Tuesday, April 21, 2026
Gut-brain axis targeting postbiotics for treatment of psychological and neurodegenerative disorders
Yoga, AI, and Neuroplasticity: Navigating the Pathways to Cognitive Resilience
I need as much cognitive reserve and resilience as possible since I probably used all of mine up just surviving my stroke. Ask your competent? doctor for EXACT PROTOCOLS TO BUILD RESILIENCE AND RESERVE! Your doctor NEEDS TO GUARANTEE REBUILDING YOR RESERVE TO PREVENT DEMENTIA!
Yoga, AI, and Neuroplasticity: Navigating the Pathways to Cognitive Resilience
Siddhant Rajhans1*, Dr. Somlata Jha2, Prakhar Singh3, Anuj Anand4, Vaibhav Saini5
1*Department Of Computer Science & Engineering, Himalayan School Of Science & Technology, Swami Rama Himalayan
University, India.
siddhantrajhanssrhu@zohomail.in
2 Assistant Professor, School Of Yogic Science, Swami Rama Himalayan University, India
3Department Of Computer Science & Engineering, Himalayan School Of Science & Technology, Swami Rama Himalayan
University, India.
4Department Of Computer Science & Engineering, Himalayan School Of Science & Technology, Swami Rama Himalayan
University, India.
5 Department Of Computer Science, Vivekananda Institute Of Professional Studies, India
*Corresponding Author: Siddhant Rajhans
siddhantrajhanssrhu@zohomail.in
Abstract
In this ever-changing modern world, people should be highly adaptable and have the ability
to adjust to any situation. We aim to do extensive research on the relationships that exist
between yoga, neuroplasticity, and artificial intelligence (AI), and also the methods for
developing a high level of cognitive resilience. In order to identify pathways to cognitive
wellbeing, we examine the cultural foundations of yoga, the transformative potential of AI,
and neuroplasticity in this paper. To get the most useful understanding of how to promote
cognitive resilience, people must be able to recognise the intersection and synergy between
these components. Only then will they be able to learn how to promote cognitive resilience
when confronted with life's challenges, as well as how to think differently going forward by
applying these useful strategies.
Low Hemoglobin Levels Linked to Higher Dementia Risk
When I donate blood every two months I'm usually good, but just to make sure a couple days before I start taking a few iron pills.
Low Hemoglobin Levels Linked to Higher Dementia Risk
Risk peaked when anemia occurred alongside abnormal Alzheimer's biomarkers
Key Takeaways
- Lower hemoglobin levels were linked with higher dementia risk over 9 years of follow-up.
- Anemia was associated with elevated Alzheimer's blood biomarkers including p-tau217 and neurofilament light chain.
- Dementia risk was highest when anemia coexisted with abnormal Alzheimer's biomarkers.
Lower hemoglobin levels were associated with progressively higher dementia risk and elevated blood concentrations of Alzheimer's disease biomarkers, data from a Swedish cohort study suggested.
In a study of 2,300 older adults without dementia, anemia was cross-sectionally associated with higher levels of serum phosphorylated tau 217 (p-tau 217; β=0.22), neurofilament light chain (NfL; β=0.25) and glial fibrillary acidic protein (GFAP; β=0.08), reported Martina Valletta, MD, of the Karolinska Institute in Stockholm, and co-authors.
Anemia was longitudinally associated with a higher risk of incident dementia over a mean follow-up of 9 years (HR 1.66, 95% CI 1.21-2.28), Valletta and colleagues reported in JAMA Network Open.
The highest dementia risk occurred when anemia and elevated biomarkers coexisted, the researchers said. For older adults with low hemoglobin and high NfL, for example, the HR was 3.64 (95% CI 2.39-5.56).
These findings suggested that anemia may interact with neuropathologic processes, potentially accelerating dementia development, Valletta and co-authors noted.
"Dementia risk was particularly high when anemia co-occurred with high levels of blood biomarkers reflecting Alzheimer's disease pathology, neurodegeneration, and glial activation. This suggests a biological interplay between anemia and neuropathology, in which low hemoglobin may not only contribute to neuropathology but also reduce the brain's resilience to it," the researchers wrote.
"Taken together, our findings suggest anemia is a clinically relevant factor in the context of dementia risk stratification and is possibly a modifiable target in dementia prevention strategies," they added.
A causal role of anemia in dementia etiology could have substantial public health implications, observed Frank Wolters, MD, PhD, of Erasmus MC-University Medical Center in Rotterdam, the Netherlands.
"Anemia is present in 25% of the global population, with the highest prevalence in countries that are expected to have the steepest increases in dementia incidence," Wolters wrote in an accompanying editorial.
The biomarker-level observations in the Swedish study "provide novel evidence that connects hemoglobin directly to Alzheimer's disease," he noted. "Although the cross-sectional design in this respect did not allow for formal mediation analyses, results point at least toward a joint role of Alzheimer's pathology and anemia, in line with earlier observations linking hemoglobin to plasma amyloid-beta," he pointed out.
To move findings from observation to effective intervention, "mechanistic insight is mandatory," Wolters emphasized. "Such insights could come from observational studies on anemia and its causes, including use of repeated measures of hemoglobin and emulated target trials, as well as from small physiological trials," he added.
Valletta and colleagues studied participants in the Swedish National Study on Aging and Care in Kungsholmen (SNAC-K), a longitudinal population-based study. Participants enrolled from 2001 to 2004 were followed up every 3 or 6 years according to age through 2019.
The analysis included 2,282 dementia-free participants with a median age of 72.2 years; 61.6% were female. Analyses were adjusted for age cohort, sex, educational level, chronic kidney disease, heart disease, cerebrovascular disease, cancer, underweight, iron and vitamin supplement intake, and interleukin-6 levels.
Hemoglobin level was measured at baseline, and anemia was defined according to World Health Organization criteria as a blood hemoglobin level of 12 g/dL or less for women and 13 g/dL or less for men. A total of 199 participants had anemia.
Alzheimer's biomarkers were measured in blood samples taken at baseline. Incident dementia was diagnosed based on DSM-IV criteria. Over a mean follow-up of 9.3 years, 362 participants (15.9%) developed dementia.
"In a previous study by our group, anemia emerged as one of the chronic conditions most significantly associated with elevated levels of Alzheimer's disease blood biomarkers. Expanding that evidence, in this study we also included p-tau217, currently regarded as the most specific blood biomarker for Alzheimer's disease, and we observed that all biomarker levels tended to be higher as hemoglobin levels declined, following a nonlinear dose-response association," Valletta and colleagues noted.
"These findings suggest a more nuanced relation between hemoglobin levels, Alzheimer's disease blood biomarkers, and dementia beyond the definition of anemia itself," they wrote.
The study had several limitations, the researchers acknowledged. Hemoglobin levels ranged from 8.2 to 17.6 g/dL, and most anemia cases were normocytic, limiting analysis of more extreme values and other anemia subtypes. Alzheimer's biomarkers were measured in serum, which typically produces lower concentrations than plasma. Blood biomarkers also were available only at baseline.
SNAC-K data collection was supported by the Swedish Research Council and by the Swedish Ministry of Health and Social Affairs. The study also received support from Stiftelsen Sigurd och Elsa Goljes minne, Hjärnfonden, the Gamla Tjänarinnor Foundation, and Svenska Läkaresällskapet.
Valletta had no disclosures. Co-authors reported relationships with the Swedish Research Council, the Karolinska Institutet Strategic Research Area in Epidemiology and Biostatistics, and the Margaretha af Ugglas' Foundation.
Wolters reported no conflicts of interest.
Study Suggests Certain Olive Oil May Help Boost Brain Function and Cognitive Health
Does your competent? doctor have enough functioning neurons to get the dietician to put this in your diet protocol? Oh, you incompetently DON'T HAVE A DIET PROTOCOL? Why not? But you also need daily EXACT AMOUNTS! To get mine I dip bread in a mixture of olive oil and balsamic vinegar, found from Italian restaurants.
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!
OH NO! your doctor KNOWS NOTHING AND DOES NOTHING!
Study Suggests Certain Olive Oil May Help Boost Brain Function and Cognitive Health
Monday, April 20, 2026
Advances in the diagnosis and management of post-stroke limb spasticity: a narrative review
Where is the CURE SPASTICITY RESEARCH?
'Management' is NOT what survivors want! They want it CURED! Are you that stupid that you believe in the idiotic opinion of the infamous Dr. William M. Landau thinks spasticity is not worth treating!
Do you believe in the do nothingism of Dr. William M. Landau on spasticity?
His statement from here:
Spasticity After Stroke: Why Bother? Aug. 2004
Wonder if he will be singing the same tune after he becomes the 1 in 4 per WHO that has a stroke, will he be satisfied with not getting recovered?
The latest here:
Advances in the diagnosis and management of post-stroke limb spasticity: a narrative review
Abstract
Objective:
This review aims to provide a comprehensive overview of the current understanding and clinical management of post-stroke limb spasticity.
Methods:
Literature searches were conducted in PubMed and CNKI databases for articles published between January 2000 and June 2025, using keywords related to post-stroke spasticity, assessment, and interventions (botulinum toxin, rehabilitation, neuromodulation, surgery). The search was restricted to English-language articles addressing post-stroke limb spasticity. After screening, 68 studies were included and categorized by research theme.
Results:
Several interventions were identified as effective in alleviating post-stroke limb spasticity. Specifically, botulinum toxin injection has emerged as the primary choice for managing focal spasticity. Neuromodulation methods, including transcranial magnetic stimulation, transcranial direct current stimulation, spinal cord stimulation, and vagus nerve stimulation, demonstrated significant therapeutic potential.(NOT GOOD ENOUGH! WHERE THE FUCK IS THE CURE?)
Conclusion:
Neuromodulation techniques exert their effects by adjusting corticospinal tract excitability and promoting neural plasticity. However, additional randomized controlled trials are necessary to optimize stimulation settings and confirm their long-term effectiveness.
More at link.
A multicenter clinical nomogram for predicting post-stroke fatigue: development and validation
Will your competent? doctor and hospital ensure research is completed to determine WHAT WILL CURE POST STROKE FATIGUE? Not manage or anything less than a FULL CURE!
This prediction crapola is COMPLETELY FUCKING USELESS!
Let's see how long everyone in stroke has been incompetent at this problem!
- post stroke fatigue
(60 posts to January 2018)
At least half of all stroke survivors experience fatigue Known since March 2017
Or is it 70%? Known since March 2015.
Or is it 40%? Known since September 2017.
A multicenter clinical nomogram for predicting post-stroke fatigue: development and validation
Abstract
Background and purpose:
Post-stroke fatigue (PSF) is a common and disabling complication after stroke, yet its pathophysiological mechanisms remain unclear and reliable prediction tools are lacking. This study aimed to identify risk factors for PSF and develop a visualized nomogram for early prediction based on clinical and laboratory data.
Methods:
We conducted a retrospective cohort study of stroke patients hospitalized in the Department of Neurology at the First Affiliated Hospital of Chongqing Medical University were randomly split into training (n = 592) and internal validation (n = 254) sets. An independent cohort of 440 patients from Nanchong Central Hospital was used as the external validation cohort. Fatigue was assessed at week 4 after admission using the Fatigue Severity Scale (FSS) and Fatigue Assessment Scale (FAS). Demographic, clinical, imaging, and laboratory data were collected. LASSO regression was used for variable selection, followed by multivariate logistic regression to construct a nomogram. Model performance was assessed using the area under the curve (AUC), calibration curves, and decision curve analysis (DCA), with internal and external validation via bootstrapping.
Results:
A total of 846 stroke patients were enrolled and randomly split into training (n = 592), internal validation (n = 254) and external validation (n = 440) sets. Eight independent predictors of PSF were identified: brainstem, basal ganglia, and thalamic lesions, female sex, older age, modified Rankin Scale (mRS) score, white blood cell (WBC) count, and C-reactive protein (CRP) level (all p < 0.05). The nomogram showed good discrimination (AUC: 0.870, 0.862, and 0.672 for training, internal, and external validation sets, respectively), calibration, and clinical utility.
Conclusion:
We developed a clinically applicable nomogram based on routinely available data for early prediction of PSF. The model demonstrated good accuracy and may aid in identifying high-risk patients to guide timely intervention.
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