A Common Smartphone Metric May Be Brain Health’s Next Frontier

 How will your competent? doctor use this to help your memory and glymphatic clearance  post stroke? Oh sorry, DOING NOTHING LIKE ALL RESEARCH IS TREATED?

A Common Smartphone Metric May Be Brain Health’s Next Frontier

Memory researcher Sara Mednick, PhD, had been chasing a mysterious signal for years when she came across a paper that changed everything.

Sara Mednick, PhD

As a cognitive scientist at the University of California, Irvine, Mednick had been studying how the brain creates memories during sleep. Her research kept pointing to the autonomic nervous system: In 2016, she reported that autonomic activity — as measured by heart rate variability (HRV), the variation in time between heartbeats — enhances brain plasticity during REM sleep, improving memory consolidation. Her 2019 study showed that autonomic and central nervous system activity together benefit memory.

“I kept saying, there’s this autonomic signal that’s really, really important, and I don’t know what it is,” Mednick said.

Things started to click when she found a 2022 study revealing a pattern in the brains of sleeping mice. Every 50 seconds, the locus coeruleus — a small nucleus in the pons of the brainstem — generated an infraslow oscillation of norepinephrine, the key neurotransmitter of the locus coeruleus. A drop in norepinephrine followed, creating spindles (bursts of brain wave activity). The rhythm determined effective memory consolidation.

Key Points

• Very low-frequency HRV may index locus coeruleus norepinephrine activity during sleep.
• HRV correlated with sleep spindle timing and memory consolidation in humans and mice.
• Non-REM norepinephrine oscillation frequency predicted glymphatic clearance in mice.
• Sleep disruption, aging, stress, depression, CV disease may impair glymphatic waste removal.
• Smartphone/smartwatch HRV could become a noninvasive biomarker for neurodegeneration risk.

How does locus coeruleus activity regulate sleep-dependent glymphatic flow?

Which HRV frequency bands best predict glymphatic clearance?

Can HRV distinguish normal aging from early neurodegeneration?

Mednick realized, “Oh, it’s the locus coeruleus. That’s what this signal that I’ve been measuring is.”

One of the study authors was Maiken Nedergaard, MD, DMSc, a neuroscientist at the University of Rochester Medicine in Rochester, New York, who in 2012 discovered the glymphatic system, the brain mechanism that clears away waste while we sleep. Nedergaard and her colleagues had put biosensors in the rodents’ prefrontal cortex, allowing them to measure norepinephrine. “If you couldn’t measure norepinephrine activity, it just looked like the locus coeruleus was kind of dead” during sleep, Mednick said. This study showed that it’s not.

Maiken Nedergaard, MD, DMSc

In 2025, the same researchers discovered a new insight: The frequency of norepinephrine oscillation during non-REM sleep predicted glymphatic clearance in mice. “You could see that the amount of waste clearance correlated to this infraslow rhythm,” said co-author Celia Kjaerby, PhD, an associate professor of neuroscience at the University of Copenhagen in Copenhagen, Denmark.

Since then, Kjaerby, Nedergaard, and Mednick have teamed up on new research — a reviewed preprint published in eLife in March — connecting HRV to glymphatic clearance. The finding suggests HRV could be used to measure how well the glymphatic system is working.

That would be a “massive breakthrough,” Mednick said. Such an accessible biomarker (standard on smartwatches and smartphones) could help identify patients at risk for neurodegenerative disease and give researchers a powerful tool to test treatments aimed at repairing a broken glymphatic system and slowing cognitive decline.

Making the Connection

Of course, none of this was on Mednick’s radar as she immersed herself in that paper in 2022. Determined to collaborate with the neuroscientists, she packed her bags for a 6-month sabbatical in Copenhagen. It was clear to her that they were all working on the same thing: “Me in my human models, and Celia Kjaerby and Maiken Nedergaard in their rodent models,” she said.

Celia Kjaerby, PhD

She and Kjaerby, who was starting her own research group within Nedergaard’s international lab, gradually learned the ins and outs of each other’s work.

“None of this was really related to [HRV] until I came,” Mednick said. “They had heart rate in their signals, but nobody was measuring it.”

In her lab, Mednick had been recording a very slow frequency heart rhythm in humans that changed whenever memory-consolidating “big infraslow spindles” appeared on their EEGs. It looked like an exact match to the rodent rhythm.

“We were sort of like, no way. This fits perfectly together,” Kjaerby said. “What you’re seeing must be what we are seeing.”

When Mednick applied her HRV algorithms to Kjaerby and Nedergaard’s rodent data, the connection was undeniable: The tiny fluctuations occurring every 50 seconds corresponded exactly to the rodents’ locus coeruleus and norepinephrine activity and predicted the same sleep spindles she’d seen in humans.

Why HRV Reflects Glymphatic Clearance

While you sleep, cerebrospinal fluid is being pumped through perivascular channels in your brain, flushing out metabolic waste. The process accelerates the longer you slumber and slows as you wake up.

When sleep is disrupted or the system falters, it increases the risk for neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and frontotemporal dementia. Stress, depression, cardiovascular disease, and aging can all disrupt sleep — potentially interrupting the process and raising risk for cognitive decline, as noted in a May review conducted by Nedergaard and published in Science.

The vascular movement helping to pump out waste is closely tied to heart rate fluctuations, explaining why HRV may provide a window into the process.

“It’s a very important observation, that it’s locus coeruleus and norepinephrine that drives [HRV],” Nedergaard said. “We know that locus coeruleus and norepinephrine is a major driver, or basically pump, of the glymphatic system.”

Measuring glymphatic flow has previously been invasive and expensive, requiring a lumbar drain and contrast MRI scans. Noninvasive glymphatic imaging platforms have seen “an explosion of studies” in recent years, Nedergaard said, but these still require specialized equipment.

HRV is already tracked on most smartwatches. If the right algorithm applied to a smartwatch could pick up the very low frequency HRV range, it could potentially provide consumers with a measure of glymphatic clearance — right from their smartphones, Mednick said.

Limitations and What’s Next

The research leaves open questions about the relationship between HRV and the autonomic nervous system.

“Our study has just done a rough correlation between the heart rate and the arousal system,” Kjaerby said. “It seems there is a link — and we have not fully characterized the link.”

Previous research suggests a strong link between the locus coeruleus and parasympathetic nervous system activity, which could explain why the heart slows when the locus coeruleus is suppressed. Or locus coeruleus activity could be coupled to the sympathetic nervous system, leading to heart rate acceleration with locus coeruleus arousal. But “these are speculations based on our paper,” Kjaerby said.

The next step is developing a robust HRV biomarker to noninvasively measure what the brainstem is doing, Mednick said. Meanwhile, all those emerging glymphatic imaging platforms could provide more evidence. “What I’m most excited about is to use it as a way to see whether treatment actually improves glymphatic function,” Nedergaard said.

For example, reduced HRV in the very low frequency range could hint at memory consolidation problems. But Kjaerby wonders if vagus nerve stimulation could restore an optimal rhythm — and an HRV measure could reveal how well that manipulation works.

For Mednick, knowing that the locus coeruleus drives HRV represents a starting point for a much deeper dive. “Every single thing that our body and minds need requires some amount of recruitment from the heart,” she said. “If we did a really good analysis of the HRV, I think we could find a lot more information.”

Nedergaard reported serving as a consultant for CNS2 Inc. for unrelated work. Kjaerby and Mednick reported having no relevant disclosures.

Scientists Discover Surprising Way To Help the Brain Recover After Stroke

 Will your competent? doctor get this written up in a protocol? NO? So completely fucking incompetent then! And your board of directors is so incompetent they don't recognize incompetence in their staff! Will your doctor at least get human testing going?

Scientists Discover Surprising Way To Help the Brain Recover After Stroke

A new study suggests that strengthening the body’s natural circadian rhythms may help the brain recover after stroke, even when treatment begins days after the injury.

Every year, millions of people survive a stroke, but recovery often continues long after the immediate medical emergency has passed. Scientists are increasingly discovering that factors beyond the initial brain injury—including sleep, the body’s internal clock, and the brain’s own cleaning system—may play important roles in determining how well the brain heals.

Now, researchers at the University of Rochester Medicine report that strengthening the body’s natural daily rhythms may help boost recovery after stroke. The study suggests that reinforcing circadian rhythms, the 24-hour biological cycles that regulate sleep and many other bodily functions, could enhance the brain’s ability to clear waste and reduce lingering inflammation.

Published in the Journal of Clinical Investigation, the research found that treatments designed to reinforce circadian rhythms improved recovery in mouse models of stroke. The benefits were associated with enhanced function of the glymphatic system, a recently discovered network that helps flush waste products from the brain, as well as lower levels of inflammatory molecules that can persist long after the initial injury.

The research builds on more than a decade of work led by URochester Medicine neuroscientist Maiken Nedergaard, MD, DMSc, whose team discovered the glymphatic system in 2012. This network circulates cerebrospinal fluid throughout the brain, helping remove waste and debris. Later studies showed that glymphatic activity is strongest during sleep and is important for maintaining brain health.

Expanding on those findings, neuroscientist Lauren Hablitz, PhD, helped show that glymphatic function is regulated not only by sleep but also by circadian rhythms, the body’s internal 24-hour clock. In a landmark 2020 study, Hablitz, Nedergaard, and colleagues demonstrated that glymphatic activity follows daily patterns even when sleep is not a factor, establishing a direct link between circadian biology and the brain’s waste-clearing system.

Stroke as a Disorder of Timing

“The discussion of stroke recovery really starts with the idea that stroke is not just a vascular event, but also a disorder of timing,” said Hablitz, lead author of the new study.

Scientists have long observed that strokes follow predictable daily patterns. They occur more frequently in the morning and are often most severe near the end of the sleep cycle. Many stroke survivors also experience disruptions to their sleep-wake schedules, which have been associated with poorer recovery, depression, and reduced quality of life.

“That led us to ask a simple question,” said Hablitz. “If timing is broken after a stroke, can we improve recovery by reinforcing the biological clock?”

Glymphatic Dysfunction and Brain Inflammation

In a healthy brain, the glymphatic system moves cerebrospinal fluid along blood vessels and through brain tissue, delivering nutrients while removing waste products and inflammatory signals. Previous research has shown that this system becomes less effective after a stroke, potentially reducing the brain’s ability to clear harmful molecules during recovery.

Traditionally, stroke research has focused on identifying harmful forms of inflammation and finding ways to suppress them. Hablitz and her colleagues suggest that impaired waste clearance may also play an important role.

“We think part of the problem may be a failure of cleaning,” she said. “If the system responsible for clearing signaling molecules isn’t working properly, everything builds up.”

According to this model, a stroke damages not only brain tissue but also the pathways responsible for removing inflammatory signals. As those molecules accumulate, they may contribute to ongoing damage and slower recovery.

Testing Circadian-Based Stroke Treatments

To determine whether restoring circadian rhythms could improve recovery, the researchers tested several approaches known to affect the body’s internal clock, including controlled light exposure, melatonin, a clock-targeting drug called KL001, and time-restricted feeding.

The team first showed that each method enhanced glymphatic function in healthy animals. They then evaluated the two most promising interventions, KL001 and time-restricted feeding, in mouse models of stroke.

Treatment began three days after the stroke, well beyond the limited window when clot-busting drugs and other emergency treatments are effective. Even with that delay, mice receiving either intervention experienced better motor recovery, smaller brain lesions, improved glymphatic flow, and lower levels of inflammatory cytokines.

“All of the cytokines moved in the same direction,” Hablitz said. “That suggests we may not be targeting one specific inflammatory pathway. Instead, we may be helping the brain clear inflammatory signals more effectively.”

Time-Restricted Feeding Shows Promise

Because time-restricted feeding produced some of the strongest results, the findings may have practical relevance for stroke rehabilitation. The approach is already being studied for conditions including obesity, diabetes, and cardiovascular disease.

“One of the exciting aspects of this work is that we’re studying interventions that could potentially be implemented not only in hospitals but also at home,” Hablitz said.

Future Directions for Circadian Stroke Therapy

The researchers emphasize that the results are currently limited to animal studies. More research is needed to better understand how circadian rhythms, glymphatic function, and inflammation interact following a stroke.

Future work will examine whether improved glymphatic flow directly contributes to recovery and whether circadian-based therapies can be advanced into clinical trials.

More broadly, the findings reflect a growing view in neuroscience that sleep, circadian rhythms, and fluid movement through the brain are central to overall brain health. By better understanding how the body’s internal clock regulates the glymphatic system, researchers hope to develop new treatments not only for stroke recovery but also for other neurological conditions involving inflammation and impaired waste removal.

“Understanding how circadian regulation shapes glymphatic clearance will help us develop more targeted therapies,” said Hablitz. “Ultimately, our goal is to find ways to improve the brain’s ability to clear waste, reduce inflammation, and recover after injury.”

Reference: “Chronotherapy to reinforce circadian rhythms improves poststroke outcomes and glymphatic function in mice” by Emma Waight, Yuxi Zhu, Ashley Caudell, Velia S. Vizcarra, Evan Newbold, Michael J. Giannetto, Evalien Duyvestyn, Estephanie Balbuena, Wei Song, Tanzil M. Arefin, Yuki Mori, Maiken Nedergaard and Lauren M. Hablitz, 15 June 2026, The Journal of Clinical Investigation.
DOI: 10.1172/JCI201800

Impaired movement of cerebrospinal fluid predicts dementia risk later in life

 With your risk of dementia post stroke is your competent? doctor testing for this so EXACT PREVENTION PROTOCOLS can be implemented? 

Your risk of dementia, has your doctor told you of this?  Your doctor is responsible for preventing this!

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

Impaired movement of cerebrospinal fluid predicts dementia risk later in life

Problems with the brain's waste clearance system could underlie many cases of dementia and help explain why poor sleep patterns and cardiovascular risk factors such as high blood pressure increase the risk of dementia.

A study led by researchers at the University of Cambridge found that impaired movement of cerebrospinal fluid (CSF) – the clear liquid that cushions and cleans the brain – predicted risk of dementia later in life among 40,000 adults recruited to the UK Biobank. Their findings are published today in Alzheimer's & Dementia: The Journal of the Alzheimer's Association.

In the healthy brain, the so-called glymphatic system serves to clear out toxins and waste materials, keeping the brain healthy. Only discovered as recently as 2012, this system functions by flushing CSF through the brain along tiny channels around blood vessels known as perivascular spaces. It collects waste then drains out of the brain, helping keep it clean and healthy.

The glymphatic system is thought to be important in protecting against many of the common forms of dementia, which are often characterised by the build-up of toxic substances in the brain – for example, Alzheimer's disease sees amyloid 'plaques' and tau 'tangles accumulate in brain tissue.

One of the most common forms of dementia is vascular dementia, caused by reduced blood flow to the brain. The most common cause of this type of dementia is cerebral small vessel disease, which affects the small blood vessels in the brain. But the impact of cerebral small vessel disease is even greater because it also interacts with other dementias making them worse; for example, a study of nuns in the US found that among those nuns whose brains showed signs of Alzheimer's disease post mortem, only around a half exhibited symptoms of dementia – but this increased to around nine in 10 if they also had cerebral small vessel disease.

Professor Hugh Markus and colleagues at the University of Cambridge wanted to see whether cerebral small vessel disease and other cardiovascular risk factors damage the glymphatic system – and whether this in turn increases the risk of dementia.

Until recently, it has only been possible to study glymphatic function in mice, but recent advances in MRI scanning have made it possible to study it indirectly in humans. Even so, it was only possible to do this practically in relatively small numbers, but Yutong Chen, while a medical student at the University of Cambridge, developed machine learning algorithms capable of assessing glymphatic functions from MRI scans at scale.

The team applied the algorithm to MRI scans taken from around 40,000 adults in UK Biobank. They found three biomarkers – biological signatures – associated with impaired glymphatic function assessed at baseline, predicted the risk of dementia occurring over the subsequent decade. One of these was DTI-ALPS, a measure of the diffusion of water molecules along the perivascular spaces. Another was the size of the choroid plexus, where the CSF is produced. The third measure reflected the flow velocity of CSF into the brain.

Although we have to be cautious about indirect markers, our work provides good evidence in a very large cohort that disruption of the glymphatic system plays a role in dementia. This is exciting because it allows to ask: how can we improve this?"

Yutong Chen, Department of Clinical Neurosciences at Cambridge

Further analysis showed that several cardiovascular risk factors impaired glymphatic function – and hence increased dementia risk, and that this was partly via causing cerebral small vessel disease, which is visible in the MRI scans.

First author Hui Hong, now a radiologist at the Second Affiliated Hospital of Zhejiang University, Hangzhou, China, said: "We already have evidence that small vessel disease in the brain accelerates diseases like Alzheimer's, and now we have a likely explanation why. Disruption to the glymphatic system is likely to impair our ability to clear the brain of the amyloid and tau that causes Alzheimer's disease."

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The research suggests possible approaches for reducing dementia risk. One is to look at strategies for improving glymphatic function. Sleep plays an important role in glymphatic function, and so disrupted sleep patterns are likely to impair its ability to clear toxins. Alternatively, there may be existing medicines that could be repurposed, or new ones that could be developed, to improve glymphatic function.

Another possible approach is to treat vascular risk factors such as high blood pressure. This is supported by recent studies: the SPRINT MIND trial, for example, showed that intensive blood pressure control (maintaining a systolic blood pressure of less than 120 mm Hg) led to a 20% reduction in cognitive decline or dementia compared to participants in the standard treatment group.

Professor Markus, who leads the Stroke Research Group at the University of Cambridge and is a Fellow of Clare Hall, Cambridge, said: "We already know the importance of cardiovascular risk factors when it comes to dementia, and our findings further emphasise this link.

"At least a quarter of all dementia risk is accounted for by common risk factors like blood pressure and smoking. If these impair glymphatic function, then we can intervene. Treating high blood pressure or encouraging people to stop smoking would be an achievable way to helping the glymphatic system work better."

Professor Bryan Williams, Chief Scientific and Medical Officer at the British Heart Foundation, said: "This study offers us a fascinating glimpse into how problems with the brain's waste clearance system could be quietly increasing the chances of developing dementia later in life. By improving our understanding of the glymphatic system, this study opens exciting new avenues for research to treat and prevent dementia. It also emphasises the importance of managing known cardiovascular risk factors, such as high blood pressure, for reducing dementia risk."

The research was funded by the British Heart Foundation, with additional support from the National Institute for Health and Care Research Cambridge Biomedical Research Centre.

Source:

University of Cambridge

Journal reference:

Hong, H., et al. (2025) MRI markers of cerebrospinal fluid dynamics predict dementia and mediate the impact of cardiovascular risk. Alzheimer's & Dementia: The Journal of the Alzheimer's Association. doi.org/10.1002/alz.70699

Brain’s Waste Clearance System Implicated in Dementia

 Your competent? doctor created protocols to fix this problem this years ago, right?

brain waste removal (19 posts to February 2018)

glymphatic clearance (6 posts to June 2022)

Glymphatic dysfunction (2 posts to April 2023)

Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING?

Brain’s Waste Clearance System Implicated in Dementia

Impaired glymphatic function — the brain’s waste clearance system — could help explain how cardiovascular disease (CVD) risk factors may drive dementia. 

In a large UK Biobank study, MRI markers of disrupted cerebrospinal fluid (CSF) and glymphatic flow predicted future dementia and were closely linked to vascular risk factors, including high blood pressure, diabetes, smoking, and arterial stiffness.

Discovered just over a decade ago, the glymphatic system depends on the efficient circulation and drainage of CSF. When this process is impaired, the brain’s ability to clear amyloid, tau, and other toxins diminishes, potentially accelerating the development of dementia.

“The study shows, with very convincing data, that these markers predict dementia risk, and also that the markers relate to cardiovascular risk factors,” study author Hugh S. Markus, MD, professor of stroke medicine in the Department of Clinical Neurosciences, University of Cambridge, UK, told Medscape Medical News.

“This offers a novel way in which one might be able to target or treat dementia. If one could improve glymphatic flow, one could then reduce the risk of dementia.”The study results were published online on October 23 in Alzheimer's & Dementia and simultaneously presented at the 17th World Stroke Congress (WSC) 2025 in Barcelona, Spain. 

Human Glymphatic Function Revealed

Over the years, studies in animal models of dementia and cerebral small-vessel disease have helped clarify how the glymphatic system functions. 

As the authors explain, CSF is continuously produced by the choroid plexus (CP), creating pressure that drives its flow from the brain’s ventricles into the subarachnoid space. From there, CSF enters the brain tissue via perivascular spaces (PVS), where it exchanges with interstitial fluid. This exchange facilitates the clearance of metabolic waste from the brain through the PVS.

Until recently, glymphatic function could be studied only in mice. Advances in MRI now make it possible to assess this system indirectly in humans. Researchers are using machine learning-based methods to quantify imaging markers of glymphatic function across large populations.

“We applied these techniques to see whether glymphatic drainage in the brain was impaired in people who had cardiovascular risk factors or had small-vessel disease of the brain, and, particularly importantly, to see whether this predicted dementia,” said Markus.

MRI-Based Biomarkers

The researchers examined several MRI-based biomarkers that serve as proxies for CSF and glymphatic dynamics. These included:

• PVS volume, reflecting the size of the small channels that run alongside blood vessels
• Diffusion tensor imaging–analysis along the PVS (DTI-ALPS), which measures the movement of water molecules along perivascular spaces — higher values indicate more efficient CSF clearance
• Blood oxygen level–dependent CSF (BOLD–CSF) coupling, which captures the relationship between cerebral blood flow and CSF inflow from the spinal cord into the brainstem — impaired coupling signals reduced CSF and glymphatic flow
• CP volume, as enlargement of the CP has been linked to decreased CSF production and waste clearance

The study included 44,384 participants (median age, 65 years; 47.9% male) with available MRI data. Over a median follow-up of 5.3 years, 133 participants developed dementia. Higher baseline DTI-ALPS values were associated with a lower risk for dementia after adjustment for age, sex, and education (hazard ratio [HR], 0.866; 95% CI, 0.797-0.942; P = .001).

Higher CP volume predicted dementia conversion (corrected HR, 1.185; 95% CI, 1.088-1.291; P < .001), as did lower BOLD-CSF coupling (corrected HR, 0.875; 95% CI, 0.806-0.951; P = .001).

However, PVS volume did not predict dementia conversion (corrected HR 1.013; 95% CI 0.940-1.091; P = .730).

Vascular Damage Impairs Brain Cleanup

All major CVD risk factors were associated with signs of impaired glymphatic flow across multiple imaging markers. Higher systolic blood pressure, for instance, correlated with larger PVS volume, lower DTI-ALPS, higher CP volume, and weaker BOLD-CSF coupling (P <.001 for all). Diabetes showed a similar pattern, with lower DTI-ALPS, higher CP volume, and reduced BOLD-CSF coupling, although it was not associated with PVS volume.

When the researchers examined potential mediators of dementia risk, diabetes emerged as particularly important, said Markus. Both DTI-ALPS and CP volume partially mediated the associations between white-matter hyperintensities and dementia, as well as between diabetes duration and dementia. 

The imaging markers were also linked to measures of cardiac and arterial function — including maximum carotid intima-media thickness, left ventricular ejection fraction, and arterial stiffness — though the strength of these associations varied.

The findings shed light on how CVD risk factors could contribute to dementia. Conditions such as hypertension and diabetes can damage the brain’s small blood vessels, leading in turn to glymphatic dysfunction, Markus said.

In addition to the vascular risk factors examined in the study, impaired sleep can also disrupt the brain’s waste-clearance system, Markus noted. It has been suggested that poor sleep is an important factor that interferes with glymphatic function and reduces the clearance of toxins from the brain, he said. 

With a clearer picture of the pathologic processes driving dementia, the next step is to identify ways to target the glymphatic system to reduce risk. Markus pointed to emerging research testing investigational agents designed to restore or enhance the brain’s natural waste clearance function.

Aside from controlling blood pressure, there are at present few effective treatments for vascular dementia, which results from reduced blood flow to the brain, Markus said. The same is true for Alzheimer’s disease, where antiamyloid therapies “don’t help all that much,” he added. 

Lifestyle Matters

Commenting on the research for Medscape Medical News, Ozama Ismail, PhD, director of scientific programs at the Alzheimer’s Association, said the study helps clarify the complex relationships among vascular changes in the brain, removal of harmful waste, and incident dementia.

“In this way, it may help us identify future targets for treatment and risk reduction,” he said.

Ismail added that research has consistently shown a close link between heart health and brain health and noted that the Alzheimer’s Association’s US POINTER study recently demonstrated that a heart-healthy diet and regular exercise can help delay cognitive decline in individuals at increased risk. 

Researchers plan to incorporate in-home sleep assessments into a US POINTER substudy to examine whether lifestyle changes can improve sleep. The glymphatic system appears to be most active during sleep, Ismail noted.

The study was supported by the British Heart Foundation, Cambridge British Heart Foundation Centre of Research Excellence, Cambridge University Hospitals National Institute for Health and Care Research Biomedical Research Centre. Markus reports no relevant conflicts of interest.