New dementia warning sign is hiding in our muscles

 

Make damn sure your competent? doctor has EXACT PROTOCOLS that prevent frailty post stroke! Doesn't have them; fire him/her and replace your incompetent board of directors!

• frailty (41 posts to January 2018)

New dementia warning sign is hiding in our muscles

Losing muscle as we age could be an important warning sign for dementia, according to new Curtin University research. Researchers analyzed more than 80 studies examining the links between body weight, body fat, muscle health and dementia, finding people with sarcopenia—the loss of muscle mass and strength—had a 42% higher risk of dementia. Sarcopenia is a condition in which people lose muscle mass, strength and physical function, often as they get older.

The findings, published in the International Journal of Food Sciences and Nutrition, also revealed a surprising difference in how obesity was linked to dementia depending on a person's age. People with obesity in middle age, or before 65, had a 9% higher risk of dementia, while obesity in people 65 and older was linked to a 17% lower risk.

Lead researcher Dr. Uraiporn Booranasuksakul, from Burapha University, said the findings showed that body weight alone did not tell the full story when it came to dementia risk.

"It's not just about how much you weigh—maintaining muscle strength and function also appears to be important as we age," Booranasuksakul said. "Our findings suggest losing muscle could be an important warning sign for dementia risk."

 Related video: World Alzheimer's Day highlights hearing loss as dementia risk factor (KYTX-TV Tyler-Longview)

 Booranasuksakul said the findings highlighted the importance of looking after muscle health throughout life. "Maintaining muscle is an important part of healthy aging, and regular physical activity and good nutrition can help support muscle strength and function," she said.

Corresponding author Professor Mario Siervo, from Curtin's School of Population Health, said the findings also challenged the idea that dementia risk could be understood simply by looking at a person's weight.

"We found that obesity in middle age was linked to a higher risk of dementia, but this relationship changed in later life," Siervo said. "This does not mean people should gain weight as they get older. Rather, it shows us that the relationship between body weight, aging and dementia is complex."

The researchers also looked at sarcopenic obesity, in which a person has both low muscle mass or function and excess body fat. Only four studies met the criteria for this part of the analysis, and researchers found no statistically significant link between sarcopenic obesity and dementia.

Siervo said more research was needed to understand whether the combination of muscle loss and excess body fat affected dementia risk.

"There is still a lot we don't know about how changes in muscle and body fat interact over time," Siervo said. "More long-term research is needed to understand whether having both low muscle mass and excess body fat increases dementia risk."

The researchers said the findings reinforced the importance of taking a lifelong approach to maintaining healthy body composition, including preventing unhealthy weight gain during middle age and maintaining muscle strength and function as people get older.

Professor Warren Harding AM, chairman and head of research and partnerships at Alzheimer's WA, welcomed the findings and congratulated Curtin on its investment in dementia research.

"Dementia is a $2.8 trillion global challenge, and the findings from the World Health Organization and the Lancet Commission on the 14 lifestyle risk factors are powerful reminders of the importance of early detection and good eating, exercise, weight, hearing, vision and brain training," Harding said. "The Curtin findings around muscle mass and strength also reinforce the importance of exercise and underline the importance of good mobility and stability to reduce falls as people age."

The study was led by researchers from Curtin University's School of Population Health and Dementia Center of Excellence, in collaboration with researchers from Australia, the U.K., Canada, Thailand and Italy.

More information: Uraiporn Booranasuksakul et al, Sarcopenia, obesity, sarcopenic obesity and dementia risk: a systematic review and meta-analysis of cohort studies, International Journal of Food Sciences and Nutrition (2026). DOI: 10.1080/09637486.2026.2722926

Provided by Curtin University

This story was originally published on Medical Xpress.

Experts link protein quality to slower biological aging

 Will your competent? doctor get the dietician to create a diet protocol on this?

 I'm sure your incompetent? doctor never instructed the dietician to create EXACT diet protocols for you; both hospital and home. And your board of directors is so incompetent, they don't recognize incompetence in their hospital! 

NO can do is PURE INCOMPETENCE!

Experts link protein quality to slower biological aging

Protein reduces risk of frailty in aging populations

Adequate protein intake lowers the likelihood of developing frailty, a condition characterized by weakness and reduced resilience in older adults. This contributes to better quality of life and longevity.

References

Biological aging may be slowed by eating this nutrient | EatingWell
The Longevity Diet: 8 Essential Plant-Based Proteins to Help You Live Longer | hi.kormedi.com
Best Diet for Longevity: What to Eat to Live Longer - ScienceInsights | scienceinsights.org

Plant proteins providing fiber, polyphenols, and anti-inflammatory benefits

Plant-based proteins contribute additional nutrients such as fiber and polyphenols, and they offer anti-inflammatory effects. These properties can support overall health beyond muscle maintenance.

References

For healthy aging, which protein you eat may matter more than how much | welltica.com
Best protein sources after 50: A longevity-focused guide | superage.app
Protein, Leucine & Longevity: Sarcopenia & mTOR Balance | The Private Practice | theprivatepractice.co

Protein-rich breakfast to support muscle protein synthesis

Including a protein-rich breakfast is one approach to ensure adequate leucine intake early in the day. This strategy supports stimulation of muscle protein synthesis in older adults.

References

Protein for Longevity: The Secret to Aging Well | getstride.com
Protein & Amino Acids for Longevity: Optimization Protocol | TPP | theprivatepractice.co
Protein, Leucine & Longevity: Sarcopenia & mTOR Balance | The Private Practice | theprivatepractice.co

Animal studies on amino acid restriction and lifespan extension

Research conducted in animals indicates that reducing specific amino acids, such as isoleucine or methionine, can induce metabolic changes associated with increased lifespan. These findings suggest that amino acid composition, rather than just total protein intake, may play a role in longevity outcomes observed in experimental models.

References

For healthy aging, which protein you eat may matter more than how much | welltica.com
Reducing This Nutrient in Diet May Help You Live Longer | Knowridge

Core Contractions Drive Brain Blood Flow

 Does your competent? doctor have enough brains to see this need and provide cerebral blood flow protocols? OH NO, your doctor has been INCOMPETENT FOR OVER A DECADE!

• cerebral blood flow (59 posts to December 2015)

Core Contractions Drive Brain Blood Flow

Summary:

Contracting core abdominal muscles through everyday activities like exercise, walking, or coughing directly regulates blood flow within the brain by causing ultrafast constrictions in major cerebral veins. The findings reveal that cerebral circulation is directly coupled to peripheral mechanical forces, offering fresh clues into the neurovascular benefits of exercise and the mechanics behind movement-triggered migraines.

Key Facts:

• Ultrafast Venous Constriction: In response to abdominal muscle activation, major cerebral veins, including the superior sagittal sinus and bridging veins, constrict in approximately one-tenth of a second, far outpacing the multi-second response time typical of cerebral arteries.
• Mechanical Spine-to-Brain Signaling: Core contractions elevate pressure in venous structures connected through the spinal column into the skull, momentarily driving blood flow alterations inside the dural membrane.
• Relevance to Headaches and Exercise: Because dural veins are embedded in pain-sensitive tissue, these movement-induced pressure fluctuations may explain why physical exertion can exacerbate migraines while simultaneously promoting long-term brain vascular health.

Source: Penn State University

Neuroscientists have long viewed cerebral blood flow as a self-contained system regulated locally within the skull. When a specific brain region increases its metabolic activity, nearby arteries and capillaries relax to supply incoming oxygen and nutrients.

However, a study published in the Proceedings of the National Academy of Sciences (PNAS) demonstrates that cerebral circulation is intimately tethered to mechanical forces generated elsewhere in the body. Researchers discovered that activating core abdominal muscles—whether during purposeful locomotion or involuntary actions like coughing, transmits rapid pressure changes upward through the spinal column to dynamically alter venous blood flow in the brain.

“The brain may be protected inside the skull, but it is not isolated from the mechanical forces generated by the rest of the body,” explained lead author Qingguang Zhang, Ph.D., an assistant professor of physiology at Michigan State University who began the project while at Penn State. “We were surprised by how rapidly and consistently the veins responded to movement… Our findings show that mechanical signals generated by the body can have immediate consequences for the circulation inside the skull.”

Beyond “Passive Pipes”: Veins as Active Regulators

Blood flow throughout the body requires continuous redistribution depending on dynamic organ demands. Senior author Patrick Drew, Ph.D., professor of biology, engineering science and mechanics, neurosurgery, and biomedical engineering at Penn State, compares this coordination to a municipal utility.

“A city’s water system has to be able to accommodate different use needs of an apartment building or a single-family home, or even a full stadium on gameday,” Drew said. “Blood flow in the body must be precisely controlled because different organs need different amounts of blood at different times.”

Historically, arteries and capillaries have taken center stage in neurovascular studies because they are encircled by smooth muscle cells that dilate and constrict in response to local chemical signals. Cerebral veins, possessing far less musculature, have often been viewed as passive drainage channels.

The new findings challenge that assumption. By monitoring vascular dynamics during natural mouse movement, the researchers observed rapid, marked constrictions of the superior sagittal sinus, the primary vein running along the superior midline of the brain, and its feeding bridging veins. While arterial contractions generally unfold over several seconds, these cerebral veins reacted within roughly 100 milliseconds of core abdominal engagement.

“Veins are not simply passive pipes,” noted Zhang. “When we think about brain blood flow regulation, we tend to focus heavily on arteries. Our results highlight the other side of circulation. What happens to blood as it leaves the brain can be just as dynamic and physiologically important.”

Implications for Exercise, CSF Flow, and Migraine Pain

The physical mechanism originates in the abdomen. Engaging the abdominal wall increases pressure across the vascular networks that link the torso to the cranial vault via the spinal column. This mechanical surge creates an instantaneous narrowing of cerebral outflow channels, momentarily boosting blood flow.

In previous research, the team showed that abdominal contractions also physically displace the brain by tiny increments, helping to circulate protective cerebrospinal fluid (CSF). Because mouse and human vascular architectures share close physiological homology, the investigators expect this core-to-brain hemodynamic coupling to operate similarly in humans.

The findings may clarify several clinical enigmas:

• The Exercise-Brain Connection: Regular physical activity provides proven cognitive and neuroprotective benefits. The continuous pumping and constriction of dural veins during physical exertion could be a driving force behind improved clearance and circulation.
• Headaches and Migraines: Unlike brain tissue itself, the surrounding protective dura mater is dense with sensory pain receptors. Rapid pressure spikes and venous shifts within dural veins could explain why movements like bending over, coughing, or exercising often trigger or intensify migraine pain.

By mapping the mechanical pathways linking core movement to the cerebral vasculature, the researchers aim to lay the groundwork for better identifying neurovascular dysfunctions and designing future interventions.

Funding: The work was funded by the U.S. National Institutes of Health’s National Institute of Neurological Disorders and Stroke under grants R01NS078168 and U19NS128613, the American Heart Association and neuroscience seed funds from Henry Ford Health and Michigan State University Health Sciences. The content is solely the responsibility of the authors and does not necessarily represent the official views of the funders.

Editorial Notes:

• This article was edited by a Neuroscience News editor.
• Journal paper will be reviewed in full once available.
• Additional context added by our staff.

About this Neuroscience Research:

• Media Contact: Sam Sholtis
• Source: Penn State
• Image Credit: Image credited to Neuroscience News
• Original Research: The findings will appear in PNAS.

Sex-Specific Biological Clocks Reveal How Aging Differs Across Women and Men: Study

 Make sure your competent? doctor has the correct sex-specific protocols to recovery  your 5 lost years of brain cognition due to your stroke.

Sex-Specific Biological Clocks Reveal How Aging Differs Across Women and Men: Study

New Blood Thinners Could Help Slow Cognitive Decline in Alzheimer's, Study Finds

 With your risk of dementia post stroke, just maybe you want your doctor to be competent in this! Up to you to ensure competence. 

Your doctor is responsible for preventing this! Is s/he willing to prevent this?

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:

New Blood Thinners Could Help Slow Cognitive Decline in Alzheimer's, Study Finds

The pan-immune-inflammation value predicts stroke-associated pneumonia and poor outcome in spontaneous intracerebral hemorrhage: a machine learning approach

 You're that incompetent you don't know predictions DO NOTHING TOWARDS RECOVERY! Solve the correct problem!  You've known of the need to prevent pneumonia for years! I'd have you all fired for incompetence!

• 11% Stroke-associated pneumonia (21 posts to October 2020)

The pan-immune-inflammation value predicts stroke-associated pneumonia and poor outcome in spontaneous intracerebral hemorrhage: a machine learning approach

• 

  Anni Chen †

• J

  Jiahui Wang †

• Q

  Qiaoying Huang †

• 

  Chaoxiong Shen

• 

  Zhizhou Hu

• 

  Xiaohong Hu *

• Department of Neurology, Longyan First Affiliated Hospital of Fujian Medical University, Longyan, Fujian, China

Abstract

Objective: 

Stroke-associated pneumonia (SAP) constitutes a major complication following spontaneous intracerebral hemorrhage (sICH), posing a significant clinical challenge for accurate prediction. This study aimed to evaluate whether integrating the pan-immune-inflammation value (PIV) enhances the predictive performance of machine learning (ML) models for SAP and poor functional outcome.

Methods: 

A retrospective cohort of 371 sICH patients was analyzed. Feature selection was performed using the least absolute shrinkage and selection operator (LASSO). Predictive models for SAP and poor outcome [modified Rankin Scale score (mRS) > 2 at 90 days] were developed and compared across nine ML algorithms. Model performance was assessed by discrimination (area under the receiver operating characteristic curve, AUC), calibration, and decision curve analysis (DCA). Interpretability was achieved via SHapley Additive exPlanations (SHAP).

Results: 

Elevated PIV was independently associated with SAP [odds ratio (OR) 13.55, 95% confidence interval (CI) 4.14–44.39; p < 0.0001] and poor 90-day functional outcome (OR 25.27, 95% CI 7.75–82.34; p < 0.0001). Among the algorithms, extreme Gradient Boosting (XGBoost) and logistic regression (LR) demonstrated the highest predictive performance for poor outcome (AUC 0.912) and SAP (AUC 0.856), respectively. Incorporating PIV significantly improved discriminatory ability (XGBoost: 0.926–0.942; LR: 0.905–0.931; both p < 0.05). The models demonstrated good calibration, provided net clinical benefit on DCA, and were interpretable through SHAP analysis, which consistently identified PIV as a critical predictor.

Interpretation: 

The integration of PIV into interpretable ML models significantly improves the accuracy of predicting SAP and functional outcome after sICH. This strategy, combining a systemic inflammatory biomarker with explainable ML, holds promise for advancing personalized risk stratification in neurocritical care.

Development and validation of a machine learning model based on multi-source clinical data for predicting the risk of early neurological deterioration in patients with ischemic stroke

 

Totally wrong objective; Survivors actually want early neurological deterioration prevented! Predictions DO NOTHING TOWARDS RECOVERY! 

What prevents early neurological deterioration is the needed research, not this crapola! You've known of the need for almost a decade but INCOMPETENTLY did this instead! You're fired!

• Early neurological deterioration (36 posts to January 2017)

Development and validation of a machine learning model based on multi-source clinical data for predicting the risk of early neurological deterioration in patients with ischemic stroke

• 

  Yue Li

• W

  Wei Wang

• Y

  Yilan Wei

• J

  Jing Han

• Y

  Yuan Shi

• Q

  Quping Ouyang *

• Neurological Disease Center, Beijing Shunyi District Hospital, Beijing, China

Abstract

Background and objective: 

Early neurological deterioration (END) is a critical clinical event associated with poor patient outcomes after acute ischemic stroke. Early identification of high-risk patients is crucial for timely clinical management. This study aimed to develop and validate a model for predicting END risk for acute ischemic stroke patients using machine learning algorithms.

Methods: 

This study retrospectively and consecutively enrolled 1,151 patients with acute ischemic stroke from the Stroke Center of Beijing Shunyi District Hospital between January 2021 and December 2024. END was defined as progressive worsening of neurological deficit symptoms after onset. Predictive variables were screened using univariate analysis and multiple feature selection methods (Treebag, Boruta, Bayesian). Nine machine learning algorithms (Decision Tree, Efficient Neural Network, K-Nearest Neighbors, Light Gradient Boosting Machine, Logistic Regression, Multilayer Perceptron, Random Forest, Simplified Support Vector Machine, Extreme Gradient Boosting) were employed to construct prediction models. Hyperparameters were optimized via 10-fold cross-validation, and model performance was evaluated in an internal validation cohort (30% of the sample). Primary evaluation metrics included the area under the receiver operating characteristic curve (AUC), sensitivity, specificity, accuracy, F1 score, and net benefit from decision curve analysis (DCA). The SHAP method was used to interpret the optimal model.

Results: 

A total of 161 patients (14.0%) developed END. Feature selection ultimately identified five key predictors: ischemic stroke etiological subtype, Oxford Community Stroke Project (OCSP) classification, age, atrial fibrillation history, and prior stroke history. In both the development and internal validation cohorts, the logistic regression model demonstrated favorable and stable performance (development cohort AUC: 0.787, 95% CI: 0.735–0.839; internal validation cohort AUC: 0.751, 95% CI: 0.668–0.834), with a low log-loss value. DCA suggested potential clinical utility of the logistic regression model. SHAP analysis revealed that the etiological subtype of ischemic stroke and age were the features contributing most to the model’s predictions.

Conclusion: 

This study successfully developed and validated a logistic regression model for predicting END risk. The model incorporates five routinely available clinical variables and demonstrates satisfactory predictive performance and interpretability. The developed online tool may assist clinicians in early risk stratification, providing a reference for personalized intervention.

Association between lactate-to-albumin ratio and in-hospital mortality in ICU patients with acute ischemic stroke: a retrospective cohort study

 And you think predicting mortality is more important than research to prevent mortality? YOU'RE FIRED!

Association between lactate-to-albumin ratio and in-hospital mortality in ICU patients with acute ischemic stroke: a retrospective cohort study

• 

  Xiaocui Yang

• Y

  Yue Zhang

• M

  Min Ou

• 

  Yiwen Liu *

• West China Hospital, Sichuan University, Chengdu, Sichuan, China

Abstract

Background: 

Early risk stratification is critical for critically ill patients with ischemic stroke. The prognostic value of the lactate-to-albumin ratio (LAR) remains unclear in this population.

Methods: 

This single-center retrospective cohort study enrolled adult ICU patients with ischemic stroke from West China Hospital. LAR was calculated using the first lactate and albumin values on ICU admission. Log-transformed LAR was adopted as the main exposure, and the primary outcome was in-hospital mortality. Multivariable logistic regression, ROC analysis, quartile stratification, subgroup, and sensitivity analyses were performed among 749 patients with complete exposure and outcome data, of whom 576 had complete covariate data and comprised the primary multivariable regression cohort.

Results: 

A total of 749 patients were included, with an in-hospital mortality rate of 30.7%. In complete-case multivariable analysis (N = 576; deaths = 172), log-transformed LAR was independently associated with in-hospital mortality (OR = 1.44, 95%CI: 1.09–1.91, p = 0.010) after full adjustment. Each two-fold increase in LAR was associated with a 29% increase in mortality odds. The highest LAR quartile had a significantly higher mortality risk than the lowest quartile (OR = 2.16, 95%CI: 1.21–3.92). LAR showed modest predictive ability (AUC = 0.628). When modeled as a raw continuous LAR, the direction of association remained consistent but did not reach conventional statistical significance (OR 1.23; 95% CI 0.97–1.56; p = 0.083). Moreover, no significant interaction or non-linearity was found.

Conclusion: 

Elevated LAR is independently linked to higher in-hospital mortality among critically ill ischemic stroke patients. It may serve as a simple adjunctive marker for early risk stratification.

Serial immune-inflammatory recovery trajectories after acute ischemic stroke: associations with early neurological deterioration and 90-day functional outcome in a retrospective cohort

 

'Associations' don't get you recovered, or are you too fucking stupid to see that? What prevents early neurological deterioration is the needed research, not this crapola! You've known of the need for almost a decade but INCOMPETENTLY did this instead! You're fired!

• Early neurological deterioration (36 posts to January 2017)

Serial immune-inflammatory recovery trajectories after acute ischemic stroke: associations with early neurological deterioration and 90-day functional outcome in a retrospective cohort

• 

  Ruihan Ni 1

• 

  Lan Chu 1,2*

• 1. Suzhou Medical College, Soochow University, Suzhou, Jiangsu, China

• 2. Department of Neurology, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China

Abstract

Background: 

Systemic inflammation after acute ischemic stroke is usually assessed using admission biomarkers, which may not distinguish transient stress from sustained immune-inflammatory activation. We examined whether serial immune-inflammatory recovery trajectories were associated with early neurological deterioration (END) and 90-day functional outcome.

Methods: 

This single-center retrospective cohort included 760 adults with acute ischemic stroke identified from a hospital stroke database. NLR, SII, SIRI, and hs-CRP measured at admission, 24 h, 72 h, and day 7 were log-transformed and standardized, and equally weighted values were averaged at each observed time point. Latent class mixed models with 2–5 classes were compared without using outcome information, and a five-class solution was selected before association and prediction analyses. The primary outcome was 90-day mRS 3–6. END was defined as an NIHSS increase of ≥2 points within 72 h; the landmark END analysis excluded END within 24 h and tested 0–24 h immune change for END from 24 to 72 h.

Results: 

The five LCMM classes comprised 182 low-stable, 223 transient moderate, 161 delayed recovery, 122 persistent high, and 72 extreme persistent high patients. Among 751 patients with 90-day outcome data, the observed rate of mRS 3–6 increased from 21.5 to 30.6%, 44.2, 71.9, and 98.6% across these classes. After adjustment, persistent high (OR 2.46, 95% CI 1.31–4.61; p = 0.005) and extreme persistent high inflammation (OR 20.24, 95% CI 2.48–165.26; p = 0.005) were associated with mRS 3–6; a bias-reduced sensitivity estimate for the extreme class remained large (OR 13.61, 95% CI 2.34–79.26). Ordinal analysis showed progressively worse mRS for delayed recovery (common OR 2.73), persistent high (4.18), and extreme persistent high (6.72). The 0–24 h composite immune-change metric was not associated with landmark END (OR 1.12, 95% CI 0.92–1.36; p = 0.265). Adding LCMM-5 to the clinical model increased AUC from 0.828 to 0.841, but did not clearly outperform adding admission NLR/SII.

Conclusion: 

Longitudinal classification identified five immune-inflammatory recovery trajectories with a marked gradient in 90-day disability. Persistent-high and extreme persistent-high classes retained independent associations with poor functional outcome.