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.

Wednesday, September 24, 2025

Association of Frailty With Dementia and the Mediating Role of Brain Structure and Immunometabolic Signatures

 


Your competent? doctor has had years to come up with a protocol to prevent frailty post stroke. 

Did that occur? NO? So, you don't have a functioning stroke doctor or hospital, do you? RUN AWAY!

  • frailty (26 posts to January 2018)
  • So, your doctor isn't up to the task of new knowledge? I'd suggest forced retirement of the doctor if your hospital is any good at all!

    Association of Frailty With Dementia and the Mediating Role of Brain Structure and Immunometabolic Signatures

  • Abstract

    Background and Objectives

    Physical frailty is associated with a higher risk of developing dementia, but it remains unclear whether this relationship is causal and whether the biological biomarkers and neurologic underlying mechanisms are involved. We aimed to elucidate the link between physical frailty and dementia, establish their causal relationship, and investigate the underlying biological mechanisms.

    Methods

    This prospective cohort study was based on UK Biobank participants without dementia at enrollment (between 2006 and 2010). Physical frailty was defined by 5 criteria (weight loss, exhaustion, physical inactivity, slow walking speed, and low grip strength). Incident dementia was tracked through linked hospital admission records and death registries, using the International Classification of Diseases, Tenth Revision (ICD-10) codes. Cox proportional hazard regression models and bidirectional Mendelian randomization (MR) analyses were used to evaluate the causal association of physical frailty with incident dementia. In addition, the potential roles of genetic background, brain structures, and biological biomarkers in the association were evaluated using structural equation modeling.

    Results

    Among 489,573 participants (mean age 57.03 years, 54.4% female), 8,900 dementia cases were documented over a median follow-up of 13.58 years. Compared with nonfrail individuals, the risk of dementia was 50% higher in those with prefrailty (hazard ratio [HR]:1.50, 95% CI 1.44–1.57) and 182% higher in those with frailty (HR: 2.82, 95% CI 2.61–3.04). Participants with frailty and high genetic risk had the highest risk of dementia compared with those with low genetic risk and nonfrailty (HR: 3.87, 95% CI 3.30–4.55 for high polygenic risk score; HR: 8.45, 95% CI 7.51–9.51 for APOE-ε4 carriers). The forward MR analysis indicated a potential causal relationship between physical frailty and dementia (odds ratio [OR]:1.79, 95% CI 1.03–3.12) while the reverse MR suggested a null causal association (OR: 1.00, 95% CI 0.98–1.01). Structural equation modeling points to genetic background and neurologic and immunometabolic function as potential underlying mechanisms linking physical frailty to dementia.

    Discussion

    Our findings support the causal association between physical frailty and dementia, which is possibly mediated through genetic background and neurologic and immunometabolic function. However, this association deserves close consideration because frailty may also be a correlative marker of dementia vulnerability.

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