attorney for Jeffries, responded that other doctors had previously found his client incompetent to proceed.
“A doctor from the Bureau of Prisons is of a different opinion,” he said in an email Wednesday. “We look forward to the Judge hearing the medical evidence, and deciding on the appropriate course of action moving forward.”
The letter comes as prosecutors and Jeffries’ lawyers are expected to confer by phone Thursday with U.S. District Court Judge Nusrat Choudhury on the status of the case.
Jeffries pleaded not guilty last year to federal charges of sex trafficking and interstate prostitution.
His lawyers had argued that the former executive required around-the-clock care and was unable to understand the nature and consequences of the case against him or to assist properly in his defense.
They had said at least four medical professionals concluded that Jeffries’ cognitive issues were “progressive and incurable” and that he would not “regain his competency and cannot be restored to competency in the future.”
Jeffries’ lawyers and prosecutors had requested that he be hospitalized in federal Bureau of Prisons custody so he could receive treatment that might allow his criminal case to proceed.
Choudhury agreed, ordering him placed in a hospital for up to four months. Before then, Jeffries had been free on a $10 million bond.
Prosecutors say Jeffries, his romantic partner and a third man used the promise of modeling jobs to lure men to drug-fueled sex parties in New York City, the Hamptons and other locations. The charges echoed sexual misconduct accusations made in a civil case and the media in recent years.
Jeffries left Abercrombie in 2014 after more than two decades at the helm. His partner, Matthew Smith, has also pleaded not guilty and remains out on bond, as has their co-defendant, James Jacobson.
An oral version of semaglutide, the active ingredient in blockbuster drugs Ozempic and Wegovy, failed to slow the progression of Alzheimer’s disease in closely watched trials, Novo Nordisk said Monday.In two Phase 3 trials of more than 3,800 adults receiving standard care for Alzheimer’s, the company evaluated whether an older pill form of semaglutide worked better than a placebo. The drug was shown to be safe and led to improvements in Alzheimer’s-related biomarkers, the company said, but the treatment did not delay disease progression.Novo had long treated Alzheimer’s as a long-shot bet for the popular GLP-1 drugs. Use of these drugs for diabetes and weight loss has exploded in recent years, and they have shown benefits for a wide range of additional health conditions, such as protecting the heart and kidneys, reducing sleep apnea and potentially helping with addiction.Smaller trials and animal studies had suggested GLP-1s might help slow cognitive decline or reduce neuro-inflammation but larger trials like Novo’s were needed to confirm whether patients saw actual benefits.”Based on the significant unmet need in Alzheimer’s disease as well as a number of indicative data points, we felt we had a responsibility to explore semaglutide’s potential, despite a low likelihood of success,” said Martin Holst Lange, chief scientific officer and executive vice president of Research and Development at Novo Nordisk said in a statement on Monday that thanked trial participants.A one-year extension of the trials will be discontinued, Novo said. Results from the trials have not yet been peer-reviewed or published but will be presented at upcoming scientific conferences.Novo has been facing increased competition in the weight loss market and recently announced lowered prices for some cash-paying patients using Ozempic and Wegovy. Novo shares fell Monday after the Alzheimer’s trial announcement.
CNN —
An oral version of semaglutide, the active ingredient in blockbuster drugs Ozempic and Wegovy, failed to slow the progression of Alzheimer’s disease in closely watched trials, Novo Nordisk said Monday.
In two Phase 3 trials of more than 3,800 adults receiving standard care for Alzheimer’s, the company evaluated whether an older pill form of semaglutide worked better than a placebo. The drug was shown to be safe and led to improvements in Alzheimer’s-related biomarkers, the company said, but the treatment did not delay disease progression.
Novo had long treated Alzheimer’s as a long-shot bet for the popular GLP-1 drugs. Use of these drugs for diabetes and weight loss has exploded in recent years, and they have shown benefits for a wide range of additional health conditions, such as protecting the heart and kidneys, reducing sleep apnea and potentially helping with addiction.
Smaller trials and animal studies had suggested GLP-1s might help slow cognitive decline or reduce neuro-inflammation but larger trials like Novo’s were needed to confirm whether patients saw actual benefits.
“Based on the significant unmet need in Alzheimer’s disease as well as a number of indicative data points, we felt we had a responsibility to explore semaglutide’s potential, despite a low likelihood of success,” said Martin Holst Lange, chief scientific officer and executive vice president of Research and Development at Novo Nordisk said in a statement on Monday that thanked trial participants.
A one-year extension of the trials will be discontinued, Novo said. Results from the trials have not yet been peer-reviewed or published but will be presented at upcoming scientific conferences.
Novo has been facing increased competition in the weight loss market and recently announced lowered prices for some cash-paying patients using Ozempic and Wegovy. Novo shares fell Monday after the Alzheimer’s trial announcement.
In medicine, there’s almost no such thing as a free lunch. Just about every drug or intervention will have its side effects.
Ideally, rigorous studies and the regulatory process will ensure that an approved drug’s benefits clearly outweigh any potential harms. But sometimes, researchers (and patients) will uncover side effects that went unnoticed during the approval process. Other times, more rarely, a drug’s maker is revealed to have buried incriminating information about their drug’s harms from the public or to have created a product that doesn’t work at all as intended. And when that happens, a bad or ineffective treatment can spark a major scandal.
There’s no shortage of pharmaceutical scandals that have occurred over the years, but to keep things short, let’s just focus on some of the biggest ones to have happened in this quarter-century.
1. Johnson & Johnson’s talcum powder products
For decades, people had unsuccessfully tried to sue J&J over its consumer products containing talc, particularly baby powder, claiming that the products had contributed to their cancers.
In 2018, however, an explosive report from Reuters found the company had hidden evidence that the talc it used could sometimes contain detectable levels of asbestos, a known carcinogen. The report helped fuel a new wave of lawsuits and growing public distrust in the company’s baby powder products. In the years since, the company has repeatedly lost civil suits over its talc products, some totaling into the billions, and its appeals continued to fail, even before the Supreme Court.
Though J&J has maintained that its products are safe, the company eventually removed talc from all its powder brands (instead using cornstarch), tried and failed to cover its liability over these lawsuits by having a subsidiary declare bankruptcy, and even this year has continued to lose court cases tying its products to people’s cancer.
Interestingly enough, though asbestos is known to cause cancer, past research hasn’t found a clear link between talc as a whole (including asbestos-free talc) and cancer, and there remains some disagreement over the extent of the risk posed by talcum powder products. The American Cancer Society states that if talc can raise a person’s risk of ovarian cancer (the primary type of cancer linked to talc), the “overall increase is likely to very be small” for an individual woman. The World Health Organization has stated that asbestos-containing talc should be considered carcinogenic, while talc in general is “probably carcinogenic.”
2. Biogen and the Alzheimer’s drug that wasn’t
In June 2021, the FDA approved Biogen and Eisai’s antibody-based Alzheimer’s drug Aduhelm. At first glance, the approval should have been good news: the first drug of its kind, and one intended to actually target a key driver of the degenerative disorder, beta amyloid. But in actuality, it was anything but.
In a rare move at the time, the FDA went against the recommendations of its expert advisory panel, who voted against approval. The outside experts rightly noted that the data supporting the drug’s effectiveness was mixed at best. The FDA also granted Aduhelm accelerated approval, a special category that requires less rigorous evidence. Media outlet STAT News later uncovered an unusually friendly relationship between top Biogen employees and FDA officials, which prompted a Congressional investigation into the matter. And to add insult to injury, Biogen initially set Aduhelm’s list price at $56,000 a year—a cost high enough to potentially devastate the pockets of patients and Medicare if the drug saw widespread use among older Americans.
Many doctors soon rebelled against the approval, refusing to prescribe it to their patients, while Medicare decided to severely restrict its coverage of the drug. Biogen eventually gave up trying to make Aduhelm a thing, following years of poor sales, and pulled the drug from the market in early 2024.
This saga does have a bit of a happy ending, at least. There have been other similar drugs developed and approved in recent years, and unlike Aduhelm, these drugs do seem to have a real, if still modest, effect on treating the condition.
3. Purdue Pharma and OxyContin
Purdue Pharma has perhaps become the most infamous poster child for the opioid crisis.
Its blockbuster drug, OxyContin, helped fuel growing rates of opioid use disorder following its release to the public in 1996. And though there are many drivers of the crisis, including the proliferation of more potent agents like fentanyl in later years, the company did eventually admit to downplaying the addictive risk of its products, paying doctors illegal kickbacks to prescribe their drugs, and turning a blind eye to the widespread diversion of its drugs from pharmacies to the black market.
Following a glut of civil and federal lawsuits over OxyContin, Purdue Pharma shuttered its doors, and its sole owners—the Sackler family—agreed to pay out more than $4 billion as part of a far-reaching settlement in 2021. The courts bumped this up to $6 billion in 2023. That settlement, however, also provided immunity from further civil charges against the Sacklers themselves. And though the situation has finally started to improve as of late, roughly 50,000 Americans still died from opioid overdoses last year.
4. Martin Shkreli’s drug price surge
Sometimes the scandals aren’t about the drugs themselves, but what they’re being sold for.
In 2015, Martin Shkreli became public enemy number one when his company, Turing Pharmaceuticals, bought the anti-parasitic and anti-HIV drug Daraprim and raised its $13.50 price tag per pill by over 5,000 percent. Shkreli’s cocky, unrepentant attitude toward his many critics earned him the nickname of the “Pharma bro.”
Ironically enough, his initial downfall had nothing to do with Daraprim. Soon after he became infamous, federal prosecutors in New York charged Shkreli with securities fraud, and in 2017, he was convicted and sentenced to seven years of federal prison.
Though Shkreli was released early in 2022, his company’s management of Daraprim did later come back to bite him. In 2020, the FTC and others sued the company, now called Vyera Pharmaceuticals after Shkreli’s imprisonment, alleging that it carried out an “elaborate anticompetitive scheme” to maintain its monopoly on the drug. The company reached a settlement with the FTC a year later, and the legal battle eventually required Shkreli himself to pay out a $64 million fine and to stay away from the pharmaceutical industry entirely. In 2023, Vyera declared bankruptcy and sold the rights to Daraprim. Last year, the U.S. Supreme Court snubbed Shkreli’s attempt to dismiss his personal fine and ban.
Don’t feel too bad for Shkreli, though. Since his release from prison, he’s been busy trying to shill crypto and AI knockoffs of WebMD.
In early 2022, the FDA warned families to stay away from certain powdered baby formulas produced by the company Abbott Nutrition. The products, it turns out, were contaminated by Cronobacter bacteria.
Several children were hospitalized, and two infants who had consumed the products later died. Abbott issued a widespread recall of its products and shut down its formula production facility in Sturgis, Michigan. The FDA’s investigation concluded that Abbott had failed to maintain sanitary conditions and that the facility had at least eight recent instances of Cronobacter contamination dating back to 2019.
It would take four months for the company’s Sturgis plant to reopen, following an agreement with the FDA to overhaul its safety practices, the length of which helped contribute to a nationwide formula shortage that year. Lawmakers on both sides also criticized the FDA for its delayed response to the crisis, since the agency first caught wind of potential issues as early as September 2021.
Though there haven’t been similar recalls or reported outbreaks since, an extensive ProPublica report in April 2025 interviewed workers who claimed that the Sturgis plant continues to have serious safety and sanitary risks to this day. One employee reported what they found to the FDA, but it’s unclear whether the new Trump administration will take action.
6. Elizabeth Holmes and Theranos
Elizabeth Holmes founded the company Theranos in 2003. It centered around the development of a device intended to make blood tests easier than ever. With just a few drops of blood from a single finger prick, Holmes claimed, her company’s “Edison” device could accurately detect a litany of health conditions. By the mid-2010s, Holmes’ marketing of Theranos had allowed her to become a darling of the biotech world: a young, self-made entrepreneur styled after Steve Jobs, who at one point was worth nearly $5 billion.
The trouble was, as the world eventually found out, it was all based on falsehoods. Starting in late 2015, Wall Street Journal reporter John Carreyrou exposed the fraudulent practices of Holmes and Theranos. Though Holmes had struck a partnership with retail chain Walgreens in 2013 to provide the Edison device to its customers, the Edison could simply never do what Holmes claimed it could. And eventually, the company secretly resorted to using other commercially available machines to perform most of its blood testing services.
Holmes’ deception didn’t just mislead investors; several people reported that the faulty test results provided by Theranos made them fearful about having medical conditions they didn’t actually have, such as HIV, or otherwise harmed their health.
Holmes was convicted of investor fraud and other charges over Theranos in 2022 and was sentenced to an 11-year stint in prison (later reduced by two years), while her co-executive and one-time romantic partner Ramesh “Sunny” Balwani was sentenced to nearly 13 years the next month. As of this year, she’s made her return to social media (via having someone else post her words).
Ahead of Solano County’s Walk to End Alzheimer’s Saturday morning in Fairfield, one Rio Vista man reflects on how the meaning behind the walks has changed for him in recent years.
Over the past couple of years, Dennis Beck has raised more than $10,000 through the Walk to End Alzheimer’s, supporting Alzheimer’s research.
Beck has a long family history of dementia. Flipping through photos of his mother, Lillian, he reflected on just how much they had in common.
It wasn’t just their shared sweet tooth but the fact that both would be diagnosed with dementia. Lillian passed from the disease more than a decade ago.
Dennis Beck and his mother, Lillian
“It was very, very, very difficult,” Beck said.
His diagnosis of late-stage, mild-onset Alzheimer’s came about a year and a half ago. It followed his sister’s diagnosis, too. However, her disease has progressed to the point where she has to be cared for in an assisted living facility.
“It did come to mind that, you know, maybe I’m in line for this. But it didn’t own me,” Beck said of his family history.
Beck started to notice just over a year ago that he was having trouble using his computer and with his short-term memory.
He decided he would not sit back and let the disease just take over his life.
“It slows the disease down so it allows you more time to be cognitively alert before the decline,” Beck said. “I’m forgetful, but I’m not as forgetful as I was during that peak period before the infusions had started.”
Today, Beck sees a big difference in his own cognitive function.
“I am grateful because of the treatment that I’m getting that wasn’t available to my sister, it wasn’t available to my mother, it wasn’t available to my aunt. So, I am beyond blessed,” Beck said.
There is no fear when he looks to the future, even though he knows all he can do is slow down this terrible disease.
“I find worrying about the future is not a positive. So, I don’t take my days for granted at all. I’m just grateful that I have a good day every day,” Beck said.
Hope outshines the darkness of dementia. Beck believes one day, Alzheimer’s disease will be forgotten.
“I believe that one day there’s going to be a cure. Maybe because I have it and I’m hopeful. I don’t know if it’s going to be in my lifetime. But I think it’s going to come about and this killer disease can be reversed,” Beck said.
CBS Sacramento anchor Marlee Ginter is emceeing the Solano County Walk to End Alzheimer’s Saturday morning.
With approximately one in eight elderly Long Islanders diagnosed with Alzheimer’s disease, treatments for this progressively debilitating disease are essential.
And as the population ages, yet even more people will be diagnosed with dementia and/or Alzheimer’s and require memory care services either at home or in a group living facility, making services and treatment for people with cognitive impairment more vital than ever.
Improving outcomes with lifestyle change
DANIEL KNECHT: ‘For several years, the medical community viewed Alzheimer’s as a fixed, chronic and ultimately fatal condition, not one impacted by lifestyle.’ Courtesy of EmblemHealth
Providing health insurance coverage for 3 million New Yorkers, EmblemHealth continually strives to bring evidence-based, holistic care to the communities it serves, notes Daniel Knecht, the company’s chief medical officer.
Currently, EmblemHealth is partnering with Dr. Dean Ornish, a lifestyle medicine pioneer, and CookUnity, which prepares home-delivered meal kits. The pilot program—which follows Ornish’s research demonstrating improved health outcomes with intensive lifestyle changes—is designed for those diagnosed with early Alzheimer’s disease.
According to Knecht, Ornish has found that diet, exercise, stress management and social connectedness–when adhered to by patients with early stage Alzheimer’s or memory loss—significantly changes the trajectory of the condition. Further, Ornish has done clinical studies that show that people on this kind of diet have reduced symptoms of memory loss, experience less of a foggy mind and have more energy through the day.
Knecht added that the U.S. POINTER Study (conducted by the Alzheimer’s Association), demonstrated that a similar approach to lifestyle changes can reduce the risk of developing Alzheimer’s in the high-risk population.
For several years, the medical community viewed Alzheimer’s as a fixed, chronic and ultimately fatal condition, not one impacted by lifestyle, notes Knecht .
“We’re starting to really understand that it [Alzheimer’s] is a chronic condition akin to diabetes or cardiovascular disease where there are many drivers that can cause or worsen Alzheimer’s,” he shared.
Knecht added that studies have shown that up to 45 percent of Alzheimer’s cases are avoidable by embracing a healthy lifestyle.
“This is incredibly groundbreaking to have a health plan to advance access to a holistic lifestyle program for cognitive health. And we’re also using our clinics and our neighborhood care centers to bring this program to life,” he said. “We’re hopeful that the information and data will demonstrate efficacy to a point where we’ll just cover this more broadly.”
Another aspect of Emblem Health’s pilot program entails exercise, Tai chi, mindfulness and meditation–activities offered at their 15 neighborhood care centers, many of them in underserved communities, according to Knecht.
BRUNO DIDIER: ‘It was a very interesting challenge for the chefs to come up with the recipes that would adhere to the diet.’ Courtesy of CookUnity Business
Because food is highly personal and has an important cultural aspect to it, the company wanted to “make sure we were bringing culturally relevant, delicious food that certainly aligns with the guidelines Dr. Ornish has set out and top quality,” Knecht said. “That’s where CookUnity fits in.”
According to Bruno Didier, head of CookUnity Business, the pilot program— which is geared for up to 150 patients—is set to commence on Oct. 22.
He says it will be a plant-based diet, which will consist of three daily meals, absent of sugar, salt, oil, dairy and meat.
“It was a very interesting challenge for the chefs to come up with recipes that would adhere to the diet,” Didier added.
Memory care ‘neighborhood’
A 20-bed memory care “neighborhood,” The Grove is the newest part of Jefferson’s Ferry’s life plan community.
Set up in a circular pattern, The Grove is a ground floor unit where residents live in a more homelike setting, with access to a courtyard and an open kitchen. Group programming includes music and art, cooking classes, pet therapy, aromatherapy and virtual reality.
ANTHONY COMERFORD: ‘An enclosed garden [at Jefferson’s Ferry] provides an additional safe space for enjoying outdoor activities, such as gardening, or for just enjoying fresh air and sunshine.’ Courtesy of Jefferson’s Ferry
“Grove activities are specifically tailored to the interests and abilities of the residents, including smaller, more intimate activities that encourage greater opportunities for meaningful and engaged participation.” said Anthony Comerford, vice president of health services/administrator for the South Setauket facility.
To ensure the safety of residents, The Grove is a standalone unit where all activities are conducted within the neighborhood, according to Comerford.
“An enclosed garden provides an additional safe space for enjoying outdoor activities. such as gardening, or for just enjoying fresh air and sunshine,” Comerford said. “The residents love spending time outdoors.”
Secure unit and community programs
Parker Jewish Institute for Health Care and Rehabilitation in New Hyde Park has a secured, high acuity 42-bed memory care unit for those who have been diagnosed with Alzheimer’s or dementia.
“The programming is tailored to people with dementia, and we’re able to successfully maintain people when, unfortunately, they’ve had a diagnosis of dementia,” said Michael Rosenblut, Parker Jewish president and CEO.
Rosenblut adds that for the most part, residents “may have Alzheimer’s or dementia and another related illness.”
The patients, who are medically managed by physicians, nurses, social workers and nurse’s aides, receive specialized programming through Parker’s recreational department.
MICHAEL ROSENBLUT: ‘The programming is tailored to people with dementia, and we’re able to successfully maintain people when, unfortunately, they’ve had a diagno-sis of dementia.’ Courtesy of Parker Jewish Institute
Parker Jewish also operates the “Willing Hearts Helpful Hands” community-based program where people caring for their loved ones at home can get relief outside of their homes at memory cafes with live entertainment in Queens, Nassau and Suffolk counties. Since its inception in 2016, the program has engaged with almost 11,000 caregivers and their care recipients throughout Long Island.
“We have one patient from years ago who participated in that program, I’ll always remember the wife said to us, she hadn’t been out with her husband—the last family wedding was 20 years earlier—even though he has dementia, she hadn’t been dancing with him in 20 years, and now she was dancing with him,” Rosenblut said.
In July, Parker Jewish introduced another community-based program—GUIDE (Guiding an Improved Dementia Experience), which offers caregiver support, education and respite, medication management, and home visits and assessments.
Some dolphins found stranded on beaches may have ended up their because they suffer from a form of Alzheimer’s disease linked to toxins in the water.
This is the conclusion of a study led by researchers from Florida’s Hubbs-SeaWorld Research Institute, who suspect that—just like some adult humans with dementia are occasionally found wandering far from their homes—dolphins may become similarly disoriented when suffering from Alzheimer’s.
Their findings, published in the journal Communications Biology, point to chronic exposure to toxins produced by microorgansims known as cynobacteria—which are frequently found in freshwater, estuarine and marine waters—as a possible trigger.
The cyanobacterial toxin β-N-methylamino-L-alanine (BMAA), as well as its isomers 2,4-diaminobutyric acid (2,4-DAB), and N-2-aminoethylglycine (AEG), have been found to be extremely toxic to neurons.
BMAA triggers Alzheimer’s-like neuropathology and cognitive loss in experimental animals. These toxins can be biomagnified as they accumulate up the food chain in the marine ecosystem towards top predators like dolphins.
The resarcher’s study, which involved 20 common bottlenose dolphins stranded in the Indian River Lagoon in eastern Florida during the summer cyanobacterial bloom season, identfied markers of Alzheimer’s disease.
The duration of cyanobacterial blooms is increasing due to climate change and nutrient pollution from agricultural runoff and sewage discharges. Cyanobacterial-laden waters have often been released down the St. Lucie River from Lake Okeechobee into the Indian River Lagoon, intensifying exposure risks even in humans.
“Since dolphins are considered environmental sentinels for toxic exposures in marine environments, there are concerns about human health issues associated with cyanobacterial blooms,” said paper author and neuropathologist Dr. David Davis of the University of Miami said in a statement.
Studies of villagers on the island of Guam show that chronic dietary exposure to cyanobacterial toxins are associated with misfolded tau proteins and amyloid plaques characteristic of Alzheimer’s disease.
“Among Guam villagers, exposure to cyanobacterial toxins appeared to trigger neurological disease,” explained Dr. Paul Alan Cox, of the Brain Chemistry Labs in Jackson Hole, in a statement.
In 2024, Miami Dade County had the highest prevalence of Alzheimer’s disease in the United States.
“Although there are likely many paths to Alzheimer’s disease, cyanobacterial exposures increasingly appear to be a risk factor,” adds Dr. Davis.
Do you have a tip on a science story that Newsweek should be covering? Do you have a question about dolphins? Let us know via science@newsweek.com.
Reference
Noke Durden, W., Stolen, M. K., Garamszegi, S. P., Banack, S. A., Brzostowicki, D. J., Vontell, R. T., Brand, L. E., Cox, P. A., & Davis, D. A. (2025). Alzheimer’s disease signatures in the brain transcriptome of Estuarine Dolphins. Communications Biology, 8(1), 1400. https://doi.org/10.1038/s42003-025-08796-0
The Alzheimer’s Foundation of America (AFA) will host a community event on Saturday, Sept. 27, at its new, 11,500-square-foot Barbara Rabinowitz Education & Resource Center in Amityville to mark Grandparents Appreciation Month and raise funds for local dementia support programs.
The “Family Fun Day” will feature activities, resources and a special appearance by former New York Giants player and two-time Super Bowl champion Leonard Marshall. A $25 donation includes an autograph and photo with Marshall, with proceeds benefiting the center’s services for Long Islanders affected by dementia.
“We are thrilled to open our doors to the community and invite families to come together for a day of fun, connection and discovery,” Charles Fuschillo, Jr., AFA’s president and CEO, said in a news release about the event.
The event “is more than just a celebration – it is our way of saying: this center belongs to you,” he added. “This intergenerational event is a celebration of family and community. We encourage everyone to attend, have fun, learn about the importance of brain health, and take a tour of the facility.”
About one in eight Long Island older adults have Alzheimer’s disease, according to published reports. The AFA aims to provide support, services and education to individuals, families and caregivers affected by Alzheimer’s disease and related dementias nationwide and to fund research for better treatment and a cure.
At the Sept. 27 event, attendees can learn about the center’s programs and services. Intergenerational activities will include creative arts, brain games and additional games for children, face painting, food, music, balloon artists and more.
The event will feature raffle prizes, including an autographed Giants football helmet signed by Marshall.
Diagnosed in 2013 with chronic traumatic encephalopathy, a progressive brain disease linked to repeated head trauma, Marshall has since become an advocate for brain health. He has pledged his brain to the Concussion Legacy Foundation and founded two organizations – Brain Unity Trust and the Game Plan Foundation – to support research and raise awareness of neurological trauma in athletes.
Chef-prepared, plant-forward meals are tailored for early-stage Alzheimer’s patients
Meals are based on the “Ornish lifestyle” to promote brain health and slow disease progression
Program includes 14 culturally relevant, vegetarian meals, expanding to 28 soon
EmblemHealth, a health insurer with locations on Long Island, is partnering with physician-researcher Dr. Dean Ornish and chef-led meal service CookUnity to provide medically tailored meals as part of a new Alzheimer’s program, according to a news release about the initiative.
Based in Williamsburg, Brooklyn, CookUnity, which serves Long Island, said it is providing medically tailored meals for participants in the program for those with early-stage Alzheimer’s disease. Backed by emerging research, the meals are delivered to participants’ homes and are designed to slow the onset and progression of the disease.
“Lifestyle and diet play a critical role in how we live and how we age,” Dr. Dan Knecht, chief medical officer at EmblemHealth, said in the news release.
“Yet access to healthy, affordable, and delicious meals remains a major challenge for many,” Knecht said. “That’s why our collaboration with CookUnity is so unique and exciting. Their local chefs are helping us bring high-quality, plant-forward meals to participants in our Alzheimer’s program, making it easier to support health through food.”
The program – it’s in a pilot phase, currently – comes at a time when Alzheimer’s affects more than 426,000 New Yorkers, according to the New York State Office for the Aging. More than 7 million are living with Alzheimer’s across the United States, according to Alzheimer’s Association. And, experts say, there are limited treatment options.
“For this program to succeed, the food must be both culturally relevant and delicious,” Knecht said. “This program isn’t just about science; it’s about dignity and joy. Meals that reflect our members’ heritage and taste preferences aren’t just nourishing, but they’re healing.”
Participants can choose from over a dozen chef-prepared, ready-to-eat meals from CookUnity, developed to meet the specific nutritional needs of those with Alzheimer’s while maintaining restaurant-quality flavor.
“Our chefs view this program as a testament to their ever-evolving expertise and to the belief that food is medicine,” Bruno Didier, head of CookUnity Business, said in the news release.
“It’s often said that we are what we eat, and we believe the right recipes can empower better health,” Didier added. “This collaboration reflects our mission to deliver nourishing, chef-crafted meals – and deepens our commitment to scaling medically tailored solutions.”
CookUnity’s veteran chefs – Emily Peck, Einat Admony, Ivy Stark and Lena Elkousy – worked with EmblemHealth’s clinical team and CookUnity’s in-house nutritionist to create a nourishing and flavorful custom menu based on the principles of the “Ornish lifestyle,” according to the news release.
“When my team first learned about this meal program, we couldn’t contain our enthusiasm,” Admony said in the news release.
“This initiative not only offers us a platform to showcase our culinary skills, but it also encourages us to think creatively through the lens of health by eliminating excess salt and unhealthy fats while using more nutritious alternatives,” Admony said. “It’s an exciting challenge that allows us to redefine our dishes while promoting better health.”
The program currently offers 14 vegetarian meals, with plans to double to 28 soon. Each meal is designed to meet strict clinical nutritional guidelines and features diverse global flavors – from Middle Eastern Moroccan vegetable stew to Italian mushroom Stroganoff – designed to satisfy varied palates and encourage long-term adherence.
Participants in the program are screened by EmblemHealth’s provider group, Advantage Care Physicians, to implement a comprehensive lifestyle medicine program aimed at enhancing brain health and providing crucial support for caregivers, according to EmblemHealth.
Cissy Houston, the mother of the late Whitney Houston and a two-time Grammy winner who performed alongside superstar musicians like Elvis Presley and Aretha Franklin, has died, CBS News confirmed. She was 91.
Houston died Monday morning in her New Jersey home while under hospice care for Alzheimer’s disease, her daughter-in-law Pat Houston said in a statement. The acclaimed gospel singer was surrounded by her family.
This is a breaking news story. Check back for updates.
The Food and Drug Administration approved Eli Lilly’s Kisunla on Tuesday for mild or early cases of dementia caused by Alzheimer’s. It’s only the second drug that’s been convincingly shown to delay cognitive decline in patients, following last year’s approval of a similar drug from Japanese drugmaker Eisai.
The delay seen with both drugs amounts to a matter of months — about seven months, in the case of Lilly’s drug. Patients and their families will have to weigh that benefit against the downsides, including regular IV infusions and potentially dangerous side effects like brain swelling.
Physicians who treat Alzheimer’s say the approval is an important step after decades of failed experimental treatments.
“I’m thrilled to have different options to help my patients,” said Dr. Suzanne Schindler, a neurologist at Washington University in St. Louis. “It’s been difficult as a dementia specialist — I diagnose my patients with Alzheimer’s and then every year I see them get worse and they progress until they die.”
Both Kisunla and the Japanese drug, Leqembi, are laboratory-made antibodies, administered by IV, that target one contributor to Alzheimer’s — sticky amyloid plaque buildup in the brain. Questions remain about which patients should get the drugs and how long they might benefit.
The new drug’s approval was expected after an outside panel of FDA advisors unanimously voted in favor of its benefits at a public meeting last month. That endorsement came despite several questions from FDA reviewers about how Lilly studied the drug, including allowing patients to discontinue treatment after their plaque reached very low levels.
Costs will vary by patient, based on how long they take the drug, Lilly said. The company also said a year’s worth of therapy would cost $32,000 — higher than the $26,500 price of a year’s worth of Leqembi.
The FDA’s prescribing information tells doctors they can consider stopping the drug after confirming via brain scans that patients have minimal plaque.
More than 6 million Americans have Alzheimer’s. Only those with early or mild disease will be eligible for the new drug, and an even smaller subset are likely to undergo the multi-step process needed to get a prescription.
The FDA approved Kisunla, known chemically as donanemab, based on results from an 18-month study in which patients given getting the treatment declined about 22% more slowly in terms of memory and cognitive ability than those who received a dummy infusion.
The main safety issue was brain swelling and bleeding, a problem common to all plaque-targeting drugs. The rates reported in Lilly’s study — including 20% of patients with microbleeds — were slightly higher than those reported with competitor Leqembi. However, the two drugs were tested in slightly different types of patients, which experts say makes it difficult to compare the drugs’ safety.
Kisunla is infused once a month compared to Leqembi’s twice-a-month regimen, which could make things easier for caregivers who bring their loved ones to a hospital or clinic for treatment.
“Certainly getting an infusion once a month is more appealing than getting it every two weeks,” Schindler said.
Lilly’s drug has another potential advantage: Patients can stop taking it if they respond well.
In the company’s study, patients were taken off Kisunla once their brain plaque reached nearly undetectable levels. Almost half of patients reached that point within a year. Discontinuing the drug could reduce the costs and safety risks of long-term use. It’s not yet clear how soon patients might need to resume infusions.
Logistical hurdles, spotty insurance coverage and financial concerns have all slowed the rollout of competitor Leqembi, which Eisai co-markets with U.S. partner Biogen. Many smaller hospitals and health systems aren’t yet setup to prescribe the new plaque-targeting Alzheimer’s drugs.
First, doctors need to confirm that patients with dementia have the brain plaque targeted by the new drugs. Then they need to find a drug infusion center where patients can receive therapy. Meanwhile, nurses and other staff must be trained to perform repeated scans to check for brain swelling or bleeding.
“Those are all things a physician has to have set up,” said Dr. Mark Mintun, who heads Lilly’s neuroscience division. “Until they get used to them, a patient who comes into their office will not be offered this therapy.”
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The Associated Press Health and Science Department receives support from the Howard Hughes Medical Institute’s Science and Educational Media Group. The AP is solely responsible for all content.
WASHINGTON — For the first time, researchers have identified a genetic form of late-in-life Alzheimer’s disease — in people who inherit two copies of a worrisome gene.
Scientists have long known a gene called APOE4 is one of many things that can increase people’s risk for Alzheimer’s, including simply getting older. The vast majority of Alzheimer’s cases occur after age 65. But research published Monday suggests that for people who carry not one but two copies of the gene, it’s more than a risk factor, it’s an underlying cause of the mind-robbing disease.
The findings mark a distinction with “profound implications,” said Dr. Juan Fortea, who led the study the Sant Pau Research Institute in Barcelona, Spain.
Among them: Symptoms can begin seven to 10 years sooner than in other older adults who develop Alzheimer’s.
An estimated 15% of Alzheimer’s patients carry two copies of APOE4, meaning those cases “can be tracked back to a cause and the cause is in the genes,” Fortea said. Until now, genetic forms of Alzheimer’s were thought to be only types that strike at much younger ages and account for less than 1% of all cases.
Scientists say the research makes it critical to develop treatments that target the APOE4 gene. Some doctors won’t offer the only drug that has been shown to modestly slow the disease, Leqembi, to people with the gene pair because they’re especially prone to a dangerous side effect, said Dr. Reisa Sperling, a study coauthor at Harvard-affiliated Brigham and Women’s Hospital in Boston.
Sperling hunts ways to prevent or at least delay Alzheimer’s and “this data for me says wow, what an important group to be able to go after before they become symptomatic.”
But the news doesn’t mean people should race for a gene test. “It’s important not to scare everyone who has a family history” of Alzheimer’s because this gene duo isn’t behind most cases, she told The Associated Press.
More than 6 million Americans, and millions more worldwide, have Alzheimer’s. A handful of genes are known to cause rare “early-onset” forms, mutations passed through families that trigger symptoms unusually young, by age 50. Some cases also are linked to Down syndrome.
But Alzheimer’s most commonly strikes after 65, especially in the late 70s to 80s, and the APOE gene – which also affects how the body handles fats — was long known to play some role. There are three main varieties. Most people carry the APOE3 variant that appears to neither increase nor decrease Alzheimer’s risk. Some carry APOE2, which provides some protection against Alzheimer’s.
APOE4 has long been labeled the biggest genetic risk factor for late-in-life Alzheimer’s, with two copies risker than one. About 2% of the global population is estimated to have inherited a copy from each parent.
To better understand the gene’s role, Fortea’s team used data from 3,297 brains donated for research and from over 10,000 people in U.S. and European Alzheimer’s studies. They examined symptoms and early hallmarks of Alzheimer’s such as sticky amyloid in the brain.
People with two APOE4 copies were accumulating more amyloid at age 55 than those with just one copy or the “neutral” APOE3 gene variety, they reported in the journal Nature Medicine. By age 65, brain scans showed significant plaque buildup in nearly three-quarters of those double carriers – who also were more likely to have initial Alzheimer’s symptoms around that age rather than in the 70s or 80s.
Fortea said the disease’s underlying biology was remarkably similar to young inherited types.
It appears more like “a familial form of Alzheimer’s,” said Dr. Eliezer Masliah of the National Institute on Aging. “It is not just a risk factor.”
Importantly, not everyone with two APOE4 genes develops Alzheimer’s symptoms and researchers need to learn why, Sperling cautioned.
“It’s not quite destiny,” she said.
The drug Leqembi works by clearing away some sticky amyloid but Sperling said it’s not clear if carriers of two APOE4 genes benefit because they have such a high risk of a side effect from the drug – dangerous brain swelling and bleeding. One research question is whether they’d do better starting such drugs sooner than other people.
Masliah said other research aims to develop gene therapy or drugs to specifically target APOE4. He said it’s also crucial to understand APOE4’s effects in diverse populations since it’s been studied mostly in white people of European ancestry.
As for gene tests, for now they’re typically used only to evaluate if someone’s a candidate for Leqembi or for people enrolling in Alzheimer’s research – especially studies of possible ways to prevent the disease. Sperling said the people most likely to carry two APOE4 genes had parents who both got Alzheimer’s relatively early, in their 60s rather than 80s.
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The Associated Press Health and Science Department receives support from the Howard Hughes Medical Institute’s Science and Educational Media Group. The AP is solely responsible for all content.
