Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 32,278 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.
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.
Saturday, February 14, 2026
Factors Influencing Adherence to Home-Based Exercise Rehabilitation in Stroke Patients from a Temporal Perspective: An Explanatory Sequential Mixed-Methods Study
You're that fucking clueless that you UNDERSTAND NOTHING ABOUT SURVIVOR MOTIVATION! My god, I'd have you all fired for stupidity!
My conclusion is you don't understand ONE GODDAMN THING ABOUT SURVIVOR MOTIVATION/DEMORALIZATION, DO YOU? You create EXACT 100% recovery protocols, and your survivor will be motivated to do the millions of reps needed because they are looking forward to 100% recovery. I'd fire all of you for absurd incompetence! GET THERE!
Here's my email: oc1dean@gmail.com Tell me EXACTLY where I'm wrong! Difficulty in getting to those protocols will not be tolerated as an excuse. You've known of this problem of 100% recovery since your education, so you've had years if not decades to work on it! Comeuppance is going to be a bitch when you are the 1 in 4 per WHO that has a stroke? Then you just might want 100% recovery. Or you can be like me where half my life will be disabled!
Factors Influencing Adherence to Home-Based Exercise Rehabilitation in Stroke Patients from a Temporal Perspective: An Explanatory Sequential Mixed-Methods Study
Authors Shao J , Cong S, Han Y, Xu W, Wang Q, Zhang J, Wei X, Ren R
Received 17 November 2025
Accepted for publication 30 January 2026
Published 13 February 2026 Volume 2026:20 Pages 1—18
DOI https://doi.org/10.2147/PPA.S582280
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Johnny Chen
Jianing Shao,1,2,* Sunling Cong,3,* Yuxin Han,1,2 Wenjin Xu,1 Qing Wang,4 Jiachen Zhang,3 Xiaoxiao Wei,1,2 Rui Ren1,2
1Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, People’s Republic of China; 2School of Nursing, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, People’s Republic of China; 3School of Medicine, Jiangsu University, Zhenjiang, Jiangsu, People’s Republic of China; 4Department of Nursing, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Qing Wang, Department of Nursing, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, People’s Republic of China, Email ruoyiwangqing@163.com
Purpose: This study aimed to examine the factors influencing the adherence of stroke patients to home-based exercise rehabilitation and to elucidate the potential driving mechanisms of temporal perspective on rehabilitation adherence.
Patients and Methods: This study employed a sequential, explanatory, and mixed-methods design. In the quantitative phase, a questionnaire survey was conducted among 289 stroke patients from January 2025 to May 2025 using convenience sampling. In the qualitative phase, 16 stroke patients were selected from the quantitative sample through purposive and maximum variation sampling to explain and supplement the quantitative findings using semi-structured interviews.
Results: Quantitative analysis demonstrated a significant positive correlation between temporal perspective and rehabilitation adherence, with rehabilitation intention partially mediating this relationship. Behavioral advantage exerted a negative moderating effect on the intention–adherence pathway, whereas the moderating effect of self-regulation ability did not reach statistical significance. Qualitative analysis identified four main themes: consistency belief, time-bound potency, behavioral advantage, and self-regulation ability.
Conclusion: Temporal perspective is an important driver of adherence to home-based rehabilitation among stroke patients. As rehabilitation habits develop, behavioral patterns gradually shift from being “intention-driven” to becoming “automatic habits”, thereby weakening the direct driving effect of intention. Given the potential presence of latent executive dysfunction in stroke patients, targeted assessment tools and intervention strategies should be developed to bridge the gap between intention and behavior.
Stroke survivors trial new at-home tech: 'It's given me my freedom back'
Your competent? doctor knew about non-invasive vagus nerve stimulation years ago, right? Oh no, you have a fuckingly incompetent doctor, don't you! And your incompetent president and board of directors haven't fired those incompetents yet!
Earlobe Clip-On Attenuates POTS - Vagus Nerve Stimulation May 2023
The latest here: Why do this research at all? Didn't the previous one provide a protocol on its' use? NO? They were fuckingly incompetent in not providing a protocol and the mentors and senior researchers haven't been fired yet!
Examples must be made and these incompetent persons must be fired, eliminating a lot of dead wood!
Stroke survivors trial new at-home tech: 'It's given me my freedom back'
New Drug Target Could Freeze Alzheimer’s in Its Tracks
Will your competent? doctor and hospital ensure enough research is produced to create EXACT PROTOCOLS on this?
New Drug Target Could Freeze Alzheimer’s in Its Tracks
Summary: Researchers discovered a powerful new drug target that could revolutionize how we treat Alzheimer’s disease. By focusing on an enzyme called IDOL, researchers found they could substantially reduce the buildup of toxic amyloid plaques in the brain.
Unlike current treatments that primarily focus on clearing existing plaques, targeting IDOL in neurons also lowers levels of the APOE protein—the strongest genetic risk factor for the disease—and boosts the brain’s natural resilience to cognitive decline. This multi-pronged approach not only clears the “trash” from the brain but also strengthens the connections between neurons, offering hope for a more effective way to freeze the disease’s progression.
Key Facts
- Targeting Neuronal IDOL: Removing the IDOL enzyme from brain neurons significantly reduces amyloid plaque load and improves communication between nerve cells.
- Resilience Booster: Deleting this enzyme increases the levels of receptors that regulate lipid metabolism, which has been shown to provide cognitive resilience even in patients with high plaque levels.
- APOE Reduction: The study found that targeting IDOL also lowers levels of APOE, the protein variant (APOE4) that serves as the most significant risk factor for late-onset Alzheimer’s.
Source: Indiana University
Indiana University School of Medicine scientists have identified a promising drug target for Alzheimer’s disease.
The team found that removing an enzyme from neurons in the brain substantially reduces amyloid plaques — a hallmark characteristic of the disease — and may provide further resilience against disease progression.
Over the past few years, the U.S. Food and Drug Administration has approved two disease-modifying drugs to treat Alzheimer’s disease. The drugs, lecanemab and donanemab, remove the buildup of amyloid plaques in the brain and can “freeze” a person in their current functional state.

In the study, published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, the researchers generated two different animal models of Alzheimer’s disease by deleting the IDOL gene in the brain from either within neurons or microglia, the brain’s immune cells.
Karahan, assistant research professor of medical and molecular genetics, said they expected microglia to be the major driver of removing amyloid plaques because immune cells are key players in clearing amyloid and are the main cell type that produces IDOL in the brain.
Deletion of IDOL neurons not only reduced plaques, Karahan said, but it also reduced levels of a protein called apolipoprotein E, or APOE, that is associated with Alzheimer’s disease; one of the protein’s variants, APOE4, is the strongest risk factor for late-onset Alzheimer’s disease. APOE also plays a critical role in lipid metabolism, Karahan said.
The team also discovered that levels of receptors that can regulate APOE and amyloid plaques in the brain increased when the enzyme was removed from neurons.
These receptors have a critical role in lipid metabolism and healthy neuronal communication. Karahan said a recent study shows that activating a pathway, which is also regulated by these receptors, provides resilience to cognitive decline in Alzheimer’s patients who have high amounts of plaques.
“This is especially important from a clinical perspective because patients are usually diagnosed with the disease after accumulating substantial amyloid plaque load in the brain. Not only decreasing amyloid levels but also increasing resilience to these pathological changes could maximize clinical benefits,” Karahan said.
“Targeting neuronal IDOL may offer multiple therapeutic benefits in Alzheimer’s disease by simultaneously reducing amyloid burden while enhancing neuroprotective effects.”
Kim said the team will next work on a few strategies targeting the enzyme to develop drugs for treating Alzheimer’s disease, adding it’s important to assess the safety of compounds and their functional effects in preclinical models. Kim said they’ll also determine whether IDOL inhibition preserves synaptic connections and mitigates tau pathology in Alzheimer’s disease.
Key Questions Answered:
A: While current drugs like lecanemab and donanemab focus on clearing existing plaques, targeting the IDOL enzyme does something extra: it builds resilience. It’s like not only taking out the trash but also upgrading the building’s security system. By improving lipid metabolism and neuronal communication, this method helps the brain stay functional even if some plaques remain.
A: APOE4 is the strongest genetic risk factor for Alzheimer’s. This study discovered that removing the IDOL enzyme naturally lowers APOE levels. By hitting both the plaques and the underlying genetic risk protein simultaneously, researchers may have found a way to attack the disease from two sides at once.
A: That’s the goal. Because IDOL is an enzyme with a well-defined “pocket” where a drug can attach, it is a perfect candidate for drug development. Scientists are now working on molecules that can block this enzyme’s activity, which could eventually lead to a treatment that is more precise and has fewer side effects than current options.
Editorial Notes:
- This article was edited by a Neuroscience News editor.
- Journal paper reviewed in full.
- Additional context added by our staff.
About this Alzheimer’s disease and neuropharmacology research news
Author: Rory Appleton
Source: Indiana University
Contact: Rory Appleton – Indiana University
Image: The image is credited to Neuroscience News
Can Brain Speed Training Delay Dementia? 20-Year Medicare Study Results
Will your doctor GUARANTEE NOT GETTING DEMENTIA by doing this? You are at a high risk of dementia.
I bet your fuckingly incompetent stroke medical 'professionals' DID NOTHING WITH THIS: 9+ years of incompetence and still has a job. Boy, your board of directors is a shitworthy piece of world class incompetence!
One particular type of brain training exercise cut the long-term risk of dementia by 29% November 2017
The latest here:
Can Brain Speed Training Delay Dementia? 20-Year Medicare Study Results
Key Takeaways
- Speed-of-processing training with booster sessions was tied to a lower dementia risk over a 20-year period.
- Memory and reasoning training did not show significant associations with reduced dementia risk.
- The findings provide support for developing and refining cognitive training interventions for older adults.
A subset of people who had one of three interventions in the ACTIVE trial had a reduced risk of dementia over a 20-year follow-up period, an analysis of Medicare claims showed.
Older adults in the ACTIVE trial were randomized to training in processing speed, memory, or reasoning. Those who received memory or reasoning training trended toward lower rates of dementia diagnoses over 20 years compared with controls, but the results were not significant, reported Marilyn Albert, PhD, of Johns Hopkins School of Medicine in Baltimore, and co-authors.
Only a subgroup of people who received both speed training and subsequent booster sessions had a long-term association with dementia diagnoses (HR 0.75, 95% CI 0.59-0.95), the researchers said in Alzheimer's & Dementia: Translational Research & Clinical Interventions.
Speed-trained participants who did not have booster sessions did not have a lower risk of dementia.
"The fact that the memory or reasoning trainings did not show statistical significance in any of the analyses presented here was somewhat surprising," Albert and colleagues wrote.
Speed training was adaptive and increased in difficulty with performance; the other trainings were not, they noted. "It is possible that this led to broader brain activation, contributing to the differential findings between the intervention arms," the researchers observed.
"The findings reported here suggest that moderate cognitive training could delay the onset of dementia over subsequent years," said Richard Hodes, MD, director of the National Institute on Aging (NIA), which funded the research.
While more research needs to be done, "this promising lead may move the field further into developing effective interventions to delay or prevent onset of dementia," Hodes said in a statement.
In 1999, the ACTIVE trial randomized 2,832 older adults with a mean age of 74 to a no-contact control group or to 10 sessions of memory, reasoning, or processing speed training over 5 to 6 weeks. Half of participants who completed the training were randomly chosen to have booster sessions 11 and 35 months later.
The trial was completed in 2010. Each intervention maintained effects on its specific targeted cognitive ability through 5 years. Memory training effects were no longer present at 10 years.
In the current analysis, Albert and colleagues linked 2,021 trial participants -- representing 72.1% of the original ACTIVE sample -- to Medicare claims records through 2019, excluding Medicare Advantage beneficiaries. During the 20-year follow-up period, 77% of the ACTIVE trial population died at a mean age of 84.
The primary outcome of this analysis was a diagnosis of Alzheimer's disease or related dementia that appeared in Medicare claims. Dementia diagnoses were not adjudicated.
Overall, 48.7% of participants in the control arm (239 of 491 people) had a Medicare claim for dementia, compared with 39.77% of participants who received both speed training and booster sessions (105 of 264 people).
Missing data and mortality were likely sources of bias in this study, pointed out Baptiste Leurent, PhD, of the UCL Department of Statistical Science in London, who wasn't involved with the research.
"None of the primary analyses found significant differences in dementia risk between the training groups and the control group. Although one subgroup analysis produced a significant result, this single finding is not generally regarded as strong enough evidence to demonstrate the intervention's effectiveness," Leurent wrote on the U.K. Science Media Centre website.
"Diagnoses were identified through health records rather than specialist clinical testing, so we do not know whether this training changed the underlying diseases that cause dementia or affected specific types of dementia," added Susan Kohlhaas, PhD, of Alzheimer's Research U.K. in Cambridge, England.
Still, the results may hold promise, the study authors said. "Our findings provide support for the development and refinement of cognitive training interventions for older adults, particularly those that target visual processing and divided attention abilities," noted co-author George Rebok, PhD, of the Johns Hopkins Bloomberg School of Public Health, in a statement.
"It is possible that adding this cognitive training to lifestyle change interventions may delay dementia onset, but that remains to be studied," Rebok said.
Novel Arm Therapy May Shift Stroke Rehab Focus
WOW! Proving once again that stroke medical 'professionals' don't keep current in research in their field. I'd fire everybody here for incompetence!
Exactly how is your competent? doctor using good side therapy to get you recovered! Oh, NOTHING AT ALL? Because doesn't even know about it? Incompetent for well over a decade!
Novel Arm Therapy May Shift Stroke Rehab Focus
Ipsilesional arm training improves motor function in chronic stroke survivors with severe paresis
Published on Feb. 13, 2026
Got story updates?Submit your updates here. ›
A small randomized clinical trial found that targeted therapy of the ipsilesional, or 'good' arm, improved motor function, including control and speed, in chronic stroke survivors with severe contralesional arm weakness. This is the first study to use a rigorous design to investigate ipsilesional limb training in this population, challenging the traditional rehabilitation focus on the contralesional arm.
Why it matters
Individuals with severe contralesional paresis depend almost entirely on their ipsilesional arm for daily activities, yet these impairments remain amenable to improvement even years after a stroke. This study suggests that targeting the ipsilesional arm could lead to sustained motor improvements and more efficient activities of daily living for chronic stroke survivors with severe hemiparesis.
The details
The phase 2 randomized clinical trial included 53 participants with chronic stroke and severe contralesional arm weakness. The ipsilesional therapy group received virtual reality-based motor training and real-world dexterity exercises focused on speed, accuracy, and coordination. The contralesional therapy group received traditional approaches like proximal strength training and mirror therapy. At the first post-treatment assessment, the ipsilesional group completed a standardized dexterity test 5.87 seconds faster than the contralesional group, a 12% improvement from baseline. These gains were sustained at 3-week and 6-month follow-ups.
- The study was published online on February 2, 2026 in JAMA Neurology.
- Participants were assessed before the start and end of the 5-week, 15-session trial, as well as 3 weeks and 6 months after the trial concluded.
The players
Carolee Winstein
Professor emerita and adjunct faculty, Division of Biokinesiology and Physical Therapy, University of Southern California, in Los Angeles, and study co-author.
Robert Sainburg
Dorothy F. and J. Lloyd Huck Distinguished Chair in Kinesiology and Neurology at Penn State in University Park, Pennsylvania, and study co-author.
What they’re saying
“This is the first project to use a rigorous randomized clinical trial design to investigate the use of ipsilesional limb training — training the less-impaired arm — in chronic stroke survivors with severe paresis.”
— Carolee Winstein, Professor emerita and adjunct faculty, Division of Biokinesiology and Physical Therapy, University of Southern California (News release)
“We're changing the function of the less-impaired hand so that their activities of daily living can be more efficient.”
— Robert Sainburg, Dorothy F. and J. Lloyd Huck Distinguished Chair in Kinesiology and Neurology at Penn State (News release)
What’s next
Future research should explore integration of ipsilesional training with home-based practice and combined bilateral approaches that optimize recovery and independence.
The takeaway
This study suggests that targeting the ipsilesional, or 'good' arm, could lead to sustained motor improvements and more efficient daily activities for chronic stroke survivors with severe hemiparesis, challenging the traditional rehabilitation focus on the contralesional arm.
Coffee and Tea May Protect Against Dementia but Hold the Decaf
Really? You don't read research!
How Coffee May Protect Brain Health: A New Study Suggests The Benefits Aren't Just From Caffeine December 2018
The latest here:
Coffee and Tea May Protect Against Dementia but Hold the Decaf
Regular consumption of coffee and tea was associated with a lower risk for dementia and modest improvements in cognitive performance, independent of a person’s genetic predisposition, a new study showed.
Results from two large cohorts showed that the benefits were strongest among those with a daily intake of about 2-3 cups of caffeinated coffee or 1-2 cups of tea. These associations remained consistent even when accounting for high-risk genetic factors, including APOE4 genotype and Alzheimer’s disease polygenic risk scores.
“The overall patterns were broadly similar across genetic risk groups, suggesting these behaviors may be relevant across genetic risk levels — not only among people at lower genetic risk,” lead study author Yu Zhang, MBBS, MS, Channing Division of Network Medicine, Brigham and Women’s Hospital and Harvard Medical School, Harvard University, Boston, told Medscape Medical News.
The study was published online on February 9 in JAMA.
Coffee, Tea, and Dementia: What’s the Link?
Coffee and tea contain caffeine as well as bioactive compounds such as polyphenols, catechins, and chlorogenic acid, which may reduce oxidative stress, protect vascular function, and mitigate cellular damage in the brain.
Previous research has suggested that caffeine and coffee consumption may protect against cognitive decline and dementia, but many studies dichotomized intake levels and did not examine dose-response relationships. Few have been able to distinguish between caffeinated and decaffeinated beverages, and evidence regarding tea consumption has been mixed.
In this new prospective cohort study, researchers sought to clarify these relationships using repeated, detailed dietary assessments across two independent cohorts.
Participants in the National Health Service (NHS) (n = 86,606 women; mean age at baseline, 46.2 years) and the Health Professionals Follow-up Study (n = 45,215 men; mean age at baseline, 53.8 years) completed repeated food frequency questionnaires every 2-4 years to assess caffeinated and decaffeinated coffee and tea intake.
Participants with major chronic diseases at baseline or significant changes in coffee intake were excluded to reduce confounding.
Objective cognitive function was measured in the NHS cohort using the Telephone Interview for Cognitive Status (TICS), verbal memory tests, and a composite global z score. Subjective cognitive decline was assessed in both cohorts through questionnaires covering memory, executive function, attention, and visuospatial skills.
Caffeinated coffee intake was analyzed in quartiles, and decaffeinated coffee and tea in tertiles due to right-skewed distributions.
Analyses accounted for age, education, lifestyle factors, medical history, medication use, and other dietary variables.
Links to Dementia Risk
Over a follow-up period of up to 43 years, 11,033 participants developed dementia.
Moderate caffeinated coffee intake of about 2-3 cups/d was associated with an 18% lower risk for incident dementia compared with no coffee (hazard ratio [HR], 0.82; 95% CI, 0.76-0.89).
Tea consumption showed a similar pattern, with participants who reported moderate tea intake (1-2 cups/d) showing a 16% lower risk for dementia than those who drank no tea (HR, 0.86; 95% CI, 0.83-0.90).
In contrast, decaffeinated coffee intake was not associated with a reduced risk for dementia.
“The decaf findings suggest that caffeine may be an important contributor because caffeinated coffee and tea showed more consistent associations than decaffeinated coffee,” Zhang said.
However, he cautioned against overinterpreting decaf as ineffective.
“Coffee and tea contain many compounds like polyphenols and other bioactives that relate to neuroinflammation and vascular or metabolic pathways,” Zhang said. “Decaf consumption patterns can also differ, for example, people may switch to decaf because of caffeine intolerance or underlying health issues, which can complicate interpretation. So we can’t conclude caffeine is the only factor.”
Links to Cognitive Decline
In the pooled analyses, the likelihood of subjective cognitive decline was lower among moderate coffee drinkers than those who did not drink coffee (7.8% vs 9.8%). The association remained after multivariable adjustment (prevalence ratio [PR], 0.86; P < .001).
The same held for tea drinkers, with subjective cognitive decline significantly lower among moderate drinkers than those with no tea intake (8.1% vs 9.5%), even after adjusting for confounders (PR, 1.16; P < .001)
Objective cognitive testing in the NHS cohort showed small but measurable improvements in TICS and global cognition scores, with the difference between the highest and lowest caffeinated coffee intake categories being 0.11 points, corresponding to approximately 0.6 years of cognitive aging.
The strongest benefits were seen in participants younger than age 75, and consuming more than moderate amounts didn’t provide additional protection.
“From a clinical standpoint, a small shift in mean performance doesn’t translate to an immediate, noticeable change for an individual patient. However, at the population level, even modest differences, if sustained, could be meaningful when dementia is common and develops over long periods,” Zhang said.
Caffeine Not a Prescription
The researchers acknowledged several limitations, including the study’s observational design and lack of detail on tea type or coffee preparation in dietary assessments.
Cognitive testing was limited to the NHS cohort, dementia classification relied on self-report and death records, and participants were predominantly White health professionals, which may limit generalizability.
“I’d frame it as reassurance rather than a prescription,” Zhang said about the study’s findings.
“For people who already drink coffee or tea and tolerate caffeine, our findings support that moderate intake…is associated with lower dementia risk,” Zhang said.
“Counseling should still be individualized, especially for patients with insomnia, anxiety, or caffeine intolerance. And it should be positioned as one part of the broader prevention approach — alongside regular exercise, vascular risk control, sleep, and diet quality,” he added.
Lifestyle Trumps Caffeine
Commenting for Medscape Medical News, Courtney Kloske, PhD, director, scientific engagement, Alzheimer’s Association, Chicago, emphasized that a balanced and healthful overall diet may be more beneficial for brain health than focusing on one beverage or ingredient.
“While the modest cognitive benefits for higher levels of caffeine consumption are intriguing findings, more research is needed to better understand the underlying mechanisms and connections between caffeine and cognition,” said Kloske, who was not part of the study.
The observed benefits could also relate to other lifestyle and cognitive factors of caffeine drinkers, such as sleep, exercise, and reading, she noted, advising that clinicians emphasize comprehensive healthy lifestyle practices instead of focusing on individual dietary factors like caffeine.
Does IV tenecteplase before thrombectomy improve outcomes in LVO stroke?
'Improve' IS NOT GOOD ENOUGH! You do realize survivors want 100% recovery? Or are you that blitheringly stupid you don't know that and aren't working on it?
Does IV tenecteplase before thrombectomy improve outcomes in LVO stroke?
BACKGROUND AND OBJECTIVES
The benefit of IV thrombolysis (IVT) with alteplase before endovascular thrombectomy (EVT) compared with EVT alone has been shown to be limited and time dependent. Data on tenecteplase, its recommended alternative, are limited. We aimed to assess the efficacy and safety of IVT with tenecteplase plus mechanical thrombectomy (TNK + EVT) compared with EVT in patients with large vessel occlusion stroke and determine whether its potential benefit decreases with treatment time.METHODS
We conducted a retrospective pooled analysis of 2 nationwide, real-world registries of patients with anterior circulation large vessel occlusion stroke within 4.5 hours of known symptom onset and with no contraindication to thrombolysis, treated with TNK + EVT (TETRIS) or EVT (ETIS). The efficacy outcome was the 3-month modified Rankin Scale (mRS) score, analyzed in ordinal and dichotomized (mRS score ≤2) approaches. We used propensity score-weighted logistic regression to assess associations between treatment groups and outcomes of interest.RESULTS
Among 1,890 patients who were analyzed (TNK + EVT: n = 798; EVT: n = 1,092; median age 73 years [interquartile range 61-82]; 49.6% women), the median expected onset-to-thrombolysis time was 146 minutes [interquartile range 119-180]. More than half of patients (n = 1,063; 56.2%) were admitted first to a primary stroke center. All baseline characteristics were balanced between treatment groups after overlap weighting. Overall, TNK + EVT was associated with better 3-month functional outcome(NOT GOOD ENOUGH! You'll want 100% recovery whenyou are the 1 in 4 per WHO that has a stroke
These Five Diets Are Linked to a Lower Death Risk
None of these have any specificity at all, SO BASICALLY USELESS! With no specifics your competent? doctor will gladly blame you for dying!
These Five Diets Are Linked to a Lower Death Risk
Key Takeaways
- Adherence to one of five healthy diets was tied to lower mortality risk and added up to 3 years to lifespan.
- Associations remained robust regardless of genetic predisposition for longevity.
- Diet focused on reducing diabetes risk showed the strongest link with lower death risk.
Following one of five diets was tied to a lower risk of death and a longer life expectancy, with greater adherence adding more years to a person's life, a longitudinal analysis of U.K. Biobank data showed.
Across five diet types, people who fell into the highest quintiles of dietary scores -- indicating the greatest adherence to the diets -- had an 18% to 24% reduced risk of all-cause mortality compared with those in the lowest quintiles:
- Diabetes Risk Reduction Diet (DRRD): HR 0.76, 95% CI 0.69-0.84
- Alternate Mediterranean Diet (AMED): HR 0.80, 95% CI 0.72-0.88
- Alternate Healthy Eating Index-2010 (AHEI): HR 0.80, 95% CI 0.73-0.89
- Dietary Approaches to Stop Hypertension (DASH): HR 0.81, 95% CI 0.73-0.90
- Healthful Plant-Based Diet Index (hPDI): HR 0.82, 95% CI 0.74-0.92
Diet adherence also tended to be associated with lower risks of cause-specific mortalities, including cardiovascular, neurodegenerative, and respiratory diseases, as well as cancer, Liangkai Chen, PhD, of Huazhong University of Science and Technology in Wuhan, China, and colleagues reported in Science Advances.
For a 45-year-old, the highest adherence to one of these diets added 1.5 to 2.3 life years for women, and 1.9 to 3.0 life years for men. AMED added the most years for women, while DRRD led to the most life years gained for men.
"Our results underscore the significance of adhering to healthy dietary patterns ... offering individuals the flexibility to adapt these dietary patterns according to their preferences and traditions," the researchers noted.
Of the five diets, DRRD showed the strongest association with reduced mortality. Chen's group suggested two possible reasons for this.
"Statistically, this result can be partly explained by the direct inclusion of dietary fiber intake and glycemic index in the DRRD scoring, as dietary fiber intake showed the strongest association with all-cause mortality and dietary glycemic index was also significantly associated with all deaths," they explained. "Another possible explanation is that a diet particularly effective in improving insulin sensitivity may have greater potential to prevent chronic conditions and premature death, as insulin sensitivity plays a crucial role in the development and progression of chronic disease."
When polygenic risk scores (PRS) were factored in, associations with reduced mortality remained robust regardless of genetic predisposition for longevity. Men with high genetic longevity and the highest dietary scores gained 1.0 to 3.2 life years; women gained 2.4 to 5.5 life years.
Of note, the DRRD benefits were more pronounced in individuals with a shorter predicted lifespan.
"For DRRD, the association was significantly stronger in individuals with low longevity PRS (indicating a shorter life span), as several SNPs [single-nucleotide polymorphisms] are involved in insulin regulation, BMI, and lipid metabolism -- factors closely linked to diabetes development," the researchers noted.
The study followed 103,649 participants enrolled in the U.K. Biobank from 2006 to 2010 for a median of 10.6 years. Average baseline age was 58.3 years and 56.4% were female. A total of 4,314 deaths occurred during the follow-up period.
Participants had no history of cardiovascular diseases or cancer at baseline and had at least two dietary assessments.
Dietary assessments were conducted through an online 24-hour dietary questionnaire. Food intake was compared against components of the five diets and scored for adherence. Those with higher dietary scores were typically older, better educated, less socioeconomically deprived, less likely to smoke, more physically active, consumed less alcohol, and had lower body mass indexes.
Associations with mortality weren't significantly modified by age, sex, obesity, smoking status, energy intake, and physical activity, but tended to be stronger in more socioeconomically deprived participants. The link between the DASH diet and all-cause mortality was stronger in older adults.
Dietary data were only collected at baseline and didn't include changes in diet quality over time, Chen's group acknowledged. The study population was limited to only those of European descent.
Alzheimer's Dementia Risk Nearly 40% Lower With Lifelong Learning
Will your competent? doctor provide this to reduce your dementia risk? Oh, DOING NOTHING LIKE USUAL! Because your doctor doesn't even know of the need?
With your risk of dementia, you need this.
Parkinson’s Disease May Have Link to Stroke March 2017
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 The latest here:
Alzheimer's Dementia Risk Nearly 40% Lower With Lifelong Learning
Key Takeaways
- Lifelong intellectual activity, such as reading or museum visits, was tied to lower Alzheimer's dementia risk in older adults.
- Adults with the highest level of cognitive enrichment developed mild cognitive impairment about 7 years later than others.
- Results persisted even after adjusting for Alzheimer's pathology, suggesting strong cognitive resilience.
A lifetime enriched with intellectually stimulating activities -- including reading, writing, or frequently visiting museums -- was associated with lower risks of Alzheimer's disease dementia and mild cognitive impairment in late life, longitudinal research showed.
Over nearly 8 years of follow-up, each 1-point increase in lifetime cognitive enrichment correlated with a 38% lower risk of Alzheimer's dementia (HR 0.62, 95% CI 0.52-0.73), reported Andrea Zammit, PhD, of Rush University Medical Center in Chicago, and colleagues.
The risk of developing mild cognitive impairment also was reduced by 33% (HR 0.67, 95% CI 0.58-0.78) for every 1-point increase in lifetime enrichment, Zammit and colleagues wrote in Neurology.
Compared with people in the lowest 10% of lifetime enrichment, those in the top 10% developed mild cognitive impairment an average of 7 years later and had dementia onset 5.4 years later.
The relationship between lifelong intellectual stimulation and higher cognitive function persisted after adjusting for Alzheimer's pathologies at autopsy, suggesting higher resilience, the researchers observed.
"Our findings are encouraging, suggesting that consistently engaging in a variety of mentally stimulating activities throughout life may make a difference in cognition," Zammit said in a statement. "Public investments that expand access to enriching environments, like libraries and early education programs designed to spark a lifelong love of learning, may help reduce the incidence of dementia."
Zammit and colleagues studied 1,939 adults from the Rush Memory and Aging Project. Participants completed surveys reflecting lifetime enrichment, had annual clinical evaluations, and were dementia-free at baseline.
Baseline age was 79.6 years, and 75% of the sample was female. Mean education level was 15 years.
A composite measure from baseline surveys reflected cognitive enrichment at three life stages:
- Early enrichment up to age 18 included the frequency of being read to and reading books, access to newspapers and/or an atlas at home, and learning a foreign language
- Midlife enrichment included income at age 40, household resources like magazine subscriptions, dictionaries, and library cards, and the frequency of visiting museums or libraries
- Late-life enrichment included the frequency of reading, writing, and playing games, and income from Social Security and other sources
The researchers followed participants for an average of 7.6 years; in that period, 551 people developed Alzheimer's disease dementia.
A subset of 948 participants who died during the study had neuropathology data. Each 1-point higher of lifetime enrichment was associated with higher global cognition (P<0.001) and slower rate of decline (P=0.02) proximate to death, independent of neuropathology, the researchers said.
"Individuals in the topmost decile of lifetime enrichment experienced over 43% less decline than individuals in the lowest decile, equivalent to being about 6 years younger," Zammit and co-authors observed. "These results suggest that lifelong cognitive enrichment may delay the onset of Alzheimer's disease dementia and protect cognition in the presence of neuropathology."
The findings have several limitations, the researchers acknowledged. Participants reported details about their early and midlife experiences late in life, which carries risks of potential recall bias and reliability.
The sample included mainly white individuals of European descent who were highly educated, leading to potential ascertainment bias, they added. The results support previous work linking higher cognitive activity engagement to better Alzheimer's and dementia outcomes, underscoring "the need to be replicated in more diverse cohorts," Zammit and colleagues wrote.