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.

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.

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