Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 32,639 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.
What this blog is for:
My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
You're so fucking incompetent you only describe a problem; OFFER NO SOLUTION! In the business world that would be actionable grounds for IMMEDIATE FIRINGS!
In my esteemed view, this is so fucking simple, 100% recovery, so they can get back to work immediately! You're complete blithering idiots if you can't see that!
Send
me personal hate mail on this: oc1dean@gmail.com. I'll print your complete
statement with your name(If you can't stand by your name don't bother replying anonymously) and my response in my blog. Or are you afraid
to engage with my stroke-addled mind? No excuses are allowed! You're
medically trained; it should be simple to precisely state EXACTLY WHY you aren't solving to 100% recovery protocols with NO EXCUSES! I've
never received any communications from any stroke association. You'd
think they would want to talk to their fiercest critic, but no, they are
hiding under a rock someplace, probably don't even know I exist!
Swearing at me is allowed, I'll return
the favor.
Don't even attempt to use the excuse that brain research is hard.
Younger stroke survivors, especially those out of work, had increased days of poor mental and physical health.
HealthDay News — Younger stroke survivors have more difficulty concentrating and doing errands alone than older stroke survivors, according to a study published online Feb. 26 in Geriatrics.Molly M. Jacobs, Ph.D., and Charles Ellis Jr., Ph.D., from the University of Florida in Gainesville, examined how functional, mental, and physical health outcomes differ between younger (younger than 50 years) and older (50 years and older) stroke survivors.
The researchers found that younger stroke survivors were more likely to report difficulty concentrating or remembering compared with older adults (41.1 versus 23.2 percent) and to report difficulty doing errands alone (27.11 versus 23.67 percent); however, they were less likely to report difficulty walking or climbing stairs (34.3 versus 47.6 percent). Compared with older adults, younger adults with stroke reported significantly more poor mental health days (10.81 versus 5.76). There was a consistent association seen for being out of work or out of the labor force with greater odds of functional limitations (odds ratio, 2.07 for activity difficulty) and with higher counts of poor mental and physical health days in adjusted models. Significantly higher odds of difficulty concentrating (odds ratio, 2.02) and increased days of poor mental and physical health (incidence rate ratios, 1.27 and 1.26, respectively) were seen for younger stroke survivors who were out of the labor force.
“With the growing rate of stroke among individuals under 50, the medical establishment has to acknowledge that young stroke survivors require age-specific rehabilitation strategies that include different components than they do for older stroke survivors,” Jacobs said in a statement.
Do you
prefer your doctor, hospital and board of director's incompetence NOT
KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand
action!
Plasma eMTBR-tau243 also could help identify people with high tau burden
Key Takeaways
Alzheimer's can be detected early with p-tau blood biomarkers, but some tests can lead to overdiagnosis.
Combining p-tau217 and eMTBR-tau243 may refine diagnostic accuracy and reduce false-positives.
Plasma eMTBR-tau243 also could help identify people with high tau burden.
A combination of two blood tests improved Alzheimer's disease triaging and reduced overdiagnosis in people with asymptomatic Alzheimer's pathology, a prospective cohort study showed.
Together, the two tests -- one assessing the ratio of phosphorylated tau 217 to non-phosphorylated tau (%p-tau217), the other measuring microtubule-binding region-tau243 (eMTBR-tau243) -- identified people with established Alzheimer's disease with an accuracy of 81%, a positive predictive value (PPV) of 84%, a negative predictive value (NPV) of 77%, and a sensitivity of 82%, reported Niklas Mattsson-Carlgren, MD, PhD, of Lund University in Sweden, and co-authors.
Positive eMTBR-tau243 was associated with worse longitudinal cognitive decline and longitudinal tau tangle accumulation in p-tau217-positive patients. In this group, eMTBR-tau243 had an accuracy of 87%, a PPV of 76%, and an NPV of 90% for identifying individuals with high tau-PET load, Mattsson-Carlgren and colleagues said in Lancet Neurology.
The proportion of false-positive test results for established Alzheimer's disease fell from 43% with %p-tau217 alone to 16% with %p-tau217 and eMTBR-tau24 combined, the researchers noted.
Two-step testing, with %p-tau217 as an initial test to identify Alzheimer's pathology followed by eMTBR-tau243, could refine diagnostic accuracy, Mattsson-Carlgren and colleagues suggested. Plasma eMTBR-tau243 also could help identify individuals with high tau burden who might have less benefit from amyloid-targeting therapies.
"Plasma p-tau217 is excellent to identify presence of amyloid pathology, which is a core feature of Alzheimer's disease. But amyloid pathology presents early, before clinical symptoms. By combining p-tau217 with eMTBR-tau243, which increases later in disease, in correlation with aggregated tau pathology, we can increase our confidence that Alzheimer's is not only present, but also contributes to symptoms," Mattsson-Carlgren told MedPage Today.
"Individuals with isolated increased p-tau217 without increased eMTBR-tau243 may be more likely to have Alzheimer's in very early stage, without clear relevance to the current symptoms," he pointed out.
"This type of fine-grained understanding of how different aspects of Alzheimer's disease are present and explain symptoms has not been possible with blood tests before," he added. "If these methods can be used in clinical practice, it will enable objective biological staging of Alzheimer's, which can guide patient management."
Plasma p-tau217 can reflect abnormal amyloid pathology decades before Alzheimer's symptom onset, but also can be abnormal when amyloid is a co-pathology in other diseases, noted Nicholas Ashton, PhD, of Banner Alzheimer's Institute in Phoenix.
"Therefore, interpretation of p-tau217 in isolation might increase the risk of overdiagnosis, especially in a preclinical population or when amyloid pathology is not the primary driver of the clinical syndrome," Ashton wrote in an accompanying editorial.
A growing demand for fast diagnostic testing coupled with the need for sufficient accuracy is a fundamental challenge facing the Alzheimer's field, Ashton observed. "Blood biomarkers clearly address the former, but their ability to reliably inform clinical care remains under scrutiny, despite recent regulatory approvals," he said.
A sequential framework of p-tau217 and eMTBR-tau243 tests could move the field toward biologically informed diagnosis and stratification, he pointed out. "As disease-modifying treatments become more available, the ability to distinguish early amyloid positivity from tau-driven symptomatic disease will be essential, not only for treatment selection, but also for avoiding both overdiagnosis and missed opportunities for timely intervention," Ashton wrote.
Mattsson-Carlgren and co-authors evaluated 572 adults with cognitive symptoms -- 142 participants with subjective cognitive decline, 259 with mild cognitive impairment, and 171 with dementia -- in the Swedish BioFINDER 2 study. About half (51%) were female.
Overall, 350 people had positive plasma %p-tau217. Of these, 341 people (97%) were amyloid-positive by cerebrospinal fluid biomarkers or PET. Just over half -- 194 of 350 participants (55%) -- also were positive for eMTBR-tau243.
The overall findings were validated in an independent cohort of both cognitively impaired and unimpaired patients from the Knight Alzheimer Disease Research Center (ADRC) at Washington University in St. Louis, the researchers said.
The study has several limitations, they acknowledged. The main sample was made up of Swedish participants, though results were consistent in the Knight ADRC cohort. Cross-validation in other populations and primary care settings is essential, they added.
The eMTBR-tau243 marker also needs further work, Mattsson-Carlgren noted. "The next step is to investigate whether the test can be simplified, and whether it can be used more widely -- in primary care, for example," he stated.
Judy George covers neurology and neuroscience news for MedPage Today, writing about brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy, autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep, pain, and more. Connect:
Disclosures
This study was supported by the National Institute of Aging, European Research Council, Alzheimer's Association, GHR Foundation, Swedish Research Council, ERA PerMed, Knut and Alice Wallenberg Foundation, Strategic Research Area MultiPark at Lund University, Swedish Alzheimer Foundation, Swedish Brain Foundation, Parkinson Foundation of Sweden, Cure Alzheimer's Fund, Rönström Family Foundation, Berg Family Foundation, Konung Gustaf V:s och Drottning Victorias Frimurarestiftelse, Skåne University Hospital Foundation, Michael J. Fox Foundation, Lilly Research Award Program, Regionalt Forskningsstöd, Wallenberg AI, Autonomous Systems and Software Program and Data-Driven Life Science, Greta and Johan Kock Foundation, and the Swedish federal government.
Mattsson-Carlgren received consultancy or speaker fees from BioArctic, Biogen, Eli Lilly, Merck, Novo Nordisk, Roche, and Owkin. Co-authors reported relationships with pharmaceutical companies and other groups.
Ashton reported relationships with AbbVie, Athira, ImaginationLand, MapLight Therapeutics, Spear Bio, Neurogen Biomarking, Quanterix, TauRx, Eli Lilly, Roche, Beckman Coulter, Janssen, Bristol Myers Squibb, ImmunoBrain, Alamar Biosciences, Biogen, and VJDementia.
Your competent? doctor understands these risks AND HAS EXACT PROTOCOLS TO PREVENT THEM, right? Well over a decade to prove competence in creating protocols! Did your doctor succeed?
Summary: A large-scale study has found that severe, hospital-treated infections are significantly associated with an increased risk of dementia. By analyzing nationwide Finnish health registry data of over 374,000 individuals, researchers identified 29 diseases linked to dementia risk—including 27 non-infectious conditions like Parkinson’s and alcohol-related disorders. Crucially, the link between infections (such as urinary tract infections and unspecified bacterial infections) and dementia remained strong even after adjusting for these other 27 health conditions. The researchers suggest that while they cannot yet prove a direct cause-and-effect relationship, severe infections may accelerate underlying cognitive decline in the years leading up to a diagnosis.Independent Risk: Less than one-seventh of the dementia risk associated with severe infections could be attributed to other pre-existing health conditions, suggesting infections are a standalone risk factor.
The Five-Year Window: On average, dementia-related infections occurred 5 to 6 years before a formal dementia diagnosis.
Early-Onset Vulnerability: The link was even stronger for those diagnosed with dementia before age 65, with five types of infections—including pneumonia and dental caries—showing a significant association.
Specific Infection Triggers: Hospital-treated cystitis (UTIs) and bacterial infections of unspecified sites were the most robustly linked to late-onset dementia.
Source: PLOS
Severe infections increase the risk of dementia independently of other coexisting illnesses, according to a new study published March 24th in the open-access journal PLOS Medicine by Pyry Sipilä of the University of Helsinki, Finland, and colleagues.
Severe infections have been linked to an increased risk of dementia. However, it has been unclear whether this association is explained by other coexisting, non-infectious diseases that predispose people to both infections and dementia.
Severe infections requiring hospital treatment were found to occur 5-6 years prior to many dementia diagnoses. Credit: Neuroscience News
In the new study, researchers used nationwide Finnish health registry data covering more than 62,000 individuals aged 65 or older who were diagnosed with late-onset dementia between 2017 and 2020, along with more than 312,000 matched dementia-free controls.
Taking a broad approach, they examined all hospital-treated diseases recorded during the previous twenty years, identifying 29 diseases that were robustly associated with increased dementia risk. Nearly half (47%) of dementia cases had at least one of the 29 identified diseases before their diagnosis.
Of those diseases, two were infections: cystitis (a urinary tract infection) and bacterial infection of an unspecified site. Among the non-infectious diseases, the strongest associations with dementia were seen for mental disorders due to brain damage or physical disease, Parkinson’s disease, and alcohol-related mental and behavioral disorders.
When the researchers then adjusted for all 27 non-infectious dementia-related diseases identified, the association between both infections and dementia remained largely intact. Less than one-seventh of the excess dementia risk among individuals with hospital-treated cystitis or bacterial infections was attributable to pre-existing conditions.
The link between infections and dementia was even stronger for early-onset dementia (diagnosed before age 65), where five types of infection—including pneumonia and dental caries—were associated with elevated risk.
The study was limited by the lack of baseline cognitive assessments and clinical examination data before dementia diagnoses, as well as a lack of data on infection treatments.
“Overall, our findings support the possibility that severe infections increase dementia risk; however, intervention studies are required to establish whether preventing or effectively treating infections yields benefits for dementia prevention,” the authors say.
The authors add, “We found 27 diverse severe, hospital-treated diseases that were robustly associated with an increased risk of dementia. Two of these diseases were infections, namely urinary tract infections and unspecified bacterial infections.”
“In our study, dementia-related infections occurred on average 5 to 6 years before dementia diagnosis. Given that the development of dementia often takes years or even decades, these findings suggest that severe infections might accelerate underlying cognitive decline.
“However, as these findings were observational, we cannot exclude the possibility that some unmeasured confounding factors might also have affected our findings. Thus, we cannot prove cause and effect.”
“Ideally, intervention trials should examine whether better infection prevention helps reduce dementia occurrence or delay the onset of this disease.”
Key Questions Answered:
Q: Does having a minor infection like a cold increase my dementia risk?
A: This study specifically looked at severe, hospital-treated infections. While everyday sniffles weren’t the focus, the data suggests that infections severe enough to require significant medical intervention are the ones linked to future cognitive decline.
Q: Why would a UTI or a tooth infection affect my brain?
A: Researchers believe severe infections cause systemic inflammation. This “biological storm” can cross into the brain, potentially damaging neurons or accelerating the buildup of plaques already present in the early, silent stages of dementia.
Q: Can I lower my dementia risk by treating infections faster?
A: It’s a strong possibility. The researchers are calling for new trials to see if better infection prevention and more aggressive treatment can actually delay or prevent the onset of dementia in high-risk groups.
Editorial Notes:
This article was edited by a Neuroscience News editor.
Journal paper reviewed in full.
Additional context added by our staff.
About this neurology research news
Author: Claire Turner Source: PLOS Contact: Claire Turner – PLOS Image: The image is credited to Neuroscience News
As is, this is useless; the Mediterranean diet has NO SPECIFICS WHATSOVER! So go ask you competent? doctor and hospital for SPECIFICS! Not being able to provide them means your board of directors is so incompetent they can't recognize incompetence in their hospital!
Ask your competent? doctor which one is better for recovery; lucid dreaming or immersive dreaming? Only an incompetent? doctor won't know the answer! Over a decade of incompetence, going for a record, are we? And just to prove the point I bet your doctor hasn't created a sleep protocol for you either!
ummary: New research reveals that the feeling of “deep sleep” depends more on the quality of our dreams than previously thought. While scientists have long believed that slow-wave brain activity was the sole driver of restorative sleep, this study shows that immersive, vivid dreaming actually enhances the subjective feeling of having slept deeply.
By waking 44 participants repeatedly over four nights and analyzing their brain activity (EEG) alongside their dream reports, researchers found that emotionally intense and bizarre dreams were linked to the highest perceived sleep depth. Conversely, abstract, “thought-like” dreams led to a feeling of shallow sleep, suggesting that our internal dream worlds are what truly allow us to feel disconnected and rested.
Key Facts
Beyond Slow Waves: While slow brain waves generally correlate with deep sleep, this relationship weakens when dreaming occurs; the dream itself becomes the primary driver of perceived restfulness.
Vividness Matters: Dreams that are “immersive”—vivid, bizarre, and emotionally intense—are associated with a much deeper subjective sleep experience than reflective or abstract thoughts.
The Disconnection Shield: Researchers suggest that immersive dreaming helps “lock” us into an internal world, keeping us disconnected from the external environment and improving sleep satisfaction.
The “Short Sleep” Mystery: This discovery may explain why some people feel fully rested after only five hours of sleep while others feel exhausted after eight; the quality of the “dream experience” may be the missing variable.
Source: PLOS
Researchers led by Guilio Bernardi at the IMT School for Advanced Studies Lucca in Italy have discovered a key relationship between dreaming and the feeling of having had a good night’s sleep.
Published in PLOS Biology on March 24th, the study shows that the feeling of deep sleep is not determined solely by slow-wave brain activity. Rather, immersive dreaming that comes with increases in wake-like brain activity leads to a greater feeling of deep sleep.
Why is it that sometimes we sleep 8 hours and don’t feel rested, while other times we feel like we had a great night’s sleep after only 5 hours? Research has shown that our feeling of deep sleep is related to a shift from high- to low-frequency brain waves, which is thought to drive unconsciousness.
At the same time, other reports indicate that dream (REM) sleep is also perceived as deep, despite its wake-like brain waves. To better characterize the effects of dream sleep on perceived sleep depth, the researchers analyzed EEG recordings from 44 adults who were repeatedly awoken during non-REM sleep over the course of 4 nights.
Analysis showed that shifts from faster to slower waves were indeed associated with a feeling of deep sleep. However, this relationship weakened when participants reported having had a dream, even if they could not remember the content.
Perceived sleep depth was thus higher after dreaming even though this state is associated with wake-like brain activity. Specifically, vivid, bizarre, and emotionally intense dreams were all associated with subjectively deeper sleep, while abstract, reflective thought-like dreams with meta-awareness were related to more shallow feeling sleep.
These findings are contrary to the longstanding view that the feeling of deep sleep is governed solely by slow brain waves and the depth of unconsciousness, and suggest that perceptually immersive dreaming is what allows us to feel well rested – even if we can’t remember what we dreamed.
The authors add, “We already know that dreaming extends beyond REM sleep and occupies a large portion of the night, yet its function remains unclear. Our study suggests that dreams may help shape how we experience sleep by immersing us in an internal world that keeps us disconnected from the external environment.”
“Understanding how dreams contribute to the feeling of deep sleep opens new perspectives on sleep health and mental well-being. Alterations in dreaming — for example, a reduction in the richness or frequency of dreams — could influence how people perceive their sleep depth or duration, and may contribute to dissatisfaction with sleep quality.”
“This kind of research is extraordinarily demanding. Serial awakening studies require waking participants repeatedly across multiple nights and collecting detailed reports each time. It was only possible thanks to the dedication, resilience, and coordination of an exceptional team of researchers.”
Key Questions Answered:
Q: I never remember my dreams—does that mean I’m not getting deep sleep?
A: Not necessarily. The study found that even if participants couldn’t remember the content of their dreams, simply having had one was enough to increase their feeling of deep sleep. Your brain is likely doing the work behind the scenes!
Q: Why do “weird” dreams make me feel more rested than “normal” ones?
A: Bizarre and intense dreams are more “immersive.” This intensity creates a stronger barrier between you and the outside world, allowing your brain to feel more profoundly “offline” and disconnected from reality.
Q: Can I “train” myself to have better dreams for better sleep?
A: While we can’t fully control our dreams, this research suggests that a reduction in dream richness can lead to sleep dissatisfaction. Focusing on sleep hygiene and mental well-being may help foster the “immersive” states needed for that rested feeling.
Editorial Notes:
This article was edited by a Neuroscience News editor.
Journal paper reviewed in full.
Additional context added by our staff.
About this sleep and dreaming research news
Author: Claire Turner Source: PLOS Contact: Claire Turner – PLOS Image: The image is credited to Neuroscience News
Original Research: Open access. “Immersive NREM2 dreaming preserves subjective sleep depth against declining sleep pressure” by Adriana Michalak, Davide Marzoli, Francesco Pietrogiacomi, Damiana Bergamo, Valentina Elce, Bianca Pedreschi, Giorgia Mosca, Alessandro Navari, Michele Emdin, Emiliano Ricciardi, Giacomo Handjaras, and Giulio Bernardi. PLOS Biology DOI:10.1371/journal.pbio.3003683
A multidisciplinary(Useless big word, you're just trying to make it sound important!), home-based intervention significantly reduced fall rates in community-dwelling stroke survivors, achieving a 33% decrease in falls over 12 months compared with usual care.
Improvements in mobility, balance, self-efficacy, and community participation suggest that tailored exercise, home hazard reduction, and goal-directed coaching can meaningfully enhance recovery and safety for ambulatory post-stroke patients.
The findings were published in the BMJ.
“More than twice as many people with stroke have falls compared with the general older population, and they are also likely to be repeat fallers,” said lead author Lindy Clemson, University of Sydney, Sydney, Australia. “Falls after stroke can lead to serious injury and hospitalisation, delaying recovery and rehabilitation, and jeopardising long-term health and wellbeing. The decrease we saw in the rate of falls among people receiving the active intervention program was underpinned by worthwhile improvements in their mobility, balance, community participation, and self-efficacy.”
The study enrolled 370 adults aged >50 years who were within 5 years of a stroke and able to walk 10 metres with or without an aid. Participants were randomised to either usual care or a 6-month, 3-part intervention program delivered by a physiotherapist and an occupational therapist working together, via a series of 10 home visits and follow-up phone calls. The individualised program encompassed 3 components: (1) habit-forming exercise to improve balance and strength, embedded into daily activities, based on the Lifestyle integrated Functional Exercise (LiFE) program; (2) fall hazard reduction focused on adapting the home environment and encouraging protective behaviours to reduce risk; and (3) coaching participants towards a goal for mobility outside the home, such as walking in the park, a shopping trip or using public transport.
After 12 months, the intervention group experienced a 33% reduction in the rate of falls compared with usual care (P = .02). While the proportion of participants experiencing a fall did not differ significantly, those in the intervention group showed meaningful improvements in self-efficacy, mobility, balance, and community participation, indicating enhanced confidence and functional independence.
“By focusing on stroke survivors living in their communities and testing an intervention delivered in the home, we’ve ensured the intervention reflects something that can readily be implemented,” Catherine M. Dean, Macquarie University, Sydney, Australia. “We believe our world-first finding could help reduce the global burden of falls after stroke.”
While
nature’s mental health benefits are well-documented, the specific
effects of birdwatching remain underexplored. This study addresses this
gap by examining the mental health benefits of a combined birdwatching
and preparatory education compared to nature walks through a randomized
controlled trial with 170 urban participants in Iran. The birdwatching
group engaged in educational birdwatching sessions and a full-day
birdwatching trip, while another group participated in general nature
walks. Anxiety and stress reductions were significantly greater in the
birdwatching group compared to participants who went on nature walks.
However, there was no significant difference in depression scores
between the groups. Participants with higher baseline distress and male
participants showed more pronounced improvements. These findings suggest
that birdwatching offers unique benefits as a mental health
intervention in urban settings, particularly for reducing anxiety and
stress, with further research needed to explore its long-term impacts.
Do you
prefer your doctor, hospital and board of director's incompetence NOT
KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand
action!
Some people with the gene did not have expected outcomes if they were heavy meat-eaters
Key Takeaways
Higher meat intake was tied to better cognitive outcomes and lower dementia risk in people with certain genetic risk for Alzheimer's disease in a cohort study.
This association was seen in people with APOE3/4 and APOE4/4 genotypes, but not in those with lower genetic risk.
Regardless of genotype, consuming more processed meat was associated with increased dementia risk.
People with a genetic risk for Alzheimer's disease did not have an expected increase in cognitive decline or dementia if they consumed relatively large amounts of meat, a Swedish cohort study showed.
Higher total meat consumption -- comparing the top and bottom quintiles -- was tied to better-than-expected cognitive trajectories (β=0.32, P=0.01) and reduced dementia risk (subdistribution HR 0.45, P=0.04) in people who were either APOE4 homozygotes (APOE4/4) or had one APOE3 and one APOE4 allele (APOE3/4), said Jakob Norgren, PhD, of the Karolinska Institute in Huddinge, and colleagues.
This association was not seen in people who had less genetic Alzheimer's risk, the researchers reported in JAMA Network Open.
"These findings suggest that higher meat consumption than conventionally recommended may be associated with benefits in a genetically defined subgroup comprising approximately one-quarter of the global population," Norgren and co-authors wrote.
Regardless of APOE genotype, a higher ratio of processed meat to total meat was unfavorably associated with dementia risk (subdistribution HR 1.14, P=0.04). There was no substantial difference between unprocessed red meat and poultry. In post-hoc analyses, all-cause mortality was lower in APOE3/4 and APOE4/4 carriers who ate more unprocessed meat.
When meat consumption was analyzed in relation to other food groups, the favorable associations in people with APOE3/4 or APOE4/4 genotypes were strongest when meat replaced cereals, Norgren told MedPage Today.
"The study shows that different subgroups of the population can respond very differently to the same diet," he said. "It suggests that the potential for dementia prevention through lifestyle changes may be greater than previously thought -- if future research confirms these findings and allows us to develop more individualized recommendations."
While the outcomes may seem surprising, they align with patterns observed in two large cohort studies, the researchers said.
"Viewed alongside reinterpreted evidence from the Nurses' Health Study and U.K. Biobank focusing on unprocessed meat, these findings point to a consistent gene-diet interaction, with important implications for public health," Norgren and co-authors wrote.
In the U.K. Biobank study of 494,000 participants, unprocessed red meat was inversely associated with dementia (P=0.01), which was driven by APOE4 carriers. In the Nurses' Health Study, supplementary analyses showed an APOE4 interaction (P<0.001) for unprocessed red meat. These patterns were not emphasized in the original publications, Norgren and colleagues noted.
Apolipoprotein E is essential for transporting cholesterol and fats in the brain and blood. The protein is encoded by the APOE gene, which has three main variants: epsilon 2, 3, and 4. All people have two APOE genes, leading to six possible combinations. The APOE3 variant is most common.
People carrying at least one APOE4 allele have a higher risk of Alzheimer's disease compared with APOE3/3 carriers; people with two APOE4 alleles have the highest risk. The APOE2 allele is associated with lower Alzheimer's risk.
The oldest variant is APOE4, which may have arisen during a period when evolutionary ancestors ate a more animal-based diet, while APOE3 emerged around the same time as modern humans, Norgren observed.
"Our findings are consistent with the idea that these variants may have evolved under different dietary conditions -- but this is still speculative, and we can't say whether diet drove the genetics or vice versa," he said.
The researchers studied participants in the Swedish National Study on Aging and Care-Kungsholmen (SNAC-K), an ongoing population-based study of older adults near Stockholm. The mean age of the cohort was 71, and 62% were women. Participants had repeated dietary assessments and cognitive evaluations for up to 15 years.
Among 2,157 participants without dementia, 1,680 had longitudinal cognition data and 569 had APOE3/4 or APOE4/4 genotypes. During follow-up, 296 people developed dementia, and 690 died without dementia.
Median consumption in the highest quintile of meat intake was 869 g/week, standardized for a 2,000 kcal/d diet, while meat consumption in the lowest quintile was 247 g/week.
The study has several limitations including potential survival bias, the researchers acknowledged. Ethnic ancestry was predominantly Northern European, which may limit generalizability. Self-reported dietary data may include errors.
"This is still a relatively new area of research, and the findings should be interpreted with caution," noted Jacqui Hanley, PhD, of Alzheimer's Research U.K., who was not involved with the study.
"Studies like this can spot links between eating meat and dementia risk but cannot prove whether it is the cause," she wrote on the U.K. Science Media Centre website. "More research is needed before suggesting that specific foods can determine whether someone will develop the condition."
Judy George covers neurology and neuroscience news for MedPage Today, writing about brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy, autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep, pain, and more. Connect:
Disclosures
SNAC-K data collection is supported by the Swedish Ministry of Health and Social Affairs, county councils and municipalities, and the Swedish Research Council.
Norgren was funded by the Swedish Alzheimer Foundation and the Swedish Dementia Foundation. Co-authors reported relationships with BioArctic AB, Eli Lilly, Eisai/BioArctic, and Novo Nordisk.
