Groundbreaking Study Finds That Grandparents Who Help With Their Grandkids May Get Protected From Cognitive Decline

 Friends who have grandkids(2, 4, 8; all boys) are being run into the ground, with no time to see how their cognition is going.

Groundbreaking Study Finds That Grandparents Who Help With Their Grandkids May Get Protected From Cognitive Decline

A recent study has unveiled an uplifting connection between grandparents and their cognitive well-being, highlighting the enriching experience of caring for grandchildren. Engaging with younger generations not only nurtures family bonds but also appears to play a vital role in maintaining brain health as we age.

Lead researcher Flavia Chereches, a doctoral candidate at Tilburg University in the Netherlands, expressed the intrigue surrounding this vital question: “Many grandparents provide regular care for their grandchildren—care that supports families, and society more broadly—but an open question is whether caregiving for grandchildren may also benefit grandparents themselves.” This research aimed to explore the potential health advantages for grandparents who dedicate time to their grandchildren, particularly in slowing cognitive decline.

Chereches and her team analyzed data from 2,887 grandparents in England, all over the age of 50, with an average age of 67. Participants answered survey questions and underwent cognitive assessments three times from 2016 to 2022. The survey inquired about the frequency of their caregiving—whether they were spending nights with grandchildren, caring for them during illness, engaging in play, assisting with homework, or even preparing meals.

The results were heartening! Grandparents who actively participated in childcare, regardless of how often or in what capacity, performed better in memory and verbal fluency tests compared to those who did not engage in caregiving. This trend remained significant even after adjusting for age and health variables. Excitingly, grandmothers who provided care displayed a slower decline in cognitive performance throughout the study.

“What stood out most to us was that being a caregiving grandparent seemed to matter more for cognitive functioning than how often grandparents provided care or what exactly they did with their grandchildren,” Chereches noted. This suggests that the sheer joy and experience of being involved in caregiving may be more beneficial than the specifics of the activities undertaken.

In the UK, approximately five million grandparents regularly embrace childcare duties, with nearly 90% babysitting at least once a week, as reported by Age UK. A remarkable one in ten grandparents cares for their grandchildren daily, often stepping in to help their own children navigate the demands of family life.

Age UK has highlighted the immense benefits of this so-called “gran-nannying,” which keeps older adults mentally and physically active while combating loneliness—as long as the caregiving experience remains enjoyable and fulfilling.

In a delightful example, a CBS news host shared a heartwarming moment with his mother, who often assists with his children. When asked about the study’s findings, she replied with joy, “They energize me, more than drive me down.”

This research illuminates the beautiful cycle of care and connection that exists within families, proving that the act of being a grandparent not only enriches the lives of grandchildren but also enhances the lives of grandparents, fostering happiness and vitality in their golden years. Let’s share this wonderful news, encouraging families to embrace the joys of grandparenting!

AI Analyzes Sleep Data to Predict Cognitive Decline and Health

 How soon will your competent? doctor get this in to verify you have the correct sleep protocol? Oh, no plans, so NEVER! That IS PURE INCOMPETENCE!     

AI Analyzes Sleep Data to Predict Cognitive Decline and Health

Summary: Researchers developed an artificial intelligence model capable of extracting hidden physiological signals from routine polysomnography data to predict long-term health risks.

Analyzing data from Cleveland Clinic’s STARLIT registry alongside a nationwide cohort, the AI model identified five distinct patient risk subtypes with vastly different health trajectories. Patients categorized into the highest-risk group faced double the five-year mortality risk compared to the lowest-risk group, a prognostic distinction invisible to conventional sleep apnea diagnostic measures.

Key Facts

• Two-Fold Mortality Risk Separation: The AI model stratified patients into five distinct risk categories, showing that individuals in the highest-risk tier had a 100 percent increase in five-year mortality risk compared to those in the lowest-risk tier.
• Superiority Over Conventional AHI: The prognostic risk stratification succeeded where the traditional Apnea-Hypopnea Index (AHI) failed, capturing latent physiological features across brain, lung, muscle, and cardiac signals that standard metrics miss.
• Sex-Balanced Predictive Accuracy: While the traditional AHI metric historically performs better in male populations, the new AI foundation model predicted cardiovascular, neurological, and mortality outcomes with equal high accuracy across both men and women.
• Unlocking Underutilized Clinical Data: Demonstrates that routine polysomnograms, 1 to 4 million of which are conducted annually in the United States, contain vast amounts of unused prognostic data capable of driving early preventative healthcare.

Source: Cleveland Clinic

A novel AI model can use information collected during routine sleep studies to identify patients’ long-term health risks, according to a new study published in Nature Communications. Developed by a multidisciplinary research team, the model uncovered hidden sleep patterns linked to risks including heart disease, cognitive decline and death.

The findings also suggest that routine medical tests may contain substantially more physiologic information than current clinical practice extracts from them. In this case, AI identified meaningful signals in standard overnight sleep study data that are not captured by conventional summary measures alone.

An AI model can analyze routine polysomnography signals to identify patient sub-groups with double the five-year mortality risk. Credit: Neuroscience News

The research revealed clinically meaningful patient subtypes with sharply different long-term health risks. Patients in the highest-risk group had twice the mortality risk over the next five years compared to those in the lowest-risk group, a distinction that was not captured by the standard clinical measure used to assess sleep apnea severity, the apnea-hypopnea index.

Each year, an estimated 1 to 4 million polysomnograms, or in-lab sleep studies, are performed in the United States, typically to evaluate sleep apnea. While these studies collect rich data on each patient’s brains, lungs, muscles and heart, clinicians historically have focused on a small subset of that information to grade sleep apnea severity.

“For decades we have distilled an overnight sleep study into a handful of summary measures,” said Reena Mehra, M.D., professor of medicine at the University of Washington and the study’s senior clinical author. “AI gives us the opportunity to move beyond those summaries and learn from the full richness of sleep physiology.”

The model was developed by a collaborative team of sleep physicians, AI researchers, data scientists and neuroscientists brought together through the Discovery Accelerator, a 10-year joint research partnership between Cleveland Clinic and IBM aimed at advancing the pace of discovery in life sciences through AI and quantum computing.

Using data from the Cleveland Clinic Sleep Signals, Testing, and Reports Linked to Patient Traits (STARLIT) registry, the researchers grouped patients into five risk categories. The model also predicted outcomes well for men and women, while the apnea hypopnea index has historically performed better in men. The findings were independently confirmed in a nationwide patient cohort.

“Modern AI lets us recover much more of the information contained in a night’s worth of sleep physiology, revealing clinically meaningful patient groups with very different long-term health risks,” said Jeffrey Rogers, Ph.D., the corresponding author and professor adjunct, neurosurgery, Yale School of Medicine.

“These findings demonstrate that routine medical tests can contain substantially more physiologic information than current clinical practice extracts from them.”

The model could also help researchers better understand how sleep impacts health outcomes. By looking beyond traditional measures, the approach uses AI to detect latent physiologic features invisible to the human eye and extract prognostic biomarkers that help stratify risk for cardiovascular and neurologic disease, and survival, opening the door to earlier and more personalized care.

“Sleep is foundational to health and wellness,” said Matheus Lima Diniz Araujo, Ph.D., a sleep researcher at Cleveland Clinic.

“Nearly 70 million Americans live with chronic disorders of sleep and wakefulness, affecting daily functioning and overall health. This discovery offers a more personalized approach to sleep medicine, by potentially expanding the value of routine sleep testing and reinforcing the key role sleep plays in chronic disease.” 

Carl Saab, Ph.D., a professor of biomedical engineering and Chief Scientist of Cleveland Clinic’s Discovery Accelerator, said, “The next step is to validate these findings in diverse populations and expand collaborations among medical and technical experts, industry partners and professional society stakeholders.”

“Sleep is increasingly recognized as a critical component of health, yet the physiological information captured during sleep remains largely underused,” said Erhan Bilal, Ph.D., lead author of the study.

“Because everyone sleeps, sleep studies offer a remarkable window into human health that extends far beyond the diagnosis of sleep disorders. Our work shows how foundation models can begin to unlock the richness of these complex signals. And this is only the beginning.”

The research team included Erhan Bilal, Ph.D.; Matheus Lima Diniz Araujo, Ph.D.; Kristen Beck, Ph.D.; Catherine Heinzinger, D.O.; Samer Ghosn, B.S.; Nancy Foldvary-Schaefer, D.O.; Carl Saab, Ph.D.; Jeffrey Rogers, Ph.D.; and Reena Mehra, M.D.

Key Questions Answered:

Q: Why is the traditional Apnea-Hypopnea Index (AHI) insufficient for predicting long-term health risks?

A: AHI compresses an entire night of complex physiological recordings into a single summary number measuring breathing pauses per hour. This oversimplification discards detailed continuous data regarding heart rate variability, brainwave architecture, muscle tone, and subtle oxygen desaturation patterns that directly reflect cardiovascular, neurological, and metabolic strain.

Q: How does this new AI model improve diagnostic equity between men and women?

A: Clinical sleep studies have historically exhibited sex bias because the AHI metric correlates better with male presentation of sleep apnea. By analyzing full-spectrum physiological signals rather than relying solely on upper-airway obstruction counts, the AI model achieves equal predictive power for cardiovascular disease, cognitive decline, and mortality across both female and male patients.

Q: What are the next steps before this AI tool can be used in routine clinical practice?

A: The research team plans to validate the model across diverse international populations, expand technical and industrial collaborations, and integrate the algorithm into existing sleep lab software to provide automated risk stratification reports alongside standard clinical metrics.

Editorial Notes:

• This article was edited by a Neuroscience News editor.
• Journal paper reviewed in full.
• Additional context added by our staff.

About this AI and sleep research news

Author: Alicia Reale
Source: Cleveland Clinic
Contact: Alicia Reale – Cleveland Clinic
Image: The image is credited to Neuroscience News

Original Research: Open access.
“A foundation model for sleep-based risk stratification and clinical outcomes” by Erhan Bilal, Matheus Lima Diniz Araujo, Kristen L. Beck, Catherine M. Heinzinger, Samer Ghosn, Carl Y. Saab, Nancy Foldvary-Schaefer, Jeffrey L. Rogers & Reena Mehra. Nature Communications
DOI:10.1038/s41467-026-75326-9

First Evidence That Targeting Tau May Slow Cognitive Decline

 Are your competent? doctor and hospital closely following this? NO? So, incompetent in not caring about preventing dementia from your stroke!

First Evidence That Targeting Tau May Slow Cognitive Decline

LONDON — The investigational tau-targeting therapy diranersen (BIIB080) reduced tau pathology and showed evidence of slowing cognitive decline in people with early Alzheimer's disease (AD) in the phase 2 CELIA trial. 

Although the study did not meet its primary endpoint, it demonstrated robust biomarker effects across all doses, with the strongest clinical benefit observed at the lowest dose evaluated.

The new results follow a phase 1b study that showed the drug had a robust impact on tau biomarkers.

“This is the first randomized phase 2 trial of a tau-targeting agent to show that a reduction in tau pathology, which has been clearly and consistently shown across both trials, may slow early Alzheimer's progression,” said study investigator Catherine Mummery, PhD, professor of clinical neurology at the University College London (UCL) Queen Square Institute of Neurology.

Key Points

• Diranersen (BIIB080) ↓ tau pathology in early AD; phase 2 CELIA.
• Primary endpoint missed; no significant dose-response on CDR-SB (P=.21).
• 60-mg dose showed best clinical signal: CDR-SB ↓26%, ADAS-Cog13 ↓42%, MMSE ↓50%.
• CSF total tau ↓50%-65%; tau PET signal also ↓ across all doses.
• Generally well tolerated; AEs mainly lumbar puncture-related, mild-moderate.

What tau reduction threshold predicts cognitive benefit in early AD?

How does intrathecal tau ASO compare with anti-amyloid therapy?

Which biomarkers best monitor response to tau-lowering therapy?

The findings were presented July 14 at the Alzheimer's Association International Conference (AAIC) 2026.

‘Clear Target Engagement’

AD is a progressive neurodegenerative disorder characterized by the accumulation of amyloid plaques and pathological tau, the latter of which is more closely associated with disease progression and clinical symptoms, Mummery said. 

Although anti-amyloid therapies are available, no tau-targeting therapies have been approved for AD.

Diranersen is an investigational intrathecally administered antisense oligonucleotide (ASO) designed to reduce production of tau protein by targeting microtubule-associated protein tau (MAPT) messenger RNA, thereby lowering both intracellular and extracellular tau.

In a phase 1b study in patients with early AD, diranersen was well tolerated, produced robust reductions in tau biomarkers, and showed favorable trends on exploratory cognitive endpoints. 

"There was a dose-dependent reduction in levels of total tau," with levels falling to about 40% of baseline by week 48 in the 60-mg group and remaining at that level, Mummery said. "So there was a clear target engagement."

The double-blind phase 2 CELIA trial enrolled 416 adults aged 50-80 years with mild cognitive impairment due to AD or mild AD dementia and confirmed amyloid pathology. 

Participants were randomly assigned to intrathecal diranersen 60 mg every 24 weeks, 115 mg every 24 weeks, 115 mg every 12 weeks, or placebo for 76 weeks. Although the numbers were small, exploratory analyses showed positive trends on cognitive tests. 

Baseline characteristics were well balanced across treatment groups. The mean participant age was 68 years, which Mummery noted is slightly younger than that of a typical AD population. 

Primary Endpoint Not Met

Approximately 60% of participants had mild cognitive impairment (MCI) due to AD, while 40% had mild AD dementia. Participants underwent quarterly cerebrospinal fluid (CSF) sampling throughout the placebo-controlled phase of the trial. 

At its conclusion, all participants were invited to enroll in a 2-year long-term extension (LTE) study.

Overall, study retention was high. More than 80% of participants completed the placebo-controlled phase, and 94% enrolled in the long-term extension study, suggesting people “weren't put off by having quarterly intrathecal administration of the drug," Mummery said. 

The primary endpoint was dose response for change from baseline to week 76 in the Clinical Dementia Rating — Sum of Boxes (CDR-SB), a global measure of cognition and daily function. 

Although the 60-mg dose slowed decline on the CDR-SB by 26% compared with placebo, the trial did not meet its primary endpoint of demonstrating a dose-response relationship across treatment groups (P = .21).

Analyses of the CDR-SB subdomains also showed consistent improvements in both cognitive and functional domains with the 60-mg dose, Mummery said.

Although the trial missed its primary endpoint, secondary cognitive outcomes consistently favored diranersen. On the 13-item Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-Cog13), all three dose groups showed less decline than placebo, with the greatest effect seen in the 60-mg group (42% slower decline; P = .01). A similar pattern was observed on the Mini-Mental State Examination (MMSE), where the 60-mg dose slowed decline by 50% vs placebo (P = .01).

In contrast, the Alzheimer's Disease Cooperative Study-Activities of Daily Living Inventory for Mild Cognitive Impairment (ADCS-ADL-MCI) showed no significant difference between the 60-mg dose and placebo, suggesting that the functional findings warrant further study, Mummery said. 

‘Unprecedented’ Tau Reduction

Biomarker analyses showed robust target engagement. Cerebrospinal fluid (CSF) total tau levels remained stable in the placebo group but fell by 50% to 65% from baseline across all three diranersen dose groups. Most of the reduction occurred during the first 12 months and was sustained through the remainder of the study, Mummery reported.

Tau PET standardized uptake value ratio (SUVR) analyses showed the expected increase in whole-brain gray matter tau burden in the placebo group over time. In contrast, all three diranersen dose groups showed reductions in tau PET signal, which Mummery described as "unprecedented."

Referring to a brain scan from a participant receiving the 60-mg dose, Mummery highlighted the drug's effect on tau pathology. "In brain areas with particularly high levels of tau, like the lateral temporal and inferior parietal, you see quite a marked reduction," she said.

The drug was generally well tolerated. Most adverse events were mild to moderate in severity and did not result in treatment discontinuation or study withdrawal.

The most common adverse events were procedural pain, post-lumbar puncture syndrome (including headache and low back pain), and confusional state. Mummery noted that post-lumbar puncture syndrome is "incredibly common" in trials involving intrathecal administration. 

In 2025, the FDA granted Fast Track designation to diranersen for the treatment of AD. 

During the discussion, a conference delegate asked about the episodes of confusion reported in the trial. Mummery said investigators "are actively collecting data to try and understand more about it." She emphasized that most cases were mild or moderate, resolved within a week, and rarely led to treatment discontinuation. 

Asked whether a threshold of tau reduction is needed before a clinical benefit emerges, Mummery said important questions remain. "The fact that we're starting to see changes on tau-PET is really exciting, but we're going to learn a huge amount more about what the threshold is and how long it takes for that to mean something," she said.

Encouraging Findings, Important Caveats

The most interesting and noteworthy aspect of the study is that it demonstrates diranersen's ability to effectively reduce tau production, Jessica Langbaum, PhD, senior director of Alzheimer's prevention and research at Banner Alzheimer's Institute, told Medscape Medical News. 

Langbaum said the findings could open the door to therapies for other tauopathies, particularly if future technologies enable tau-targeting drugs to cross the blood-brain barrier and be administered subcutaneously. 

These findings provide the first evidence from a randomized trial that a tau-targeting therapy can produce both robust biomarker effects and a signal of clinical benefit, Laura Nisenbaum, PhD, interim chief science officer at the Alzheimer's Drug Discovery Foundation, said in a press release.

“Tau is one of the two defining pathologies of Alzheimer’s disease and has long been difficult to target, which makes these results all the more notable.”

However, Nisenbaum said the discordance between the biomarker and clinical findings raises important questions about the optimal degree of tau reduction and the dose of diranersen that should be evaluated in future studies. "Those questions will be central to designing the strongest possible phase 3 program."

Mummery has served as a consultant to Alector, Aerska, Biogen, Eisai, Ionis, Lilly, MSD, Neuroimmune, Novartis, Prevail, Roche/Genentech, Switch, Voyager, and Wave. She has received honoraria for teaching and educational activities from Biogen, Eisai, and Lilly, and an academic research funding award from Biogen. She is supported by the NIHR University College London Hospitals Biomedical Research Centre.

Neurologists warn this everyday noise could be aging your brain

 You don't want to live in any large city of Madagascar then, honking is the polite way to notify pedestrians in the street that your car is coming thru. Sidewalks are taken up by street vendors, so the only place to walk is in the street.

Neurologists warn this everyday noise could be aging your brain

Those traffic honks might be doing more than testing your patience.

Key Points

• Chronic exposure to environmental noise has been linked to increased risk of cognitive decline.
• A neurologist explains how traffic noise may age your brain.
• Wearing ear protection and spending time outside may help protect your brain.

Hearing loss is associated with changes in brain health, with even slight hearing loss increasing the risk of brain-volume loss and dementia. But it’s not just factory workers and rock concert lovers who may be at risk. While short bursts of intensely loud sound can damage hearing, long-term exposure to everyday noise, like traffic, may also affect hearing and expose the brain to chronic stress. 

“Whether it comes from busy roads, highways, airports or constant urban activity, chronic exposure to environmental noise has now been linked to accelerated brain aging and an increased risk of cognitive decline,” says David Perlmutter, M.D. 

Keep reading to learn how traffic noise may affect your brain, how to protect it, and strategies to support a healthy brain now and as you age. 

How Traffic Noise Could Be Aging Your Brain

It Increases Stress Levels

Living or working in a high-traffic area means your body may be exposed to a near-constant source of stress. “Persistent noise elevates stress hormones like cortisol, promotes inflammation and can contribute to the chronic activation of microglia,” says Perlmutter. While high-level noises, like an airplane taking off or a car horn honking, can trigger the stress response directly, even lower levels of noise can indirectly create stress in the body through annoyance or disruptions to communication, daily tasks or sleep.

Related video: Nearly half of dementia cases may be preventable, doctor explains (FOX 32 Chicago)Over time, increased stress can make it more difficult for the brain to enter into a restorative state, explains Perlmutter: “When these cells remain in a prolonged inflammatory state, they become less effective at protecting and repairing the brain, thereby increasing vulnerability to neurodegenerative diseases.”

It Can Cause Hearing Loss over Time

While excessively loud noises like jackhammers and explosions can cause significant damage to your hearing in a short amount of time, repeated exposure to moderately loud noises, including traffic, may also damage the microscopic hair cells in your inner ear. These cells help convert sound vibrations into signals your brain interprets as sound.

People regularly exposed to higher levels of road traffic noise have been found to have more hearing damage than those exposed to lower levels. And the effects of that hearing loss go beyond asking people to repeat themselves. Recent research links hearing loss from noise exposure to earlier dips in memory and thinking skills. This acceleration of brain aging is likely due, in part, to the increased strain on your brain as it works to make sense of the sound inputs around you. 

It Disrupts Your Sleep

Getting enough quality sleep is essential for brain health, and chronic sleep disruption is a known risk factor for dementia. If you live near high-traffic areas, you may not even notice the noise disrupting your sleep, but its impact can still result in brain aging, as it fragments deep restorative sleep. 

“This is especially concerning because deep sleep is when the brain clears metabolic waste through the glymphatic system (the waste clearance pathway in the brain), consolidates memories and resets immune function,” says Perlmutter.  

It’s not just the noise you hear at night that disrupts your sleep, either. Research suggests that for every 10-decibel increase in sound levels over a 24-hour period, poor sleep quality increases and sleep duration decreases. While one night of poor sleep won’t lead to brain aging, these sleep disruptions night after night add up. “Chronic sleep disruption has consistently been associated with poorer cognition and a higher risk for Alzheimer’s disease and other forms of dementia,” says Perlmutter. 

It’s Linked to Poor Cardiovascular Health

Aside from the direct impact traffic noise can have on your brain health, it indirectly affects your cardiovascular system, which supplies the brain with oxygen and nutrients and helps remove waste. “Long-term exposure to traffic noise has been linked to higher blood pressure, insulin resistance and vascular dysfunction,” says Perlmutter. These effects are most likely related to an increase in oxidative stress markers that influence blood vessel function and inflammation in the body. “Since the brain depends on healthy blood vessels and efficient energy metabolism, these downstream effects can further increase the risk of cognitive decline,” says Perlmutter. 

The World Health Organization recognizes 53 decibels over a 24-hour period as the upper limit to avoid health risks. However, recent research suggests that some cardiovascular and metabolic risks may begin to increase at even lower levels, around 45 decibels over 24 hours. To put this in perspective, regular traffic noise falls between 12.8 and 88.3 decibels, from rural country roads to high-traffic city streets.

Ways to Protect Your Brain Health from Noisy Traffic

Unless you’re able and willing to pack up and move to the middle of rural America, escaping traffic noise may not be possible. To help protect your ears and your brain from daily and nightly traffic noise, experts recommend these strategies. 

• Wear ear protection. While it may not be safe to wear noise-canceling headphones while walking near traffic or driving, you may want to consider them if you’re a passenger, working or living near loud traffic noises. 
• Turn on a noise machine.  While white noise machines are often used to help people fall and stay asleep, researchers have found that pink noise may be specifically beneficial for reducing the impact traffic noise has on the brain.
• Spend time in green spaces. If you live or work in a high-traffic area, getting out in nature as often as you can is a way to help offset some of the negative effects. “Even brief exposure to green spaces has been shown to reduce stress,” says Perlmutter. Research has found that even just 10 minutes in nature can improve mental health and potentially reduce stress biomarkers.

Other Strategies to Support Brain Health

“While we can’t eliminate every source of environmental noise, we can significantly strengthen the brain’s ability to withstand its effects,” says Perlmutter. Here are some proven strategies to support your brain’s health and help protect it against chronic stress. 

• Maintain social connections. Regular social connection is linked to improved memory, attention and language skills, while loneliness and isolation are risk factors for cognitive decline and dementia. Even small routine interactions with people you love or groups you feel connected with can help. 
• Eat a nutrient-rich diet. A diet rich in fruit, vegetables, whole grains, fatty fish, nuts, olive oil and fermented foods helps your brain counteract the negative effects of oxidative stressors, like noise and other pollutants.
• Engage in regular physical activity. Regular physical activity helps regulate glucose levels, improves oxygen and nutrient flow to your brain, supports the growth of new neurons and eases stress., In fact, research suggests that regular exercise may even reduce brain age.
• Prioritize restorative sleep. Deep, uninterrupted sleep is when your brain does its most important maintenance tasks, including clearing waste, consolidating memories and resetting its stress response systems. Simple, but effective interventions including blackout curtains, a cool room and a consistent bedtime can help make your sleep as restorative as possible. 

Our Expert Take

While traffic noise may appear to be just a daily annoyance, over time it can speed up how fast your brain ages. Traffic noise can damage hearing, elevate stress hormones, disrupt your sleep and strain your cardiovascular system, impairing nutrient and oxygen flow to your brain. While it may feel impossible to avoid noisy streets or subways if you live in an urban area, taking steps to protect your hearing and reduce your stress can help minimize its impact. Everyday habits, including quality sleep, eating a nutrient-rich diet, getting regular physical activity and maintaining meaningful social connections, can help protect your brain from traffic noise and other everyday stressors. 

Read the original article on EatingWell

Experimental Alzheimer's drug that fights a tough-to-target protein shows promise at slowing cognitive decline in a clinical trial

 Is your competent? doctor closely following this? NO? So COMPLETELY FUCKING INCOMPETENT THEN?

Experimental Alzheimer's drug that fights a tough-to-target protein shows promise at slowing cognitive decline in a clinical trial

An experimental drug might slow early Alzheimer’s disease by targeting a hallmark of the illness that researchers have historically had less success with: toxic tangles of tau proteins inside the brain.

Accumulations of these tau tangles and sticky clumps of the protein amyloid beta are the neurodegenerative disease’s defining features. In recent years, two drugs that clear amyloid plaques have been approved by the Food and Drug Administration—the first new Alzheimer’s therapies in about two decades. Meanwhile, many experimental treatments targeting tau have failed, despite research suggesting that tau tangles are a stronger predictor than amyloid of brain deterioration.

Now, findings from a mid-stage clinical trial presented on July 14 at the Alzheimer’s Association International Conference in London could change that. Researchers revealed that an experimental anti-tau drug slowed cognitive decline at a level on par with the approved anti-amyloid drugs—although puzzlingly, that result came about in the treatment group that received the lowest dose. The work offers hope for the treatment of a disease that affects more than seven million Americans ages 65 and older, though a larger follow-up study will need to confirm the therapy’s benefits.

“This is really quite promising if it were to hold up” in further testing, says Jessica Langbaum, senior director of Alzheimer’s prevention and research at the Banner Alzheimer’s Institute who wasn’t involved in the trial, to Lauran Neergaard at the Associated Press.

The drug, called diranersen, was developed by Biogen, a Massachusetts-based biotech company. It works by attaching itself to genetic instructions for making tau, forcing the brain to produce less of the protein.  

Related video: Study challenges link between super-aging and Alzheimer’s risk genes (KYTX-TV Tyler-Longview)The recent trial involved more than 400 patients with early-stage Alzheimer’s split into four groups. One received 60 milligrams of diranersen every six months via injection into the spinal cord, one received 115 milligrams every six months, one received 115 milligrams every three months and one group received a placebo. They were tracked for 18 months and given several cognitive tests.

In all three treatment groups, the drug lowered tau levels in brain and spinal fluid by 50 to 65 percent compared to the participants’ starting baseline. Brain imaging of 131 participants also showed decreases in tau tangles relative to baseline across all doses.

But the drug defied one of the researchers’ main expectations: that cognitive outcomes would strengthen with dose. In the trial, the lowest-dose group experienced the greatest slowing of cognitive decline—by 26 percent in one test—and the smallest decrease in tau levels. The middle-dose group’s cognitive decline slowed by 14 percent based on that test, and the highest-dose group’s slowed by 9 percent.

While many outside experts welcome the findings, they highlight the deviation from the expected dose-dependent response. And some participants who received higher doses suffered from a state of confusion for up to one week following injection. That’s why the findings represent “a double, not a home run,” says Adam Boxer, a neurologist at the University of California, San Francisco who is working on a different anti-tau therapy, to Jennie Erin Smith at Science.

Rob Howard, a psychiatrist at University College London who wasn’t involved in the study, explains to R.J. Mackenzie at Science News that the counterintuitive cognitive results could be due to the study’s small cohort or the drug’s small effect sizes.

The size of change in cognitive scores was “pretty tiny,” and it’s unclear how it would translate to patients in the real world, he adds. “It’s the age-old question: Are these clinically meaningful differences?”

What’s more, the side effect of confusion was unexpected, Boxer tells Science. It may have happened because the drug affected something it wasn’t supposed to, but a more troubling possibility is that it’s related to lowering tau, he says. “Maybe we can’t knock down tau without some effects.” Biogen, for its part, notes that the confused state was temporary.

“This was a well-tolerated trial where people wanted to continue on treatment,” neurologist Cath Mummery of University College London said as she presented the study at the conference, reports Andrew Joseph at STAT.

The company now plans to test diranersen in a late-phase clinical trial to see how it fares with a larger group of participants. And perhaps it could one day be tested in conjunction with amyloid-targeting drugs, Heather Snyder, a neuroscientist and senior vice president of medical and scientific relations at the Alzheimer’s Association, tells Science News. She notes that other trials are studying combinations of different anti-tau and anti-amyloid drugs.   

“We are seeing the entire movement of thinking about these different targets and how [we can] start putting tau together with amyloid,” Snyder says.

This article was originally published on Smithsonian Magazine. Read the full story here: Experimental Alzheimer's Drug That Fights a Tough-to-Target Protein Shows Promise at Slowing Cognitive Decline in a Clinical Trial © 2026 Smithsonian Institution.