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. Did your doctor somehow miss the recovery protocol that Pedro Bach-y-Rita used to recover fully back in 1958 with only a partial brain?

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 solve the correct problem. Show all posts
Showing posts with label solve the correct problem. Show all posts

Sunday, October 25, 2026

Depression, Not Anxiety, Linked to Poorer Cognition After Stroke

 It doesn't make a damn bit of difference what causes that poor cognition! SOLVE THE DAMN PROBLEM!

Prevent that cognition problem from occurring! Luckily my cognition remained intact since my doctor would have failed at that like he failed at my motor recovery and spasticity!

Depression, Not Anxiety, Linked to Poorer Cognition After Stroke

TOPLINE

Depression, but not anxiety, was independently linked to poorer executive function over 5 years after ischaemic stroke. The association between depression and visuospatial function was less robust. Anxiety was present in 27%-36% of patients at each assessment. 

METHODOLOGY

  • Researchers analysed data from the single-centre, observational STROKDEM cohort, which included 191 patients with ischaemic stroke (119 men and 72 women) assessed at 6, 12, 36, and 60 months after stroke.
  • Data on anxiety were available for 157 patients at 6 months and 85 patients at 60 months; patients with poorer baseline cognition were more likely to be lost to follow-up.
  • Patients completed neuropsychological testing across five domains (memory, executive function, attention, visuospatial abilities, and language), with results expressed as domain-specific z-scores.
  • Anxiety was measured using the Hamilton Anxiety Rating Scale (scores ≥ 8 indicated clinically relevant anxiety), depression was assessed using the Center for Epidemiologic Studies Depression Scale (scores ≥ 16 indicated clinically relevant depression), and stroke severity was evaluated using the National Institutes of Health Stroke Scale.
  • Researchers fitted two models, each using one affective score as the outcome and the five cognitive domains as predictors, with adjustment for the other affective score, time, sex, age, education, and stroke severity. Sensitivity analyses used multiple imputation and pattern-mixture models to address attrition.

TAKEAWAY

  • After mutual adjustment and false discovery rate correction, depression was independently associated with executive function (standardised regression coefficient [b], -0.167; P = .021) and visuospatial abilities (b, -0.208; P = .043). 
  • No cognitive domain was independently associated with anxiety after adjustment for depression. 
  • The association between depression and executive function held across all sensitivity analyses, including multiple imputation (b = -0.178; P = .015) and pattern-mixture analysis (P = .008 to .025). The association between depression and visuospatial abilities was not significant after multiple imputation (P = .195). 
  • Anxiety prevalence ranged from 26.6% to 36.1% across assessments (28.7% at 6 months and 31.8% at 60 months), whereas depression prevalence declined from 27.1% to 17.8%. 

IN PRACTICE

"Distinguishing between [depression and anxiety] requires joint modelling; failing to do so risks misattributing depression-related cognitive impairment to anxiety. For clinical practice, screening for depression is the more informative route for identifying stroke survivors at cognitive risk," the authors wrote. 

"This does not diminish the importance of anxiety, which is prevalent, persistent, and detrimental to quality of life and rehabilitation participation in its own right," they added. 

SOURCE

The study was led by Florine Ruthmann, Université de Lille, Inserm, Lille, France. It was published online on October 12 in the Journal of Affective Disorders.

LIMITATIONS

Attrition was substantial, and patients with poorer baseline cognition were more likely to be lost to follow-up; the COVID pandemic further contributed to the loss to follow-up at 60 months. Few patients had persistent anxiety. Psychiatric history was not available, psychotropic medication use was not adjusted for, and education was the only measure of cognitive reserve. The study was observational and conducted at a single centre, and the cohort included mostly men; effect sizes were modest.DISCLOSURES

Hauts-de-France Regional Council funded the study. The authors reported having no conflicts of interest.

The daytime habit linked to a higher risk of dementia

 Napping IS NOT THE PROBLEM, you blithering idiots! It's the symptom, solve the underlying problem causing naps!

The daytime habit linked to a higher risk of dementia

A common daytime habit many older adults do could be increasing their risk of developing dementia, a new study has found.

Researchers at Johns Hopkins University said that daytime napping, specifically how often, how intentionally and how long, was found to influence a person’s risk of developing dementia.

However, the experts emphasized that the findings were observational and do not establish that napping directly causes dementia. The study was published online in The Journals of Gerontology: Medical Sciences on October 5.

These findings follow on from previous research in the field, some of which has indicated that sleepiness has been associated with an abnormal accumulation of proteins associated with dementia in the brains of otherwise healthy adults, Dr. Andrew Varga, a sleep neurologist and neuroscientist at the Icahn School of Medicine at Mount Sinai, told Newsweek.

They found that those who napped frequently, meaning either most days or every day, had a 48 percent higher risk of developing dementia compared to those who either rarely or never napped.

 Related video: New study identifies possible early sign of dementia (Welltica+) 

The researchers said this was the case even after several demographic factors were accounted for, such as health conditions and nighttime sleep characteristics.

Unintentional napping, so falling asleep without intending to, was linked to a 39 percent higher risk of developing dementia as well.

They also identified that duration of the nap had an impact too. Daytime sleeping for 30 minutes or less was associated with a 40 percent higher risk.

A ‘Two-Way’ Association

The scientists noted that there could be a “two-way” nature to the association, meaning that cognitive decline can cause more frequent intentional and unintentional napping, as well as napping potentially increasing risk of the disease.

Varga said that as the proteins amyloid and tau – which are associated with dementia development – “start to accumulate and neurons start to become dysfunctional or die, some of the earliest neurons affected are ones that control the regulation of sleep and wake as well as the circadian rhythm.”

“So, this means that periods of sleep can come on during the day at inappropriate times,” he said.

However, as the researchers followed some participants for 10 years, who did not have dementia at the start of the study, they said that the findings seem to suggest that napping pattern could have an influence on dementia development, and not just be a reflection of the disease.

How Could Napping Affect Dementia Risk?

In terms of how napping could affect dementia risk, Adam Spira, the study author and a professor of mental health at Johns Hopkins University, told Newsweek that one possibility is daytime napping may affect nighttime sleep.

“This matters because disturbed nighttime sleep is linked to brain changes associated with dementia, such as the accumulation of proteins like beta-amyloid and increased neuroinflammation,” he said.

He said, specifically, “napping may reduce ‘homeostatic sleep drive,’ the body’s natural drive for sleep that builds up throughout the day, potentially disrupting nighttime sleep.”

Both sleep deprivation and sleep apnea have been “shown to raise risk for dementia, with proposed mechanisms including increased production of amyloid and tau (the bad proteins that accumulate in Alzheimer’s disease), decreased clearance of amyloid and tau from the brain, increased inflammation, and altered immune function,” Varga said.

Dr Omonigho Bubu, the director of the Aging Research in Sleep Equity and Dementia Prevention program at New York University, told Newsweek that daytime napping may also reflect “underlying sleep disruption, excessive daytime sleepiness, or early neurodegenerative changes already affecting the brain systems that regulate sleep and wakefulness.”

“In that sense, napping may be either a contributing factor, an early warning sign, or both,” he said.

What The Findings Mean

Kening Jiang, the study’s first author and postdoctoral fellow at Johns Hopkins University, told Newsweek the findings suggest daytime napping “may be an important potential risk factor for dementia,” and “highlight the importance of considering daytime napping, in addition to nighttime sleep, as napping behaviors may help identify older adults at higher risk of dementia and inform dementia-prevention strategies.”

“However, whether daytime napping causes dementia has not yet been established, and more research is needed to understand whether this is a causal relationship,” he said.

Varga said that it’s important to note “not all napping is bad, and there are documented benefits of napping,” but it becomes a worry when “the napping is in response to either insufficient nighttime sleep or, sleep that is of sufficient duration but is interrupted by some disorder.”

Bubu said the findings suggest that “daytime sleep behaviors should not be overlooked in older adults.” He added that “the key message is not that all napping is harmful, but that changes in napping patterns deserve attention.”

Reference

Kening Jiang, Alden L Gross, Catriona Tingsea Wu, Junxin Li, Halima Amjad, Emerson M Wickwire, Jennifer S Albrecht, Atul Malhotra, Chien-Yu (Irene) Tseng, Marc Kaizi-Lutu, Chunyu Liu, Christopher N Kaufmann, Adam P Spira, (2026) Napping characteristics and incident dementia: results from the National Health and Aging Trends Study, The Journals of Gerontology: Series A. https://doi.org/10.1093/gerona/glag208

Newsweek’s reporters and editors used Martyn, our AI assistant, to produce this story. Learn more about Martyn here.

Contact Newsweek editors on this story: Kara Dolman and Paul Donnelley.

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Friday, October 2, 2026

Associations between wearable‐device‐measured daytime and nighttime light exposures and dementia risk: A prospective cohort study

 Not getting you into daylight as often as possible IS EXTREME INCOMPETENCE OF YOUR DOCTOR!

Associations between wearable‐device‐measured daytime and nighttime light exposures and dementia risk: A prospective cohort study


PMCID: PMC13291554  PMID: 42358626

ABSTRACT

Background

Identifying reliable predictors for dementia remains a critical unmet need(You ARE that blitheringly stupid you think predictions are helpful! SOLVE THE CORRECT PROBLEM! PREVENTING DEMENTIA!) Light exposure plays a crucial role in regulating circadian rhythms, which influence cognitive function. However, the association between light exposure and dementia risk remains unclear.

Aims

This study examined the associations of daytime and nighttime light exposure with dementia risk.

Methods

A total of 87 577 dementia‐free participants (mean age: 62.36 years; 56.98% female) were included. Daytime and nighttime light exposures were measured using 7‐day free‐living wrist‐worn accelerometry. Incident dementia was identified from primary care, hospital inpatient admissions and death registry data. Cox proportional hazards models assessed associations, and mediation analyses evaluated circadian rest–activity rhythms (CRARs), brain structures and vitamin D as potential mediators.

Results

Over a median follow‐up of 8.1 years, 741 participants developed dementia. Daytime light exposure above 1000 lux was associated with reduced dementia risk (hazard ratio [HR] 0.84, 95% confidence interval [CI] 0.71–0.99, p = 0.039). Longer exposure to brighter light (e.g., ≥ 0.70 h at ≥ 5000 lux; HR 0.83, p = 0.036) was associated with a further reduction in risk. In exploratory analyses, CRARs and brain structures mediated up to 33% of the association. Protective associations were stronger in those with high levels of nighttime light exposure, an evening chronotype or apolipoprotein E (APOE) ε4 carrier status, with a risk reduction of up to 41%. Furthermore, < 0.70 h per day of bright daytime light (≥ 5000 lux) outperformed six established dementia predictors (e.g., obesity, alcohol consumption, traumatic brain injury and so on). Nighttime light showed no significant association with dementia risk.

Conclusions

High levels of daytime light exposure were significantly associated with lower dementia risk. Further research should explore its role in dementia screening and inform the development of light‐based interventions.