Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective 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.

Showing posts with label cognitive improvement. Show all posts
Showing posts with label cognitive improvement. Show all posts

Thursday, October 1, 2026

Proof that puzzles can reverse cognitive impairment

 Ask your competent? doctor FOR EXACTLY WHICH ONES TO DO! 

Can't do that; PURE INCOMPETENCE!

Your doctor obviously doesn't ever read or understand research AND DOESN'T FUCKING CARE!     

Proof that puzzles can reverse cognitive impairment

Scientists have proven for the first time that simple activities and small lifestyle changes can reverse cognitive impairment.

Puzzles, learning new skills and social interaction have been linked with maintaining cognitive function.

Now – in the first large-scale trial in community settings – researchers have found that even very brief brain stimulating activities, alongside physical activity and a healthy diet, have a significant impact.

They studied more than 11,500 people aged 60 to 85 with mild to severe cognitive impairment.

After 12 months, 28 per cent of study participants no longer had cognitive impairment.

Paul Little, Professor of Primary Care Research at the University of Southampton and study co-lead, said: “This is the first large trial to test brief interventions over a sustained period with people recruited in primary care via GPs and nurse practitioners. We have shown that simply giving advice and pointing people towards brain stimulating activities has a real impact. That’s important because it can happen with minimal input and cost. Previous trialled interventions have been shorter term and requiring a lot more resource from health service providers.”

Participants in the study were split into three groups. Members of the first group (the control group) were asked about their brain stimulating activities, their cognitive function was tested and they were given brief advice about how to protect cognitive health via physical activity, a heathy diet and brain stimulating activities.

Brain stimulating activities are things that engage the brain to think, learn and be social – such as puzzles, online brain training games, playing a musical instrument, singing in a choir, learning a new language, and social activities and interaction.

“We thought there would be relatively little effect from this, but there was in fact a big effect,” explained Professor Little. “After 12 months, 28 per cent of people in this first group no longer had cognitive impairment.”

Most participants already had reasonably healthy activity levels and diet, so the significant improvement in their cognitive function is believed to be a result of simple activities that use the brain.

A second group was given access to a website with brain exercises and advice, and a third group was offered two brief appointments, phone calls or emails from a facilitator, usually a nurse.

Of those who had access to the website, there was an 8 per cent reduction in the number of people who had mild cognitive impairment compared to the control group. And of those who had the extra support, there was an 18 per cent reduction.

Professor Little, who co-led the study with Lucy Yardley, Professor of Health Psychology at the Universities of Southampton and Bristol, explained: “These are really exciting findings that people can easily take on board. Simple messages and simple things that people can do really make a difference – and the NHS does not need to spend a lot of money.

“It’s an important health message. The brain remains plastic and malleable, so it can learn new things, well into older age, so you can really make a difference and combat cognitive decline.

“We have an ageing population where cognitive impairment and dementia is incredibly common. About 20 per cent of over 65s have cognitive impairment and about 10 per cent of those will go on to develop dementia each year.

“It’s probably the biggest public health danger of our time. The great thing is that we can do something about it.”

The Active Brains study is published in The Lancet Primary Care .

The University of Southampton has announced plans for a groundbreaking new medical institute which will bring medics, computer scientists and engineers together in one brand new building. The pioneering Institute for Medical Innovation will be based at University Hospital Southampton and will tackle five devastating disease areas - cancer, dementia, sight loss, infection and respiratory and allergic conditions.

Wednesday, September 2, 2026

Sunday, August 30, 2026

Causality of genetically determined glucosamine supplementation on cognition and sarcopenia: a Mendelian randomization study

 Did your competent? doctor inform you of the EXACT PROTOCOLS to get these benefits? NO? So your doctor is OK with incompetence while treating you?

But wait!

Glucosamine Supplement Linked to Accelerated Alzheimer’s Progression

 Have your competent? doctor reconcile the earlier research showing benefits!

Causality of genetically determined glucosamine supplementation on cognition and sarcopenia: a Mendelian randomization study

  • 1. Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu, China

  • 2. Laboratory of Anesthesia and Critical Care Medicine, National-Local Joint Engineering Research Centre of Translational Medicine of Anesthesiology, West China Hospital, Sichuan University, Chengdu, China

Abstract

Background:

Evidence indicates a negative link between glucosamine and age-related cognitive decline and sarcopenia. However, the causal relationship remains uncertain. This study aims to verify whether glucosamine is causally associated with cognitive function and sarcopenia.

Method:

Forty-eight genetic variants linked to glucosamine use were extracted from the MRC-IEU consortium. Besides, we gathered cognition proxy indicators [cognitive performance and fluid intelligence score (FIS)], and sarcopenia-related indicators, namely, appendicular lean mass (ALM), whole body fat-free mass (WBFM), low hand grip strength, facial aging (FA), moderate to vigorous physical activity levels, usual walking pace and DNA methylation GrimAge acceleration from the large publicly available genome-wide association studies. Initially, Mendelian randomization (MR) analyses were conducted to ascertain the causal impact of glucosamine on cognition and sarcopenia-related traits. Subsequently, the two-step MR and multivariable MR (MVMR) were employed to examine whether any mediators causally mediated the observed associations.

Result:

MR analysis indicated that glucosamine was associated with increased cognitive performance (p = 8.46E-04), FIS (p = 7.50E-04), ALM (p = 6.45E-08), WBFM (p = 1.97E-03), usual walking pace (p = 2.55E-07), and moderate to vigorous physical activity levels (p = 3.29E-03), but associated with decreased FA risk (p = 3.77E-05) and DNA methylation GrimAge acceleration (p = 0.001). However, there were no significant causal associations between glucosamine and low hand grip strength. Multivariable MR showed that glucosamine continued to have a significant effect on cognitive performance, FIS, ALM, WBFM, usual walking pace, and moderate to vigorous physical activity levels after controlling for osteoarthritis (OA) and body mass index (BMI) (p < 0.05). We further found that C-reactive protein levels (CRP) may mediate the association of glucosamine and ALM, WBFM, usual walking pace, and physical activity (p < 0.05), and basal metabolic rate (BMR) may mediate the association of glucosamine and cognitive performance, FIS, ALM, WBFM, and usual walking pace (p < 0.05).

Conclusion:

Regular glucosamine use enhances cognitive function and postpones sarcopenia for preserving the functional capacities necessary, and the impact of glucosamine on cognition and sarcopenia could be partially attributed to the mediation of BMR and CRP.

Thursday, July 30, 2026

Daily eating change linked to sharper thinking in older women, study finds

 Do your really think your doctor has enough competence and clout to get this diet protocol implemented in the hospital?

Daily eating change linked to sharper thinking in older women, study finds

Eating all meals within an eight-to-nine-hour window each day may offer benefits for brain health beyond weight loss alone, according to new research presented at a major nutrition conference. 

The research was presented at NUTRITION 2026, the annual meeting of the American Society for Nutrition in National Harbor, Maryland. 

Researchers found that participants who restricted their daily eating window showed improvements in certain cognitive abilities after six months, even though they lost a similar amount of weight as those who followed a more typical eating schedule. 

“We are confident it is due to meal timing itself, because this was a randomized controlled trial and both groups lost weight (about 8 percent) but there was a greater cognitive benefit only in the group that also was restricting their eating window to 8 hours compared to the control group eating 12 hours,” Sue Shapses, a professor at Rutgers University and Rutgers-RWJ Medical Center and the study’s principal investigator, told Newsweek.  

However, she cautioned that the findings were limited to women with overweight or obesity who were actively losing weight.  

“We did not study leaner women or those who are not losing weight during the time-restricted eating,” Shapses said. “As a result, we cannot confidently state that it applies to other women, or to men.” 

Alzheimer’s disease and other forms of dementia are becoming increasingly common as populations age.  

Previous research has linked diet and lifestyle habits to dementia risk, but relatively few studies have explored whether changing those habits can help reduce that risk. 

To investigate, researchers enrolled 47 women between the ages of 50 and 79 who were overweight or obese.  

All participants were advised to cut 500 calories from their daily diets as part of a weight-loss program. 

 Twenty-six women were assigned to a time-restricted eating plan, limiting food consumption to fewer than nine hours per day.  

Most ate between 10 a.m. and 6 p.m., resulting in an average eating window of 8.2 hours. 

The remaining participants maintained a more conventional schedule, eating over roughly 12 hours per day on average. 

After six months, women in both groups had lost about 15 pounds on average, suggesting that the amount of weight lost was not the key factor separating the groups. 

Instead, differences emerged in cognitive performance. 

Compared with women who maintained a 12-hour eating window, those who restricted eating to eight or nine hours a day performed significantly better on tests measuring spatial planning and problem-solving abilities.  

Researchers also observed a trend toward fewer mistakes on memory and learning tasks, although those improvements did not reach statistical significance. 

The findings suggest participants may have become better at remembering information during everyday activities while making fewer mistakes linked to memory, attention and problem-solving.  

The researchers also found that greater reductions in the eating window were associated with larger cognitive improvements. 

Shapses said the approach may also be practical for people who cannot follow a strict schedule every day. 

“If they can’t do this every day—due to weekend events or weekday business dinners—it is OK to have occasional aberrations,” she said, noting that participants in the study also occasionally deviated from the eating schedule. 

The team cautioned that the study was small and that the findings remain preliminary.  

“At this point, we will continue our analysis and submit the full length manuscript for peer-review for publication,” Shapses said.

Reference

American Society for Nutrition. “Eating within 8 hours may help keep the aging brain sharp.” ScienceDaily. ScienceDaily, 27 July 2026. www.sciencedaily.com/releases/2026/07/260727012125.htm

Contact Newsweek editors on this story: Kara Dolman and Emma Lee-Sang

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Monday, June 29, 2026

The effect of probiotic supplements on cognitive outcomes and neuroplasticity in elderly ischemic stroke survivors

 How soon will your competent? doctor and dietician update your diet protocols? Oh NO, you don't have any, do you?

The effect of probiotic supplements on cognitive outcomes and neuroplasticity in elderly ischemic stroke survivors


  • 1. Department of Neurology, The Second Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, China

  • 2. Department of General Affairs, The Second Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong, China

Abstract

Background: 

This retrospective cohort study investigates the effects of probiotic supplementation on the nutritional, cognitive, and motor functions of elderly survivors recovering from ischemic stroke. Given the high prevalence of nutritional deficits and cognitive impairments in this population, exploring adjunct therapies such as probiotics could provide improved outcomes.

Methods: 

The study included 223 elderly ischemic stroke survivors treated between March 2021 and February 2024, divided into two groups based on treatment modalities: the Conventional Group (n = 117) receiving standard enteral nutrition, and the Supplement Group (n = 106) receiving similar nutrition plus probiotics. Data collected included NIH Stroke Scale (NIHSS), nutritional indicators, cognitive assessments (MMSE, HDS, CDR, SES), and motor evaluations (STREAM, mRS, MBI).

Results: 

Baseline comparisons showed no significant differences between groups. Post-treatment outcomes demonstrated significant improvements in the Supplement Group across several measures. Neurotrophic and nutritional parameters, including BDNF, hemoglobin, albumin, and prealbumin levels, significantly increased (p ≤ 0.011). Cognitive function also improved, with higher MMSE and HDS scores and reduced CDR scores (p < 0.003). Motor function, evaluated by STREAM, showed enhanced upper and lower limb mobility and basic activities (p ≤ 0.014). Further, participants in the Supplement Group experienced better functional recovery with decreased mRS scores and increased MBI scores (p < 0.004). The incidence of gastrointestinal adverse events was significantly reduced in the Supplement Group (p < 0.001), and correlation analysis underscored positive associations between probiotics and improved outcomes (p ≤ 0.003).

Conclusion: 

Probiotic supplementation as part of nutritional therapy significantly enhances nutritional, cognitive, and motor function recovery in elderly ischemic stroke survivors, while also reducing gastrointestinal adverse events. These findings suggest that incorporating probiotics into recovery protocols post-stroke may facilitate better health outcomes and provide a well-tolerated therapeutic adjunct.


More at link.

Tuesday, May 12, 2026

40-Hz sensory stimulation-induced gamma oscillations enhancing brain network connectivity to improve poststroke cognitive impairment: study protocol for a prospective randomized controlled trial in China

 Why? Didn't this earlier research prove it works? And your mentors and senior researchers incompetently didn't know about it?

40-Hz sensory stimulation-induced gamma oscillations enhancing brain network connectivity to improve poststroke cognitive impairment: study protocol for a prospective randomized controlled trial in China


Abstract

Background: Poststroke cognitive impairment (PSCI) has an incidence rate ranging from 24% to 80.97%. It reduces survival rates and increases disability among stroke patients, posing a substantial socioeconomic burden. Current treatments for PSCI primarily involve medication and rehabilitation; however, therapeutic efficacy remains limited, with unsatisfactory improvement in activities of daily living. This study aims to conduct a prospective clinical trial to evaluate the safety and efficacy of 40-Hz sensory stimulation-induced gamma oscillations in the treatment of PSCI, including assessment of neuropsychology, psychiatric symptoms, cerebral blood perfusion, and functional and structural brain changes, and to investigate the underlying mechanisms by RNA-sequencing of blood samples.

Methods: This trial is designed as a prospective, randomized controlled, double-blind, non-inferiority study conducted in the Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine in China. Participants with confirmed cognitive impairment occurring after the stroke event and persisting for 3 to 6 months will be screened and recruited by the attending neurologists for participation. A total of 120 enrolled patients will be randomly assigned to one of two groups at a ratio of 1:1. The experimental group will receive 40-Hz sensory stimulation, while the control group will receive sensory stimulation at random frequencies. Both groups will receive the same standard clinical drug therapy and rehabilitation treatment. The primary efficacy endpoints include cognitive function and learning ability. Secondary endpoints encompass changes in cerebral hemodynamics, neural network connectivity, synaptic-related gene expression, and neurotransmitter levels. Safety assessments will include monitoring of major adverse events, all-cause mortality, and photosensitive epilepsy. Evaluations will be conducted at baseline, after the 14-day treatment period, and during follow-up visits (at 3 and 6 months). Differences between the two groups will be compared.

Discussion: This study will assess the safety and efficacy of gamma oscillations induced by 40-Hz sensory stimulation in treating PSCI patients. In parallel, potential mechanisms-including alterations in synaptic-related genes and neural network connectivity-will be explored. This trial is expected to provide evidence supporting the effectiveness of this novel technique for treating PSCI and improving patients' quality of life.

Trial registration: Chinese Clinical Trial Registry (ChiCTR) ChiCTR2400088535. Registered on 20 August 2024.

Wednesday, February 4, 2026

Targeting immune cells in the aged brain reveals that engineered cytokine IL-10 enhances neurogenesis and improves cognition

 We need both, do you have ANY CONFIDENCE AT ALL that your stroke medical 'professionals' will get human testing going?

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!

Targeting immune cells in the aged brain reveals that engineered cytokine IL-10 enhances neurogenesis and improves cognition


https://doi.org/10.1016/j.immuni.2026.01.016Get rights and content
Under a Creative Commons license
Open access

Highlights

  • •
    The old brain contains exhausted T cells and unbalanced microglial inflammation
  • •
    Delivery of engineered proteins into old mouse brains allows immune cell targeting
  • •
    Checkpoint inhibition in old brains activates T cells and microglial inflammation
  • •
    Engineered IL-10 restores microglial balance, neurogenesis, and cognition in old mice

Summary

The immune system could play an important role in the age-related decline in brain function, yet specific immune-based strategies to enhance brain resilience in older individuals are lacking. Here, we combined engineered proteins and direct brain delivery to target immune cell populations within the old brain. We detected T cells with an exhaustion signature in the old brain and targeted them with a potent engineered checkpoint inhibitor (RIPR-PD1). This led to T cell expansion and strong pro-inflammatory responses in many brain cell types, notably microglia. To rescue age-related inflammatory imbalances in microglia, we used the anti-inflammatory cytokine interleukin (IL)-10. IL-10 boosted anti-inflammatory responses in old microglia, but it also triggered pro-inflammatory signaling. An engineered IL-10 variant that uncouples pro- and anti-inflammatory responses positively impacted the transcriptome of multiple cell types, enhanced neurogenesis, and improved cognition in aged mice. Our findings pave the way for immunotherapies for the aged brain.

Introduction

Brain function deteriorates with age. Additionally, age-related neurodegenerative diseases (e.g., Alzheimer’s disease and Parkinson’s disease) surge in the elderly population. While many pathways are remodeled in the brain during aging,1,2,3,4 a key feature of old brains is immune cell infiltration and inflammation. Aging leads to a pronounced increase in the number of T cells across several brain regions in mice and humans,5,6,7 including neural stem cell (NSC) niches8,9,10,11 and white matter tracts.12,13,14,15,16 T cells from old brains are clonally expanded,8,17 suggesting they have encountered antigens. T cell infiltration and clonal expansion are further accentuated in age-related neurodegenerative diseases.18,19,20,21,22,23,24,25,26 In parallel, pro-inflammatory pathways are strongly upregulated during aging in many cell types, and this is exacerbated in Alzheimer’s disease.8,13,27,28,29,30,31,32,33,34,35,36 A systematic understanding of age-related changes in brain immune cells may inform strategies to mitigate brain aging.
Could immune-based interventions be designed to counter brain aging? Modulating immune cells and inflammatory pathways can affect the old brain.12,13,28,30,37,38,39 But previous studies have relied on broad interventions, often performed in the periphery13 and in young or disease model mice.18,24,40,41,42,43,44,45 We lack strategies to target specific immune cell subsets and pathways within the old brain to determine their mode of action. Moreover, identifying such brain immune interventions could help develop “aging immunotherapies” and would be critical to counter aspects of brain aging and age-related brain diseases.
Here, we developed a platform that leverages engineered proteins and direct brain delivery to test immune cell-specific interventions in old mice. We identified T cells with an exhaustion signature and targeted them with a potent engineered checkpoint inhibitor, leading to T cell expansion and strong pro-inflammatory responses in many cell types, including microglia. To rescue age-related inflammatory balance in microglia, we used an engineered interleukin (IL)-10 variant that uncouples pro- and anti-inflammatory responses and found that it had beneficial effects on multiple cell types and cognition in aged mice. Our findings pave the way for novel immunotherapies for the aged brain.

Results

Characterization of immune cells in the aged brain

We systematically characterized immune cells in the aging brain, focusing on the subventricular zone (SVZ) neurogenic niche—a region that contains adult NSCs and declines during aging.46,47,48,49 Leveraging previously published single-cell RNA-sequencing (scRNA-seq) datasets,8,50 we found that SVZ neurogenic niches contained microglia (the brain-resident myeloid population), macrophages, CD8+ T cells, CD4+ T cells, and low numbers of other immune cells (Figures 1A and S1A). CD8+ T cells were not very numerous but significantly increased in number with age (Figure 1A, upper and middle panel). Microglia were the most abundant immune cell type and showed the largest age-related changes in gene expression (Figure 1A, lower panel). We thus focused on CD8+ T cells and microglia for further characterization and targeting in the old brain.
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Figure 1. Characterization of immune cells in the old brain

(A) Analysis of immune cell populations in the SVZ neurogenic niche of young (3–4 months, n = 7) and old (22–29 months, n = 6) male mice in two merged scRNA-seq published datasets.8,50 Top panel, quantification of the proportion of different immune cell types relative to the total number of cells. Data are mean ± SEM; each dot represents one mouse. Middle panel, age-dependent changes (log2[old/young]) in the abundance of each cell type. Bottom panel, age-dependent changes in gene expression per cell type. Dots represent differential expression MAST Z score for each gene. Genes significantly changed with age (Bonferroni-corrected p < 0.05) are in color.
(B) scRNA-seq analysis of CD8+ T cells freshly isolated from the brain and lung of old male mice (22–25 months, n = 11 mice, pooled). Uniform manifold approximation and projection (UMAP) clustering of all T cells colored by organ of origin, downsampled to 3,724 cells per organ. One independent experiment.
(C) UMAP as in (B) colored by cell type.
(D) Changes in the percentage of T cell subtypes in old brains vs. old lungs.
(E) Heatmap of top six marker genes for each T cell subtype in the old brain.
(F) FACS quantification of percent PD1+ and CD44+CD69+ of CD8+ T cells freshly isolated from the brains and lungs of old male mice (24 months, n = 6). One independent experiment.
(G) Heatmap of T cell marker genes in T cells from same dataset as (A).
(H) Left, representative images showing exhaustion scores for T cells in coronal brain sections of young (6 months) and old (28 months) male mice in a spatial transcriptomics (MERFISH) dataset.7 Right, quantification of exhaustion scores in T cells from young (3–6 months, n = 5) and old (26–34 months, n = 6) male mice across four brain regions, cortex (CTX), striatum and adjacent regions (STR), white matter tracts of the corpus callosum and anterior commissure (CC/ACO), and the ventricle (VEN). One coronal section per mouse. Boxplots of median and lower and upper quartile values.
(I) Left, representative immunofluorescence images of SVZ from young (4 months) and old (28 months) male mice. Red, CD8+ (T cells); green, PD1+ (checkpoint protein); blue, DAPI (nuclei). Scale bar, 10 μm. Right, number of CD8+ and CD8+ PD1+ T cells in the SVZ of young (3–4 months, n = 7) and old (28–32 months, n = 7) male mice. Each dot represents one mouse (average of two sections per mouse). One independent experiment.
(J) FACS quantification of the percentage of CD8+PD1+ and CD8+CD44+CD69+ T cells of live/CD45+ cells freshly isolated from the brain of young (6 months, n = 6) and old (24 months, n = 6) male mice. One independent experiment.
(K) Average changes in gene expression in microglia of the SVZ neurogenic niche of young and old male mice from three published scRNA-seq datasets.8,50,51 Red, upregulated; blue, downregulated genes.
(L) Heatmap of log-normalized counts for pro- and anti-inflammatory genes in microglia from the SVZ in a published dataset.8
(M) Log-normalized expression values of Socs3 (left) and combined genes in the IL-10 pathway in microglia from the SVZ in a published dataset.8 Horizontal lines, median.
(N) IL-10 signaling scores for microglia in spatial transcriptomics dataset.7
(O and P) FACS histograms and quantification of inflammation proteins in microglia (CD45+CD11b+) freshly isolated from the SVZ of young (3 months) and old (24 months) male mice (n = 6). Each dot represents one mouse (mean fluorescence intensity [MFI] values from ∼500 microglia per mouse). One independent experiment.
Data are mean ± SEM. p values, two-sided Wilcoxon rank-sum test. NS, not significant.
See also Figure S1.
More at link.