Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 32,632 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.
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.
With ANY BRAINS AT ALL in our stroke medical 'professionals' we could do research that tells us exactly what interventions work to stop the neuronal cascade of death in the first week! Putting the brain on a chip with brain organoids and this and we could solve a lot of stroke recovery questions. But nothing will occur; OUR 'PROFESSIONALS' ARE FUCKING INCOMPETENT!
Imagine what brain surgeons could do with a three-dimensional (3D)-printed model of the brain. Not a structural model printed in plastic and uniform throughout, but one that mirrors the heterogeneity of real human brain tissue — its mechanical, thermal, and electromagnetic properties.
Christopher O’ Bryan, PhD, MS
“If somebody has a brain tumor, you could take an MRI of their brain and make a 3D model from it that includes the tumor, and then practice surgery on that model,” said Christopher O’ Bryan, PhD, MS, assistant professor of mechanical and aerospace engineering at the University of Missouri (UM) in Columbia, Missouri. “You could learn how sound, electromagnetic waves, or physical insults interact with the brain to better understand concussions and traumatic brain injury.”
A scaled-down 3D model of the brain, about 15% of a real brain’s size.
O’Bryan and colleagues in UM’s College of Engineering recently published a study in the journal Materialia describing how the researchers designed a unique 3D printer ink made from a modified polymer — called a photo-crosslinkable poly(vinyl alcohol) methacrylate polymer — and then used it to print a scaled-down 3D model of the brain, about 15% of a real brain’s size. The scientists relied on a method called embedded 3D printing, crosslinking the polymer in a microgel bath, to achieve a model that mimicked the soft tissue and the structural complexities of a real human brain.
How They Did It
To provide a broader picture of why they conducted the study, O’Bryan described his lab’s goals. “The focus areas in our lab include the designing of soft materials, the testing of these materials, and then how to actually manufacture things out of these soft materials. And that’s especially challenging when you take into account that most soft materials are hydrogels and biopolymers which start out in a liquid phase ,” he said.
Researchers used embedded 3D printing, crosslinking the polymer with a gel bath to mimic brain tissue.
The researchers’ embedded 3D printing approach uses “sacrificial support baths,” jelly-like baths, which act as a supportive matrix during the printing phase. “What this allows us to do is to print materials as liquids and keep them as liquids until we’ve completely printed our structure, and then we crosslink the printed structure using heat or UV [ultraviolet] light to make it solid. Then we take it out of the gel bath, and it’s become a soft, deformable structure — meaning it can change shape when a force is applied,” O’Bryan said.
With your extra risk of dementia post stroke will your competent? doctor use this to validate that their EXACT DEMENTIA PREVENTION PROTOCOLS WILL BE USED?
Your risk of dementia, has your doctor
told you of this? Your doctor is responsible for preventing this! Is
s/he willing to prevent this?
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!
An EEG-derived brain age index predicted dementia risk across five cohorts.
Each 10-year increase in the brain age index was linked with a 39% higher dementia risk.
The findings indicate that the predictive value of the index should be further assessed, the researchers said.
A brain age index based on microstructures of sleep electroencephalography (EEG) data predicted dementia risk, a meta-analysis showed.
Across five cohorts and 7,105 participants, each 10-year increase in the EEG-derived index was tied to a 39% higher risk of dementia (HR 1.39, 95% CI 1.21-1.59, P<0.001) after adjusting for covariates, reported Yue Leng, PhD, of the University of California San Francisco, and co-authors.
The relationship remained significant after adjusting for comorbidities and apnea-hypopnea index scores (HR 1.31, P<0.001) and APOE4 gene status (HR 1.22, P=0.03), the researchers wrote in JAMA Network Open. Links were consistent across sex and age groups.
"Sleep gives us a unique window into the brain. This study shows that we can use brain activity during sleep to estimate how the brain is aging," Leng told MedPage Today.
"Sleep isn't just rest; it reflects how well the brain is functioning and maintaining itself," she said. "By turning sleep EEG into a measure of 'brain age,' we may be able to detect risk of dementia earlier and more easily."
The brain age index captures the difference between sleep EEG-based brain age and chronological age, Leng and colleagues noted, with negative values indicating a younger brain age and positive values reflecting an older one. The index incorporated 13 microstructural features of brain waves from EEG recordings of overnight, home-based polysomnography.
Earlier work has linked sleep macrostructure -- like sleep efficiency or time spent in certain sleep stages -- to dementia risk, but results have been inconsistent.
This study "advances the field by shifting attention from macrostructure to EEG microstructure (i.e., spectral power in specific bands, spindle and slow oscillation characteristics, and waveform properties across sleep stages)," observed Omonigho Bubu, MD, PhD, MPH, of the NYU Grossman School of Medicine in New York City, in an accompanying editorial.
"What makes this work particularly compelling is that brain age index is a general marker of neurophysiologic aging, developed in an independent cohort and then tested, prospectively, against dementia outcomes," Bubu wrote. "That design enhances its plausibility as a robust marker of accelerated brain aging, rather than an overfitted prediction tool."
Dementia research is moving toward combining genetic information, blood biomarkers, imaging, and cognitive testing into integrated risk assessments, Bubu pointed out. "Within this landscape, sleep EEG-based brain age index occupies a distinctive niche as it reflects real-time brain physiology, relies on widely used clinical technology, and condenses complex neural information into an interpretable brain age," he added.
For their individual participant data meta-analysis, Leng and co-authors pooled information from five community-based longitudinal cohorts: the Multi-Ethnic Study of Atherosclerosis (MESA; 1,802 participants), the Atherosclerosis Risk in Communities (ARIC; 1,796 participants) study, the Framingham Heart Study-Offspring Study (FHS-OS; 617 participants), the Osteoporotic Fractures in Men Study (MrOS; 2,639 participants), and the Study of Osteoporotic Fractures (SOF; 251 participants).
Participants' average ages at the time of the sleep study ranged from 59.5 to 82.7 years, and more than 90% were cognitively normal. The primary outcome for the pooled analysis was incident dementia, with death treated as a competing risk.
Over follow-up, 1,088 people developed dementia, with a median time to dementia ranging from 3.6 to 16.9 years.
The findings highlight the need to evaluate the predictive value of the brain age index as a digital marker for early dementia detection in community settings, the researchers said.
The five cohorts included in the study differed in population characteristics, data collection methods, dementia ascertainment, and follow-up times, which may have introduced heterogeneity and potential bias, they acknowledged. Only death was used as a competing risk, but other life events may affect follow-up or dementia ascertainment, they added. The analysis is observational and a causal relationship between brain age index and dementia can't be inferred.
"Moreover, as a composite measure, brain age index itself is not a plausible therapeutic target," Leng and colleagues wrote. "Rather, brain age index should be viewed as a prognostic marker for future dementia risk."
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 work was supported by grants from the National Institute on Aging.
Leng reported receiving grants from the NIH and serving on the advisory board of ResMed.
Co-authors reported relationships with GLG Councils, Guidepoint, MyCardio, the Alliance of Sleep Apnea Partners, SleepHealth, the NIH, Google, Axsome, Eli Lilly, and Beacon Biosignals.
Bubu reported relationships with the ResMed medical advisory board, the NIH, the Alzheimer's Association, the Michael J. Fox Foundation, CurePSP, and the BrightFocus Foundation.
More useless blathering from our fucking failures of stroke associations. Until 100% recovery is the only thing talked about, why don't you retreat to the locker room and let real leaders solve stroke? NOTHING ON 100% RECOVERY! Get back to survivors when you've actually left stroke! Because you are absolute pieces of shit! You're not 'in the arena', so get the hell out!
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(This is you; ASA and WSO). 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.
Research roundtable highlights early detection, biomarkers, interventions
An earlier diagnosis and intervention strategy for Alzheimer's disease is on the horizon, signaling a need to overhaul current detection methods and patient care protocols, experts at the Alzheimer's Association Research Roundtable (AARR) said.
"Advances in biomarker technology, digital cognitive assessments, and amyloid-targeting therapies have redefined the opportunities for accurate and early diagnosis and care of Alzheimer's disease," reported Christopher Weber, PhD, of the Alzheimer's Association in Chicago, and co-authors in Alzheimer's & Dementia: Translational Research & Clinical Interventions.
These advances create new possibilities to intervene before the onset of cognitive impairment, Weber and colleagues wrote. Targeting the earliest stages of Alzheimer's, Weber said, "is similar to how doctors treat other diseases like heart disease and some cancers, where early detection and prevention are key parts of care."
Alzheimer's disease often remains undiagnosed until significant memory loss and functional decline have occurred, observed co-author Suzanne Schindler, MD, PhD, of Washington University School of Medicine in St. Louis. "This means that patients and care partners don't get a diagnosis until later in the disease, after the window when interventions are most helpful and patients can make truly independent decisions," she told MedPage Today.
In 2024, an Alzheimer's Association workgroup established new biologically-based criteria for Alzheimer's, incorporating biomarker classifications and a revamped disease staging system. This approach recognized Alzheimer's disease as a process detectable by abnormal biomarkers, even without cognitive symptoms.
The shift wasn't without controversy. A diagnosis based on biomarkers without symptoms sparked debate among clinicians, some of whom argued there may be potential harms to redefining Alzheimer's disease.
In spring of 2025, the AARR convened academic, industry, clinical, and government experts to discuss how to identify and treat people in Alzheimer's earliest stages. "This meeting and paper reviewed the state of the field and areas that need further work, especially if treatments for asymptomatic Alzheimer's are approved in the near future," Schindler said.
Earlier detection brings a set of complex issues, from identifying who's at highest risk and navigating treatment decisions to clear, compassionate communication with patients and families, the AARR said. Stigma and ethical concerns will need to be addressed. Economic, social, and policy factors will need to be considered.
While plasma biomarkers offer hope for broad applications in the clinic, tests must be rigorously validated, the AARR emphasized. Primary care clinicians, who will be on the front lines, will need enhanced tools, training, and support.
Two anti-amyloid therapies currently are approved to treat Alzheimer's patients with mild symptoms -- lecanemab (Leqembi) and donanemab (Kisunla). The AHEAD 3-45 trial of lecanemab and the TRAILBLAZER-ALZ 3 study of donanemab are now testing these drugs in people with biomarker evidence of Alzheimer's who are cognitively intact. "If these studies are successful, it could change how doctors manage the disease," Weber said.
If the trials are successful, it also may create new challenges, noted Eric Widera, MD, of the University of California San Francisco, who was not part of the AARR.
"We struggle currently for people diagnosed with mild cognitive impairment and mild dementia, whether the current treatments equate to a meaningful difference when we see a small but statistically significant difference in the Clinical Dementia Rating-Sum of Boxes," Widera told MedPage Today. "It will be so much more complicated in cognitively unimpaired individuals as it's such a larger population that it will apply to, the measures being studied are not generally outcomes patients truly care about, and it's unclear what a meaningful difference is in these measures."
The consensus that Alzheimer's starts years before symptoms appear has refocused dementia prevention strategies, the AARR pointed out. "Doctors need to learn more about how Alzheimer's disease starts many years before symptoms begin, and also about preventive interventions -- from exercise to hearing aids -- that may reduce the risk of cognitive impairment," Schindler said.
"Research studies, including the U.S. POINTER trial, show that healthy habits with structure and accountability can improve thinking and support brain health in older adults at risk for cognitive decline," Weber added.
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 report was supported by the Alzheimer's Association and other groups.
Weber is an employee of the Alzheimer's Association.
Schindler reported serving on scientific advisory boards of biomarker testing and clinical care pathways for Eisai and Novo Nordisk and receiving consultancy/speaking fees for biomarker testing presentations from Eisai, Eli Lilly, and Novo Nordisk.
Co-authors disclosed relationships with nonprofit groups and industry; several were employed full time by pharmaceutical companies.
Widera had no conflicts of interest.
Primary Source
Alzheimer's & Dementia: Translational Research & Clinical Interventions
