A new study found a connection between low levels of this 1 vitamin and dementia — and 60% of the world is deficient in it

 

Fairly useless, nothing on how to measure such deficiency and no protocols listed to counteract such deficiency. 

How can I check my vitamin D levels at-home?

Everlywell, Drop, and myLAB Box are other brands that offer at-home vitamin D tests. Each relies on a finger prick blood sample. “Any at-home testing should be done by individuals who know or feel they may be at risk for low levels,” Guandalini says.

How to Get Vitamin D: 7 Effective Ways - Healthline

The latest here:

A new study found a connection between low levels of this 1 vitamin and dementia — and 60% of the world is deficient in it

Many people’s vitamin D levels do not fall within a healthy range, which can cause muscle weakness, fatigue, depression, bone pain and lower immune function. In fact, an estimated 60% of the world is vitamin D deficient and needs a supplement, Dr. Michael Holick, a professor of medicine, pharmacology, physiology & biophysics and molecular medicine at Boston University Chobanian & Avedisian School of Medicine, previously told HuffPost.

But if that alone isn’t enough to convince you to prioritize getting vitamin D, which you can do through foods like salmon, tuna, and milk, new research published in the journal “Neurology” this month may do the trick. The study suggests that people with high vitamin D levels in their 30s and 40s have lower dementia risk factors later in life.

The study investigates the potential impact of vitamin D levels in early midlife by examining the prevalence of tau protein and amyloid protein in the brain, “which are key hallmarks of Alzheimer’s disease,” Dr. Thomas M. Holland, physician-scientist and assistant professor at the Rush Institute for Healthy Aging at Rush University Medical Center in Chicago, told HuffPost via email. Holland is not affiliated with the study.

Researchers followed 793 people in their 30s and 40s with an average age of 39 over 16 years. Vitamin D levels were tested at the beginning of the study; those with levels below 30 nanograms per milliliter (ng/mL) were categorized as having low vitamin D; anything above was considered high.

After a follow-up at the end of the study, it was determined that participants in the high-vitamin D group were more likely to have lower tau levels in their brains.

“Researchers looked at two different types of scans of the brain called PET scans,” said Dr. David Gill, chief of the division of cognitive and behavioral neurology at the University of Rochester in New York. Gill is not affiliated with the study.“One looks at the amyloid protein [prevalence], and one looked at the tau protein [prevalence].” 

Even though tau protein levels were lower in participants with high vitamin D, researchers found that those elevated levels did not impact levels of amyloid in the brain. This indicates someone with high vitamin D could still have elevated levels of amyloid protein, which, as mentioned above, is a characteristic of Alzheimer’s disease.

This study does have a “major limitation,” Dr. Jagan Pillai, a Cleveland Clinic neurologist and director of the Cleveland Alzheimer’s Disease Research Center, told HuffPost via email. Vitamin D levels were measured once at the beginning of the study “and after that PET scans were completed 15 or more years later,” said Pillai, who was not associated with the study..

“So, we don’t have any information in between,” Pillai added. It’s unknown if participants took supplements or followed a healthy lifestyle that helped them maintain healthy vitamin D levels, he noted. Because vitamin D levels were only measured once, it’s also unclear if someone shifted from having healthy levels to unhealthy levels (or the opposite) during the study’s time period.

While this study has solid data, it does not prove that vitamin D levels directly affect dementia risk, according to Gill. There are many studies on this topic, and they’re conflicting.

“Specifically, there’s been some studies to show that giving vitamin D might help improve memory a little bit, but those are also conflicting. There’s been all of this information out there without a firm understanding of whether there’s a real connection between low vitamin D and Alzheimer’s disease,” Gill said. “I don’t know this [study] answers that question, but it helps move us forward.”

So, does this mean having healthy vitamin D levels in your 30s and 40s will protect you from dementia? Not necessarily. But having healthy vitamin D levels can bolster many systems in your body, including the brain. And as research emerges about vitamin D and dementia risk, there are other changes you can make to take care of your cognition.

Scientists reveal daily step count that may help slow Alzheimer’s disease

 What are the EXACT PROTOCOLS from your doctor that will guarantee you recover enough to do this?

Scientists reveal daily step count that may help slow Alzheimer’s disease

A “moderate” amount of physical activity—in the form of getting your daily steps—could be help slow Alzheimer’s disease among those at risk.

This is the finding of Mass General Brigham scientists who determined that a surprisingly achievable step count was associated with slower rates of cognitive decline in older adults with elevated levels of amyloid beta, a protein linked to the disease.

Cognitive decline was delayed by three years on average for people who walked just 3,000–5,000 steps per day, according to the 14-year study of cognitively unimpaired older adults.

Meanwhile, it was delayed by seven years for people who walked 5,000–7,500 steps per day.

Those who were sedentary, however, had a significantly faster harmful buildup of tau proteins in the brain and more rapid declines in cognition and daily functioning. 

“We were able to clarify that the association with cognitive decline was not explained by differences in amyloid accumulation,” study author and cognitive neurologist Dr. Wai-Ying Wendy Yau told Newsweek.

“Instead, for a given amount of elevated amyloid burden, higher step counts were associated with slower accumulation of tau, the protein most closely tied to cognitive symptoms, which largely accounted for the association with slower cognitive decline.”

Mature woman using smart watch to track steps.“These findings show us that it’s possible to build cognitive resilience and resistance to tau pathology in the setting of preclinical Alzheimer’s disease,” added study author and neurologist Dr. Reisa Sperling.

“This is particularly encouraging for our quest to ultimately prevent Alzheimer’s disease dementia, as well as to decrease dementia due to multiple contributing factors.”

The team analyzed data on 296 cognitively unimpaired participants aged 50–90 in the Harvard Aging Brain Study.  

“This research provides strong evidence that moderate levels of physical activity are associated with slower progression of the earliest stages of Alzheimer’s disease and that this is linked to slower accumulation of tau protein, which is an important cause of brain cell loss,” said neurologist professor Charles Marshall of Queen Mary University of London—who was not involved in the study—in a statement. 

The researchers used PET brain scans to measure baseline levels of amyloid-beta in plaques (dense clumps) and tau in tangles (formed from the accumulation of abnormal tau) and assessed the participants’ physical activity using small waistband tracking devices.

The main study group received annual follow-up cognitive assessments for between two and 14 years while a subset group received repeated PET scans to track changes in tau.

More steps were linked to slower rates of cognitive decline and a slower buildup of tau proteins. In people with low baseline levels of amyloid-beta, however, there was very little cognitive decline or accumulation of tau proteins over time and no significant associations with physical activity.

“With this type of observational study, it is always hard to be sure whether the physical activity is actually the thing causing the observed difference. The authors do a good job of trying to disentangle this, but we cannot be certain whether the people doing more exercise are healthier in other ways, nor whether the development of Alzheimer’s disease changes are influencing activity levels (reverse causality),” said Marshall.

“We also cannot be sure that it is physical activity during this period in later life that makes the difference, or whether those who are more active now have been more active for decades and that the benefits accrue in the much longer term.”

“The study followed people with raised levels of amyloid in their brain—a potential early sign of Alzheimer’s—but who were not cognitively impaired. We don’t know if these people went on to develop dementia or whether walking 5,000–7,000 steps a day might reduce the risk of or prevent the condition,” added Richard Oakley, associate director of research and innovation at Alzheimer’s Society in the UK, in a statement.

“We would encourage everyone to exercise regularly if they can. Other steps like eating a healthy balanced diet, not smoking, drinking less alcohol and keeping on top of health conditions, such as diabetes or high blood pressure, can also help reduce our risk of getting dementia.”

The researchers next plan to look into both which aspects of physical activity—like intensity and longitudinal activity—may be most important and the biological mechanisms linking physical activity, tau buildup and cognitive health. This collective work may help design future clinical trials that test exercise interventions to slow late-life cognitive decline, according to the authors.

“Every step counts—and even small increases in daily activities can build over time to create sustained changes in habit and health,” added Yau. 

Do you have a tip on a health story that Newsweek should be covering? Do you have a question about Alzheimer’s? Let us know via health@newsweek.com.

Reference

Yau, W.-Y. W., Chhatwal, J. P., & colleagues. (2025). Physical activity as a modifiable risk factor in preclinical Alzheimer’s disease. Nature Medicine. https://doi.org/10.1038/s41591-025-03955-6

Scientists found a protein that drives brain aging — and how to stop it

 How long will it take for your incompetent? doctor to drive the research that solves this for humans and creates protocols that deliver this solution? Just why can't your doctor accomplish that?

Laziness? Incompetence? Or just don't care? NO leadership? NO strategy? Not my job? Not my Problem!

Your doctor has known of this for almost a year and should have preparations ready for this research NOW!

• FTL1 protein(2 posts to August 2025)

Scientists found a protein that drives brain aging — and how to stop it

Date:

April 5, 2026

Source:

University of California - San Francisco

Summary:

Scientists have uncovered a powerful new clue in the mystery of brain aging: a single protein called FTL1. In aging mice, higher levels of this protein weakened connections between brain cells and led to memory decline. But when researchers reduced FTL1, something remarkable happened — the brain began to recover, rebuilding lost connections and restoring memory performance.

FULL STORY

A protein called FTL1 was found to drive brain aging — and lowering it restored memory and neural connections in mice. Credit: Shutterstock

Aging takes a serious toll on the hippocampus, the part of the brain that plays a central role in learning and memory.

Scientists at UC San Francisco have now pinpointed a protein that appears to drive much of this decline.

FTL1 Emerges as a Key Driver of Brain Aging

To understand what changes with age, the researchers tracked shifts in genes and proteins in the hippocampus of mice over time. Among everything they examined, only one stood out as consistently different between young and old animals. That protein is called FTL1.

Older mice showed higher levels of FTL1. At the same time, they had fewer connections between neurons in the hippocampus and performed worse on cognitive tests.

How FTL1 Alters Brain Function

When the team boosted FTL1 levels in young mice, the effects were striking. Their brains began to look and function more like those of older mice, and their behavior reflected this shift.

Lab experiments revealed more detail. Nerve cells engineered to produce high amounts of FTL1 developed simplified structures, forming short, single extensions instead of the complex, branching networks seen in healthy cells.

Reversing Memory Decline by Lowering FTL1

The most surprising result came when researchers reduced FTL1 in older mice. The animals showed clear signs of recovery. Connections between brain cells increased, and their performance on memory tests improved.

"It is truly a reversal of impairments," said Saul Villeda, PhD, associate director of the UCSF Bakar Aging Research Institute and senior author of the paper, which was published in Nature Aging. "It's much more than merely delaying or preventing symptoms."

Metabolism Link Points to New Treatments

Further experiments showed that FTL1 also affects how brain cells use energy. In older mice, higher levels of the protein slowed cellular metabolism in the hippocampus. However, when researchers treated these cells with a compound that boosts metabolism, the negative effects were prevented.

Hope for Future Brain Aging Therapies

Villeda believes these findings could pave the way for treatments that target FTL1 and counter its effects in the brain.

"We're seeing more opportunities to alleviate the worst consequences of old age," he said. "It's a hopeful time to be working on the biology of aging."

Authors and Funding

Other UCSF authors are Laura Remesal, PhD, Juliana Sucharov-Costa, Karishma J.B. Pratt, PhD, Gregor Bieri, PhD, Amber Philp, PhD, Mason Phan, Turan Aghayev, MD, PhD, Charles W. White III, PhD, Elizabeth G. Wheatley, PhD, Brandon R. Desousa, Isha H. Jian, Jason C. Maynard, PhD, and Alma L. Burlingame, PhD. For all authors see the paper.

The exercise routine that turns brain 'measurably younger'

 Do you really think your doctor is competent enough to get you recovered enough to do this and at least recover some of your 5 lost years of brain cognition due to your stroke? I can almost guarantee that your  incompetent? doctor HAS NOTHING FOR 100% RECOVERY! Ask him/her and not politely!

The exercise routine that turns brain 'measurably younger'

Following a simple, guideline-based aerobic workout programme for a year could make the brain “measurably younger”, scientists claim in a new study.

Researchers found that regularly following the exercise regimen for a year led to participants’ brains appearing nearly a year younger on MRI scans.

Studies have previously shown that regular exercise plays a meaningful role in slowing ageing and keeping the mind sharp as one grows older.

In particular, a consistent aerobic workout routine has been proven to prevent the brain from ageing faster. Aerobic exercises have been linked to sharper thinking, stronger memory, and better overall well-being.

But structured long-term studies looking into measurable brain effects of such workouts have been limited, say researchers.

In a new study, scientists subjected 130 healthy adults(So your doctor needs to get further research going on stroke subjects! I bet your doctor will fail at that!) aged 26 to 58 to a 12-month intervention involving moderate-to-vigorous intensity aerobic exercise and measured changes to their brains via Magnetic Resonance Imaging (MRI) scans.

Participants in the exercise group attended two supervised 60-min sessions per week in a laboratory setting, along with at-home workouts to achieve 150  minutes of exercise per week.

They were guided to walk, jog, or run on a treadmill, as well as to record their use of aerobic exercise equipment such as bikes, elliptical machines, stair climbers, and rowers.

For the first six weeks, each participant was prescribed an exercise intensity that took them to 50 to 60 per cent of the maximum heart rate reserve (HRR), which is the difference between one’s maximum heart rate and resting heart rate.

The maximum heart rate is typically calculated using the formula of “220 – one’s age”, scientists explained.

“For the remainder of the intervention, participants increased their intensity to 60 to 75 per cent of HRR,” researchers wrote in the study published in the Journal of Sport and Health Science.

Participants’ fitness was estimated at the beginning and end of the 12-month study by measuring their peak oxygen uptake.

Brain ages of the participants were determined by estimating how old their brains appeared on MRI scans compared to their actual age.

Scientists found that the exercise group showed a measurable decrease in brain age after one year, while the control group experienced a slight increase.

“We found that a simple, guideline-based exercise programme can make the brain look measurably younger over just 12 months,” said Lu Wan, an author of the study from the AdventHealth Research Institute in the US.

“Studies like this offer hopeful guidance grounded in everyday habits,” Dr Wan said, adding that “even a one-year shift in brain age could matter over the course of decades”.

“From a lifespan perspective, nudging the brain in a younger direction in midlife could be very important,” said Kirk I. Erickson, another author of the study.

Researchers suspect exercise could be acting through additional mechanisms that haven’t been captured yet in studies.

Some subtle changes in brain structure, inflammation, vascular health, or other molecular factors due to routine exercise could be behind the slower ageing effects, they theorise.

They hope that larger studies conducted in the future with longer follow-up can determine whether exercise can reduce the risk of stroke, dementia, or other age-related brain diseases.

“If we can slow brain ageing before major problems appear, we may be able to delay or reduce the risk of later-life cognitive decline and dementia,” Dr Erickson said.

“Our findings support the idea that following current exercise guidelines – 150 minutes per week of moderate-to-vigorous aerobic activity – may help keep the brain biologically younger, even in midlife,” he added.

Association between uric acid to lymphocyte ratio and poor functional outcomes in acute ischemic stroke patients

 

Why are your predicting failure to recover RATHER THAN DELIVERING RECOVERY?

Laziness? Incompetence? Or just don't care? NO leadership? NO strategy? Not my job? Not my Problem!

You're all fired! Biomarkers  do nothing for recovery unless you are mapping EXACT RECOVERY PROTOCOLS to them!

Association between uric acid to lymphocyte ratio and poor functional outcomes in acute ischemic stroke patients

• 

  Xu Zhu 1†

• 

  Yijun Zhang 2,3,4,5,6†

• G

  Guoyuan Yu 1†

• 

  Anxin Wang 2,3,4,5,6

• X

  Xiaoli Zhang 2,3,4,5,6

• S

  Shifeng Xiang 1

• 

  Xia Meng 2,3,4,5,6*

• Y

  Yiping Wu 1*

• 1. Department of Neurology, Handan Central Hospital, Handan, China

• 2. Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China

Abstract

Background: 

Inflammation has an important impact on the pathological progression associated with ischemic stroke. Serum uric acid (UA) to lymphocyte ratio (ULR) is a biomarker that responds to the level of inflammation but is not definitively associated with the clinical outcomes in patients with acute ischemic stroke (AIS).

Methods: 

The data were obtained from the Third China National Stroke Registry (CNSR-III). Enrolled AIS patients were grouped by ULR quartiles at admission. The outcomes were poor functional outcomes (modified Rankin Scale [mRS] score of 3–6 or 2–6) and all-cause mortality at 3 months and 1 year. The associations of ULR with the risk of poor functional outcome and all-cause mortality were analyzed by multivariable logistic regression and Cox proportional hazards regression.

Results: 

A total of 8,241 patients were included from the CNSR-III study. After adjusting for confounders, it was found that patients in the highest ULR quartile had higher mRS scores of 2–6 (odds ratio [OR], 1.33; 95% confidence interval [CI], 1.15–1.53) and 3–6 (OR, 1.35; 95% CI, 1.16–1.57) at the 3-month follow-up. Additionally, the highest ULR quartile was associated with an increased risk of all-cause mortality at the 3-month follow-up (hazard ratio [HR], 1.97; 95%CI, 1.22–3.18). Similar results were observed at the 1-year follow-up.

Conclusion: 

Elevated ULR increased the risks of poorer functional outcomes and all-cause mortality in the AIS patients. However, this observational study was limited by potential unmeasured confounders, selection bias, residual confounding, and restricted generalizability to other populations.

Measuring arm function early after stroke: is the DASH good enough?

 

Look at it yourself, you can see it has no objectivity at all and nothing that could generate an EXACT RECOVERY PROTOCOL! In my opinion; TOTALLY WORTHLESS!

Free online DASH score calculator

You need to determine which of these nine options is causing your problems.

The exact same deficit could have 9 causes.

See this example of nine reasons for a movement disability:

 

You can't tell me these all have the same solution, I'm not that stupid.
1. Penumbra damage to the motor cortex.
2. Dead brain in the motor cortex.
3. Penumbra damage in the pre-motor cortex.
4. Dead brain in the pre-motor cortex.
5. Penumbra damage in the executive control area.
6. Dead brain in the executive control area.
7. Penumbra damage in the white matter underlying any of these three.
8. Dead brain in the white matter underlying any of these three.
9. Spasticity preventing movement from occurring.

The latest here: 

Measuring arm function early after stroke: is the DASH good enough?

1. Karen Baker1,
2. Louise Barrett2,
3. E Diane Playford1,
4. Trefor Aspden3,
5. Afsane Riazi3,
6. Jeremy Hobart2

1. Correspondence to Professor Jeremy Hobart, Clinical Neurology Research Group, Plymouth University Peninsula Schools of Medicine and Dentistry, Room N13 ITTC Building, Plymouth Science Park, Derriford, Plymouth PL6 8BX, UK; jeremy.hobart@plymouth.ac.uk

Abstract

Objective Despite a growing call to use patient-reported outcomes in clinical research, few are available for measuring upper limb function post-stroke. We examined the Disabilities of the Arm, Shoulder and Hand (DASH) to evaluate its measurement performance in acute stroke. In doing so, we compared results from traditional and modern psychometric methods.

Methods 172 people with acute stroke completed the DASH. Those with upper limb impairments completed the DASH again at 6 weeks (n=99). Data (n=271) were analysed using two psychometric paradigms: traditional psychometric (Classical Test Theory, CTT) analyses examined data completeness, scaling assumptions, targeting, reliability and responsiveness; Rasch Measurement Theory (RMT) analyses examined scale-to-sample targeting, scale performance and person measurement.

Results CTT analyses implied the DASH was psychometrically robust in this sample. Data completeness was high, criteria for scaling assumptions were satisfied (item-total correlations 0.55–0.95), targeting was good, internal consistency reliability was high (Cronbach's α=0.99) and responsiveness was clinically moderate (effect size=0.51). However, RMT analyses identified important limitations: scale-to-sample targeting was suboptimal, 4 items had disordered response category thresholds, 16 items exhibited misfit, 3 pairs of items had high residual correlations (>0.60) and 84 person fit residuals exceeded the recommended range.

Conclusions RMT methods identified limitations missed by CTT and indicate areas for improvement of the DASH as an upper limb measure for acute stroke. Findings, similar to those identified in multiple sclerosis, highlight the need for scales to have strong conceptual underpinnings, with their development and modification guided by sophisticated psychometric methods.

https://doi.org/10.1136/jnnp-2015-310557

Fr. Muller Medical College Hospital receives WSO Angels Diamond Award for stroke patient care

 

Any mention of 'care' rather than recovery means a COMPLETELY FUCKING FAILURE OF A HOSPITAL; DON'T GO THERE!

Fr. Muller Medical College Hospital receives WSO Angels Diamond Award for stroke patient care

Father Muller Medical College Hospital (FMMCH) has been conferred the WSO Angels Diamond Award for Q1 2026, an international recognition jointly supported by the World Stroke Organization (WSO) and the Angels Initiative, for its outstanding excellence in stroke patient care(NOT RECOVERY!) and advanced neurovascular services as of Thursday, May 28.

A release here said the award recognises hospitals that demonstrate exceptional standards in acute stroke management through rapid diagnosis, timely treatment, evidence-based thrombolysis, mechanical thrombectomy services, multidisciplinary coordination, and superior patient outcomes. The recognition reflects the collaborative efforts of multiple departments working in unison, including the Departments of Emergency Medicine, Neurology, Neuroradiology, Critical Care, and General Medicine.

The advanced Stroke Unit at FMMCH is supported by state-of-the-art neuroimaging and interventional facilities, including a 3 Tesla MRI, CT Brain Perfusion Imaging, and a sophisticated Bi-plane Cath Lab. These facilities allow rapid diagnosis, accurate patient selection, and timely neuro-interventional procedures, including acute thrombolysis and mechanical thrombectomy.

FMMCH acknowledged the dedicated contributions of the core stroke care(NOT RECOVERY!) team, including Raghavendra B.S. and Vimala Colaco from the Department of Neurology, Shailaja S. from the Department of Emergency Medicine, and Ariharan K. from the Department of Interventional Neuro-Radiology, along with the Cath Lab team, nursing staff, technicians, emergency personnel, and the hospital administration.

Hospitals from countries outside the territory of the European Stroke Organisation that capture treatment data in RES-Q, SITS-QR, or other approved stroke registries are automatically considered for the WSO Angels awards based on stringent quality measures outlined in the tier system.