Scientists reveal that neurodegenerative diseases aren’t caused by rogue genes, but by the brain’s failing cleanup systems—offering new hope for early detection and treatment.
Did you know that neurodegenerative diseases, including Alzheimer’s and Parkinson’s, primarily result from failures in clearing damaged proteins? In a recent review published in the journal Molecular Psychiatry, researchers explored how genetic variations affect the body's ability to remove harmful protein accumulations. The findings indicated that these diseases stem from declining clearance mechanisms rather than direct genetic mutations, and suggested new strategies for diagnosis and treatment.
Neurodegenerative diseases, such as Alzheimer’s and Parkinson’s, arise from progressive damage to brain cells, often linked to protein accumulation. Normally, the body has efficient clearance systems, including microglia, lysosomes, and the ubiquitin-proteasome pathway, to remove misfolded or excess proteins. However, as individuals age, these mechanisms weaken, leading to the accumulation of toxic proteins like amyloid-beta, tau, and alpha-synuclein.
Genetic research has identified several risk factors, but most associated genes are involved in clearance pathways rather than directly causing disease. Studies suggest that variations in these genes reduce the efficiency of protein removal, increasing disease risk. Additionally, many patients exhibit multiple overlapping pathologies, complicating diagnosis and treatment.
The review explored why specific proteins accumulate in neurodegenerative diseases and discussed existing research that indicates that proteins such as amyloid-beta, tau, and alpha-synuclein originate from highly expressed genes and accumulate when clearance mechanisms falter. Genetic factors, including gene duplications (e.g., APP, SNCA, MAPT) and variations in protein synthesis regulation (such as through antisense transcripts or pseudogenes), contribute to disease risk. However, late-onset cases are more influenced by reduced protein clearance than increased production of these proteins, particularly in Alzheimer’s disease.
Co-pathologies, where multiple neurodegenerative markers coexist, were also found to be common in elderly individuals. Amyloid plaques, tau tangles, and Lewy bodies frequently appear together in elderly patients, suggesting interconnected clearance pathways. The researchers discussed how spillover from one failing clearance pathway to another can overload other pathways, leading to multiple deposits. For example, the failure of the tau clearance pathway in the medial temporal lobe (a condition known as Primary Age-Related Tauopathy or PART) may allow amyloid deposition to spread tangle pathology to the cortex. However, they observed that no direct causal links between different protein accumulations have been definitively established.
Furthermore, certain genetic loci are associated with multiple neurodegenerative conditions, such as mutations in the gene encoding Leucine-Rich Repeat Kinase 2 (LRRK2), which can lead to either Parkinson’s disease with Lewy bodies or tauopathy. This suggested that genetic variations influence how the body responds to cellular damage rather than directly determining pathology.
Additionally, the review discussed the role of incomplete penetrance in near-Mendelian mutations, explaining that incomplete penetrance likely reflects age-related declines in clearance capacity and environmental factors. While some individuals with high-risk mutations remain unaffected, others develop severe symptoms, likely due to additional genetic or environmental influences.
Moreover, the researchers reported that age dependency in neurodegenerative diseases is linked to declining protein clearance efficiency. While genetic risk factors are present from birth, these diseases typically manifest later in life as clearance mechanisms weaken with age. This supported the idea that aging itself is a primary driver of neurodegeneration, emphasizing the need for therapies targeting age-related clearance failures.
The study also indicated that genetic risk is not static but shifts across an individual’s lifespan, with some risk variants having stronger effects at specific ages. For example, the APOE4 allele, which has the largest effect on Alzheimer’s risk, shows changing allele frequencies and odds ratios with age. Given that these diseases significantly contribute to mortality, the researchers stated that their genetic architecture must be analyzed in age-specific contexts to improve predictive accuracy.
The review also examined genome-wide association studies (GWAS), which have been instrumental in identifying genetic risk factors. However, it found that existing datasets often lack age-matched analyses. Most Alzheimer’s disease GWAS are based on dementia diagnoses rather than confirmed pathological markers, which complicates the interpretation of findings.
Furthermore, the researchers underscored the urgent need for genetic studies in non-European populations. Current findings are primarily derived from Northern European cohorts, limiting their applicability to diverse genetic backgrounds. The few studies conducted among African and Asian populations have already revealed differences in risk variants, such as the ABCA7 internally deleted allele in African Americans and the GBA-PD allele in African-derived populations, highlighting the necessity of broadening research efforts.
Additionally, the researchers believe future studies should integrate genetic, biomarker, and imaging data to identify high-risk individuals before clinical symptoms appear. They specifically recommended GWAS of age-specific risks, pathology-confirmed cases, disease progression rates, and analyses of quantitative biomarkers like AB peptides, GFAP, NFL, and p-Tau. Targeted interventions to slow or prevent disease onset can be developed by analyzing disease progression rates and age-specific genetic effects. The review emphasized that advancing precision medicine approaches will require moving beyond broad case-control studies to more nuanced analyses incorporating genetic and biomarker interactions over time.
Cartoon suggesting the possible relationships between the different disease pathologies: amyloid, cleared largely by the microglia; tau, clearly largely by the ubiquitin-proteasome and synuclein, cleared mainly through the lysosome.
To summarize, the study reinforced the concept that neurodegenerative diseases result primarily from failures in protein clearance rather than direct genetic mutations. Age-related declines in clearance capacity play a crucial role, making late-onset diseases an inevitable consequence of aging.
The findings suggested that future research should prioritize age-specific genetic analyses, biomarker integration, and diverse population studies to refine diagnostic tools and develop targeted therapies. Addressing protein clearance failures may be the key to delaying or preventing neurodegenerative disorders.
Alzheimer’s disease is a devastating condition that impacts millions of families around the world. But scientists are still trying to pinpoint the elements that go into why some people develop Alzheimer’s disease and others don’t. Now, a new study suggests that your sleep patterns may play a role.
The study, which was published in the journal Alzheimer’s & Dementia on January 27, specifically looked at the relationship between REM sleep and Alzheimer’s disease. But what’s the link between the two and, more importantly, how can you use this information to lower your risk of developing Alzheimer’s disease? A neurologist explains.
Meet the expert: W. Christopher Winter, MD, a neurologist and sleep medicine physician with Charlottesville Neurology and Sleep Medicine and host of the Sleep Unplugged podcast.
For the study, researchers looked at how long it took 123 people to reach rapid eye movement (REM) sleep for the first time after falling asleep, as well as several biomarkers linked to Alzheimer’s disease. (REM sleep is a stage of sleep where your eyes move quickly and you dream, per the Cleveland Clinic. It’s important for learning and memory, too.)
The researchers discovered that people who took longer to get to the REM stage of sleep were more likely to have biomarkers of Alzheimer’s disease.
The relationship between sleep and Alzheimer’s disease is still being explored. The Alzheimer’s Society notes that people living with dementia tend to have sleep issues, but the evidence is currently unclear on whether poor sleep is a risk factor for the disease.
However, some research suggests that poor sleep could raise your risk of Alzheimer’s. A study published in November found that 35 percent of people who were considered poor sleepers (and felt excessively tired during the day as a result) went on to develop motoric cognitive risk syndrome (MCR), which is considered a precursor to dementia.
It’s hard to say for sure at this point. While the researchers concluded that more studies are needed, they also said a slower movement to REM sleep could serve as a “potential marker” for Alzheimer’s disease.
Given that good sleep is linked to good overall health, it can’t hurt to try to improve your sleep.
Most people go through four to six sleep cycles a night, and REM sleep is part of that. Unfortunately, you can’t dictate the stages of sleep you enter and when. What you can do is try to focus on getting good sleep, period.
Winter offers up these tips to help support good sleep:
Have a set bedtime and wake time, and do your best to stick to it.
Limit alcohol and caffeine, especially avoiding caffeine later in the day.
Try to be physically active, and aim to work out in the mornings to support your body’s natural sleep/wake cycle.(Your doctors' complete responsibility to get you to this state)
Create a good, consistent bedtime routine that helps you wind down for the evening.
Be wary of sleep aids. “Ironically, some sleep aids affect REM sleep,” Winter says.(So, no sleeping pills, which my hospital handed out like candy at 10pm.)
Researchers don’t know exactly what causes Alzheimer’s disease and dementia, making it tough to know for sure how to prevent it. But the Centers for Disease Control and Prevention (CDC) recommends doing these things to help lower your risk:
Be physically active(Your doctors' complete responsibility to get you to this state)
Try to prevent or manage diabetes
Manage your blood pressure
Try to prevent or correct hearing loss
Try to limit or avoid drinking alcohol
Try to limit or avoid smoking
If you’re struggling with sleep, Winter says it’s important to consult with a healthcare professional sooner rather than later. They should be able to do a sleep study—which can give you more information on what’s behind your sleep issues—and make personalized recommendations from there.
Summary: Researchers have discovered that the gut bacteria Klebsiella pneumoniae can migrate to the brain, leading to inflammation and cognitive decline that mimic Alzheimer’s symptoms. The study suggests that hospital-acquired infections combined with disrupted gut microbiomes may increase the risk of developing neurodegenerative diseases.
Using a mouse model, scientists found that antibiotic exposure can cause microbiome imbalances, allowing K. pneumoniae to reach the brain. This study opens new avenues for preventing Alzheimer’s by managing infections and gut health.
Key Facts:
Source: FSU
A groundbreaking study by researchers at Florida State University’s Gut Biome Lab has revealed a potential link between an infection caused by gut bacteria and the progression of Alzheimer’s disease.
The research found that the bacteria Klebsiella pneumoniae — a common bacteria notorious for causing hospital-acquired infections — can migrate from the gut into the bloodstream and eventually into the brain.
This bacterial invasion may lead to increased inflammation in the brain and impair cognitive functions, mimicking symptoms seen in Alzheimer’s patients.
The work was published in The Journal of Infectious Diseases.
“Hospitalizations and ICU stays, combined with antibiotic exposure, may lead to a further decline in microbiome diversity that leaves older adults at high risk not only for digestive issues but also for extra-intestinal pathologies such as neurodegenerative disorders through a dysregulation of the gut-brain axis,” said Ravinder Nagpal, an assistant professor in the FSU College of Education, Health, and Human Sciences and the director of the Gut Biome Lab.
The study is the first to show a direct correlation between K. pneumoniae infection and Alzheimer’s pathology, fueling the emerging field that investigates how infectious agents may trigger or aggravate Alzheimer’s disease.
It also paves the way for future research into how to treat harmful infectious agents in vulnerable populations such as the elderly or those recovering from sepsis.
The research suggests that when antibiotics disrupt the gut, it can lead to issues not just in the gut but also in the brain. Using a preclinical mouse model, researchers showed that antibiotic exposure depletes gut bacterial diversity and causes microbiome imbalance, which promotes the proliferation of K. pneumoniae by creating a favorable niche.
When this happens, K. pneumoniae can move from the gut into the bloodstream by passing through the gut lining and eventually reach the brain, triggering neuroinflammation and neurocognitive impairment.
The findings emphasize the potential risk hospital-acquired infections like K. pneumoniae may pose in the development of neurodegenerative diseases.
“Hospital-acquired and septic infections are one of the risk factors that may increase the predispositions to future neuroinflammatory and neurocognitive impairments, especially in older adults,” Nagpal said.
The study highlights the need for innovative therapeutic approaches to combat the rising prevalence of Alzheimer’s disease, in addition to existing amyloid and tau protein therapies. Further research could provide insight into preventive strategies aimed at managing hospital-acquired pathogens and preserving cognitive health in aging populations.
Funding: The research was funded by the Infectious Diseases Society of America and the Florida Department of Health.
The paper was co-authored by graduate researchers Ian Park, Saurabh Kadyan, and Nathaniel Hochuli from the FSU College of Education, Health, and Human Sciences. Additional collaborators included Hazel K. Stiebeling Professor Gloria Salazar; Associate Professor of psychology and neuroscience Aaron Wilber; University of Florida researchers Orlando Laitano, Paramita Chakrabarty, and Philip A. Efron; and Wake Forest University School of Medicine Associate Professor M. Ammar Zafar.
Author: Bill Wellock
Source: FSU
Contact: Bill Wellock – FSU
Image: The image is credited to Neuroscience News
The study has only been done on mice, but scientists say the findings are "potentially scary for humans"
There is a credible link between picking your nose and increasing the risk of developing dementia, according to a recent study. Picking your nose can sometimes damage international tissue, meaning bacteria have a clear path to the brain, which responds to the presence of bacteria in ways that resemble signs of Alzheimer's disease.
As many as 9 out of 10 people may pick their nose, with experts warning that picking your nose and plucking your nose hair is "not a good idea" because of the potential damage it does to protective nose tissue.
So far, the supporting evidence is based on mice rather than humans, but the findings could better our understanding of how Alzheimer's begins, which remains an enigma. Tests with a bacteria called Chlamydia pneumonia, which can infect humans, cause pneumonia, and has been found in most human brains affected by late on-set dementia, were run by a team of researchers led by scientists from Griffith University in Australia last year.
Dementia can be caused by an excessive amount of daily habit which can also lead to depression and Parkinson's
Blood test that detects Alzheimer’s disease before onset of symptoms could become available next year
According to an article in ScienceAlert, the tests showed that the bacteria could travel up mice's olfactory nerve - joining the nasal cavity and the brain - and when there was damage to the nasal epithelium - the thin tissue along the roof of the nasal cavity - nerve infections got worse. This led to the mouse brains depositing more of the amyloid-beta protein.
This leads to a protein that is released in response to infections. Clumps of this protein are also found in hefty concentrations in people with Alzheimer's disease. Neuroscientist James St John from Griffith University said: "We're the first to show that Chlamydia pneumonia can go directly up the nose and into the brain where it can set off pathologies that look like Alzheimer's disease... the evidence is potentially scary for humans as well as mice."
The scientists were surprised by the speed at which C. pneumoniae took hold in the central nervous system of the mice, with infection happening within 24 to 72 hours. It is believed that bacteria and viruses see the nose as a quick route to the brain. St John continued: "We need to do this study in humans and confirm whether the same pathway operates in the same way. It's research that has been proposed by many people, but not yet completed. What we do know is that these same bacteria are present in humans, but we haven't worked out how they get there."
Summary: Researchers identified cortical gray matter thinning as a potential early biomarker for dementia. In a study involving 1,500 participants from diverse backgrounds, thinner cortical gray matter was linked to a higher risk of developing dementia 5 to 10 years before symptoms appeared.
This finding suggests that measuring gray matter thickness via MRI could be key in early dementia detection and intervention. The research highlights the importance of early diagnosis in managing and possibly slowing the progression of dementia.
Key Facts:
Source: UT San Antonio
A ribbon of brain tissue called cortical gray matter grows thinner in people who go on to develop dementia, and this appears to be an accurate biomarker of the disease five to 10 years before symptoms appear, researchers from The University of Texas Health Science Center at San Antonio (also called UT Health San Antonio) reported.
The researchers, working with colleagues from The University of California, Davis, and Boston University, conducted an MRI brain imaging study published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.
They studied 1,000 Massachusetts participants in the Framingham Heart Study and 500 people from a California cohort. The California volunteers included 44% representation of Black and Hispanic participants, whereas the Massachusetts cohort was predominantly non-Hispanic white. Both cohorts were 70 to 74 years of age on average at the time of MRI studies.
“The big interest in this paper is that, if we can replicate it in additional samples, cortical gray matter thickness will be a marker we can use to identify people at high risk of dementia,” said study lead author Claudia Satizabal, PhD, of UT Health San Antonio’s Glenn Biggs Institute for Alzheimer’s and Neurodegenerative Diseases.
“By detecting the disease early, we are in a better time window for therapeutic interventions and lifestyle modifications, and to do better tracking of brain health to decrease individuals’ progression to dementia.”
Repeating the Framingham findings in the more-diverse California cohort “gives us confidence that our results are robust,” Satizabal said.
Sifting MRIs for a pattern
While dementias can affect different brain regions, Alzheimer’s disease and frontotemporal dementia impact the cortex, and Alzheimer’s is the most common type of dementia.
The study compared participants with and without dementia at the time of MRI. “We went back and examined the brain MRIs done 10 years earlier, and then we mixed them up to see if we could discern a pattern that reliably distinguished those who later developed dementia from those who did not,” said co-author Sudha Seshadri, MD, director of the Glenn Biggs Institute at UT Health San Antonio and senior investigator with the Framingham Heart Study.
“This kind of study is only possible when you have longitudinal follow-up over many years as we did at Framingham and as we are building in San Antonio,” Seshadri said. “The people who had the research MRI scans while they were well and kept coming back to be studied are the selfless heroes who make such valuable discoveries, such prediction tools possible.”
The results were consistent across populations. Thicker ribbons correlated with better outcomes and thinner ribbons with worse, in general. “Although more studies are needed to validate this biomarker, we’re off to a good start,” Satizabal said. “The relationship between thinning and dementia risk behaved the same way in different races and ethnic groups.”
Applications
Clinical trial researchers could use the thinning biomarker to minimize cost by selecting participants who haven’t yet developed any disease but are on track for it, Seshadri said. They would be at greatest need to try investigational medications, she said.
The biomarker would also be useful to develop and evaluate therapeutics, Seshadri noted.
Future directions
Satizabal said the team plans to explore risk factors that may be related to the thinning. These include cardiovascular risk factors, diet, genetics and exposure to environmental pollutants, she said.
“We looked at APOE4, which is a main genetic factor related to dementia, and it was not related to gray matter thickness at all,” Satizabal said. “We think this is good, because if thickness is not genetically determined, then there are modifiable factors such as diet and exercise that can influence it.”
Derived in clinical MRIs
Could the MRI gray matter biomarker be used widely someday?
“A high proportion of people going to the neurologist get their MRI done, so this thickness value might be something that a neuroradiologist derives,” Seshadri said. “A person’s gray matter thickness might be analyzed as a percentile of the thickness of healthy people for that age.”
Acknowledgments
National Institutes of Health/National Institute on Aging funding for Alzheimer’s Disease Research Centers (ADRCs) at The University of Texas Health Science Center at San Antonio; The University of California, Davis; and Boston University School of Medicine supported this study.
Author: Steven Lee
Source: UT San Antonio
Contact: Steven Lee – UT San Antonio
Image: The image is credited to Neuroscience News
Original Research: Open access.
“A novel neuroimaging signature for ADRD risk stratification in the community” by Claudia Satizabal et al. Alzheimer’s & Dementia
Body composition patterns associated with weight and fat distribution were strongly correlated with neurodegenerative disease and brain aging, mediated by cardiovascular disease, according to research published in Neurology.
“This study highlights the potential to lessen people’s risk of developing these diseases by improving their body composition,” Huan Song, MD, PhD, a professor at the West China Hospital of Sichuan University in Chengdu, China, said in a related release.
Song and colleagues sought to examine examines the associations between seven different kinds of body composition and the risk of neurodegenerative diseases with cardiovascular disease (CVD) as a mediator in a cohort of midlife to older adults compiled by the U.K. Biobank from 2006 to 2010.
Their retrospective analysis included more than 412,000 individuals (mean age, 56 years; 55.1% female) with the necessary body composition measurements at the time of recruitment but without record of neurological disease at time of examination or extreme values in body composition measurement.
All who met inclusion criteria were followed from 5 years after recruitment until April 1, 2023.
The primary outcome for the study was incidence of any neurodegenerative disease, with secondary outcomes of incidence of specific neurodegenerative conditions such as Alzheimer’s disease, Parkinson’s disease, dementia or other vascular disease of that type. All cases were determined by review of inpatient hospital or death records.
The researchers employed multivariable Cox regression models to assess associations between different components and major patterns of body composition with the risk of neurodegenerative disease. They also conducted mediation analysis to determine if CVD contributed to these associations.
Song and colleagues additionally followed a subset of 40,790 participants, utilizing MRI-derived data, to assess relationships between body composition patterns and brain aging biomarkers such as atrophy and cerebral small vessel disease.
According to results, 8,224 new cases of neurodegenerative diseases (primary causes, n = 6,274; vascular causes, n = 1,194) were identified over an average follow-up of 9.1 years, with 2,427 cases of PD, 2,933 cases of AD and 6,076 all-cause dementia cases.
Data showed that lower rates of neurodegenerative disease carried associations with body condition patterns such as “fat-to-lean mass,” “muscle strength,” “bone density,” and “leg-dominant fat distribution” (HR = 0.74–0.94).
Conversely, higher rates of neurodegenerative disease were associated with patterns such as “central obesity” and “arm-dominant fat distribution” (HR = 1.13–1.18).
The researchers additionally reported that roughly 10.7% to 35.3% of the observed associations between body composition and neurodegenerative disease were mediated by CVDs, particularly cerebrovascular issues. Analysis of the study subcohort yielded positive association with brain aging biomarkers and composition patterns “central obesity,” “muscle strength,” and “arm-dominant fat distribution.”
“Our findings highlight the potential for improvement in body composition and early interventions in CVDs as a target in mitigating the future risk of neurodegenerative diseases,” Song said in the release.
Does your body composition affect your risk of dementia or Parkinson’s? https://www.aan.com/PressRoom/Home/PressRelease/5189. Published July 24, 2024. Accessed July 25, 2024.
Sources/DisclosuresCollapse
Disrupted circadian rhythms in cognitively normal adults were tied to higher subsequent amyloid-beta levels, prospective data showed.
Higher daily variability at baseline -- an indicator of fragmented 24-hour activity rhythms -- was associated with higher PET amyloid burden 8 years later (β=0.15, P=0.02) after adjusting for age, sex, APOE4 status, and other factors, according to Julia Neitzel, PhD, of Erasmus University Medical Center in Rotterdam, the Netherlands, and co-authors.
The relationship was stronger in APOE4 carriers (β=0.38, P=0.03), Neitzel and colleagues reported in JAMA Neurologyopens in a new tab or window. The findings remained largely similar after excluding participants with baseline Alzheimer's pathology.
Earlier research has suggested the relationship between Alzheimer's and sleep may be bidirectionalopens in a new tab or window and could span several decades.
"The literature on sleep and Alzheimer's disease pathology is very inconsistent," Neitzel noted. "However, the main difference between this study and other research was that we controlled for Alzheimer's disease pathology at baseline," she told MedPage Today.
"When we excluded participants with a positive Alzheimer's blood test at baseline, we still found an association between higher 24-hour rest-activity rhythm fragmentation at baseline and Alzheimer's PET burden at follow-up," Neitzel added. "This suggests that fragmentation is likely to be a risk factor, rather than a result, of Alzheimer's disease pathology."
According to the Lancet Commissionopens in a new tab or window, about 40% of dementia cases may be prevented or delayed by modifying 12 key risk factors. At this point, sleep is not one of them.
"Considerable interest surrounds the role of sleep dysfunction in the development of Alzheimer's disease and dementia," observed Matthew Pase, PhD, of Monash University in Victoria, Australia, who wasn't involved with the study.
"If poor sleep contributes to dementia, improving sleep symptomatology could be one strategy to lower dementia risk," he told MedPage Today.
Previously, the Rotterdam studyopens in a new tab or window did not find an association between fragmented 24-hour activity rhythms and incident dementia, Pase noted. But the current study -- which looked at Alzheimer's biomarker changes that occur years before dementia onset -- adds to the growing evidence that circadian disruption may increase dementia risk, he said.
In this analysis, Neitzel and co-authors evaluated sleep and 24-hour activity rhythms from 319 participants in the prospective Rotterdam study. No one had a diagnosis of dementia at baseline. At a mean follow-up of 7.8 years (from 2018 to 2021), the researchers measured amyloid burden on PET.
Mean baseline age was 61.5 years; mean age at follow-up was 69.2. About half (47%) of participants were women.
Sleep and activity were assessed by actigraphy for 7 days and nights to determine objective sleep and 24-hour activity rhythms. Participants also maintained diaries to self-report their sleep patterns. Plasma assays assessed baseline amyloid-beta 42/40 ratios and phosphorylated tau (p-tau)181 and p-tau217 levels.
While higher fragmentation of 24-hour activity rhythms was associated with more severe amyloid pathology at follow-up, no other objective or self-reported measure of sleep was, Neitzel and colleagues reported. There was no strong relationship between sleep duration and amyloid pathology, contrary to what some earlier research has shown.
"Self-reports of shorter sleep duration were associated with increased amyloid-beta pathology in most but not all studies," they wrote. "However, this association has not been confirmed in previous actigraphy studies, consistent with the current findings." Different sample sizes may be one underlying reason; actigraphy studies are typically smaller because they are more burdensome than self-reports, they added.
Because participants had only one PET scan, longitudinal analyses were limited in the study. The gold standard for measuring sleep is polysomnography, though actigraphy "shows fair associations with polysomnography," the researchers noted. And while possible sleep apnea was assessed through self-reports, it still may have influenced results.
Disclosures
This project received funding from the European Union's Horizon 2020 program, ZonMW, the Alzheimer's Association, the public-private partnership ABOARD, Topsector Life Sciences & Health, and the Tailored Activity Program (TAP)-dementia.
Neitzel and co-authors reported no conflicts of interest.
Pase reported relationships with the National Institute on Aging, the National Health and Medical Research Council of Australia, and the Alzheimer's Association.
Primary Source
JAMA Neurology
Source Reference: opens in a new tab or windowHo PTN, et al "Sleep, 24-hour activity rhythms, and subsequent amyloid-β pathology" JAMA Neurol 2024; DOI: 10.1001/jamaneurol.2024.1755.
