Microvascular Measure Gives Clues to Poor Response to Successful Thrombectomy

 You've known of 100% recovery failure after thrombectomy for a long long time! WHEN ARE YOU GOING TO DO SOMETHING ABOUT THAT?

Or just sit with your heads up your asses? That doesn't help.

Microvascular Measure Gives Clues to Poor Response to Successful Thrombectomy

Capillary bed perfusion could point to a treatment target, proof-of-concept study suggests

Microvascular hemodynamics might provide an early marker of poor recovery despite successful large-vessel thrombectomy in acute ischemic stroke, an imaging study suggested.

Poor capillary bed perfusion as indicated by relative transit time heterogeneity around the infarct on immediate post-thrombectomy perfusion MRI predicted substantial infarct progression (≥10 mL, OR 1.4 per 10% increase, 95% CI 1.0-2.0, P=0.04), with a stronger association than seen for baseline infarct volume (OR 1.1 per 1 mL, 95% CI 1.0-1.2).The microvascular measure also outperformed baseline stroke severity as an independent predictor of poor 90-day functional outcome, defined as a modified Rankin Scale score over 2 (OR 1.4 per 10% increase, 95% CI 1.0-1.9, P=0.03, vs OR 1.2 per 1-point increase on the NIH Stroke Scale, 95% CI 1.0-1.2).

In contrast, conventional post-thrombectomy perfusion parameters, such as cerebral blood flow and volume and time to maximum residue function, failed to predict outcomes, "demonstrating their insensitivity to microvascular dysfunction," reported Yannan Yu, MD, of the University of California San Francisco, at the American Society of Functional Neuroradiology meeting in Newport Beach, California.

Despite acute stroke treatment advances, "still a significant portion of the stroke patients have a bad outcome even though they have successful thrombectomy and have reperfusion of the tissue," Yu said.

While no reflow in these cases isn't well understood, animal models have shown that microvascular hemodynamic failure is one mechanism, she noted.

"In routine practice, what people get [for imaging] is maybe 24 to 48 hours after the stroke treatment, and when you evaluate no-reflow on that time point, a lot of things may have already happened," she said. "They may have late recanalization, they may have early reocclusion. ... But in this immediate post-thrombectomy MRI, we're hoping that this MRI will reflect the truth of what happened immediately after we recanalize the vessel."

The researchers aren't proposing that centers switch from their routinely done diffusion MRI to the perfusion MRI as done in this study. Rather, the findings serve as proof of concept that the microvasculature can be measured and matters in this setting.

It's one of the pieces of the puzzle to sort out what's happening to these no-reflow patients to move toward finding better treatment for them, Yu said.

"Currently our limitation is that this is a pretty small sample size. There's not a lot of analysis we can do with such a small sample size," she said. "A larger cohort will be important to validate the scientific factuality of the findings. And then after that, if we're able to validate that, I think then it could potentially become a treatment target."

The study included 47 acute ischemic stroke patients (mean 72 years, 62% women) treated for anterior circulation large vessel occlusion from 2015 through 2020 who had complete or near-complete brain tissue reperfusion (modified Thrombolysis in Cerebral Infarction score ≥2c) after thrombectomy. Participants needed to have had diffusion-weighted imaging (DWI) and dynamic susceptibility contrast perfusion MRI both pre-treatment and within 2 hours after thrombectomy as well as 24-48 hour follow-up DWI.

Among them, 43% (20 of 47) had substantial infarct progression, and the same proportion had poor functional outcomes.

Relative capillary transit time heterogeneity was calculated as the ratio of the standard deviation of mean transit time to the mean transit time of red blood cells across a capillary bed.

Noninvasive magnetic field therapy shows promise for long COVID cognitive impairment

 Ask your competent? doctor and hospital when this testing will occur on stroke survivors.

DOING NOTHING, LIKE USUAL?

Are you impressed with your doctors' world class incompetence with their head up their asses? Planning on doing anything about it, like getting them fired?

Noninvasive magnetic field therapy shows promise for long COVID cognitive impairment

A twice-weekly, at-home transcranial magnetic field intervention was associated with improvements in working memory, verbal learning, processing speed, and emotional well-being in patients with cognitive impairment associated with long COVID, according to a triple-blind pilot randomised controlled trial published in Brain Communications.

The findings represent the first randomised controlled trial of Microtesla Magnetic Therapy (MMT) for long COVID cognitive impairment, providing early evidence that noninvasive biophysical approaches may warrant further study as potential treatments for persistent neurological symptoms following severe acute respiratory syndrome coronavirus 2 infection.

Cognitive impairment -- often described as "brain fog" -- is among the most disabling manifestations of long COVID and is thought to involve sustained neuroinflammation, cerebrovascular dysfunction, and mitochondrial impairment.

Jacqueline Becker, PhD, Icahn School of Medicine at Mount Sinai, New York, New York, and colleagues randomised 30 adults with confirmed long COVID cognitive impairment 2:1 to active or sham MMT. Participants self-administered 15-minute at-home sessions twice weekly for 4 weeks, with remote monitoring, via a head-worn device delivering either a nonthermal radiofrequency magnetic field to the whole brain. Sham devices were identical in appearance and sound. Cognitive function, mood, and quality of life were assessed at baseline, week 4 (end of treatment), and week 8 (follow-up).

Adherence was 100% among participants who completed the study, and no device-related adverse events occurred. Compared with the sham group, active MMT was associated with significantly greater improvement at week 8 in Digit Span Sequencing (P = .026), Hopkins Verbal Learning Test-Revised Total Recall (P = .044), and Delis-Kaplan Executive Function System Color Naming (P = .049). Greater improvement on emotional well-being on the 36-Item Short Form Survey was also observed with active treatment (P = 0.017), and several measures continued to improve between weeks 4 and 8.

"Cognitive symptoms are among the most persistent and disabling manifestations of long COVID, yet evidence-based treatment options have been sparse," said Dr Becker. "What is particularly encouraging about these findings is that we observed improvements across several cognitive domains, as well as in daily functioning and well-being, and that these improvements persisted even after treatment ended."

"There is an urgent need to find answers and effective treatments for the hundreds of millions of people worldwide who are struggling with long COVID," said David Putrino, PhD, Icahn School of Medicine at Mount Sinai, New York, New York. "This first-in-human study is a promising start for a completely novel therapy that is showing great potential."

The authors emphasised that MMT remains investigational; they called for larger, adequately powered trials to confirm these preliminary findings and to examine the biological mechanisms underlying the observed effects.

Reference: https://academic.oup.com/braincomms/advance-article/doi/10.1093/braincomms/fcag364/8841135

SOURCE: Icahn School of Medicine at Mount Sinai

Magnetic Stimulation Improves Long COVID “Brain Fog”

 

Can your doctor rub a couple of neurons together and see if this improves stroke brain fog? Or is sitting with heads up the ass the likely outcome? 

Are you impressed with your doctors' world class incompetence? Planning on doing anything about it, like getting them fired?

Magnetic Stimulation Improves Long COVID “Brain Fog”

Summary:

A pilot clinical trial led by the Icahn School of Medicine at Mount Sinai shows that an at-home, non-invasive magnetic headset significantly improves cognitive performance and emotional well-being in adults suffering from long COVID “brain fog.”

Published in Brain Communications, the triple-blind, sham-controlled study found that twice-weekly sessions of Microtesla Magnetic Therapy (MMT) enhanced working memory, processing speed, and verbal learning, with therapeutic benefits persisting a full month after treatment ended.

Key Facts:

• Targeted Brain Stimulation: Participants self-administered 15-minute sessions twice weekly for four weeks using an investigational headset delivering nonthermal radio-frequency low-amplitude magnetic fields (MMT) to the whole brain.
• Measurable Cognitive & Mood Gains: Active treatment produced significant gains in working memory, processing speed, verbal learning, and self-reported emotional well-being compared to an identical sham device.
• Durable Aftereffects: Cognitive improvements continued between the end of the four-week treatment window and the eight-week follow-up assessment, indicating lasting neuroplastic or anti-inflammatory changes.

Source: Mount Sinai Health System

Among the constellation of symptoms defining post-acute sequelae of SARS-CoV-2 infection (PASC), commonly termed long COVID, cognitive dysfunction remains among the most debilitating. Millions of individuals describe a persistent “brain fog” characterized by slowed processing speed, executive dysfunction, working memory lapses, and attention deficits that derail employment and daily life.

Emerging neuropathological evidence indicates that long COVID cognitive deficits stem from a combination of sustained neuroinflammation, microvascular endotheliopathy, and mitochondrial metabolic exhaustion within neural tissue. Yet, despite the vast global disease burden, clinically validated therapeutic interventions remain exceedingly rare.

In a randomized, triple-blind pilot trial published in Brain Communications, investigators from the Icahn School of Medicine at Mount Sinai evaluated whether biophysical neuromodulation could counter these entrenched post-viral neurological symptoms.

The researchers tested Microtesla Magnetic Therapy (MMT), a proprietary, non-invasive technology developed by clinical-stage biophysics company Fareon® that delivers low-amplitude, nonthermal radio-frequency magnetic fields across the cortex.

“Cognitive symptoms are among the most persistent and disabling manifestations of long COVID, yet evidence-based treatment options have been sparse,” said co-senior author Jacqueline Becker, Ph.D., clinical neuropsychologist and assistant professor of medicine at Icahn Mount Sinai.

“What is particularly encouraging about these findings is that we observed improvements across several cognitive domains, as well as in daily functioning and well-being, and that these improvements persisted even after treatment ended.”

Triple-Blind, At-Home Intervention

The clinical trial enrolled 30 adults with objectively documented post-COVID cognitive impairment. Participants were randomized 2:1 to receive either active MMT or an indistinguishable sham treatment that looked, sounded, and operated identically.

Subjects wore the headset at home for 15 minutes twice a week over a four-week period, monitored remotely by Mount Sinai clinical trial coordinators. The investigators assessed cognitive performance, mood, and quality-of-life metrics at baseline, at week four (conclusion of the intervention), and at week eight (four-week post-treatment follow-up).

The home-administered protocol proved safe, feasible, and well tolerated, with participants exceeding the 80% protocol completion threshold without significant device-related adverse events.

Patients receiving active MMT demonstrated marked improvements in objective neuropsychological endpoints, including:

• Working Memory: Enhanced capacity to retain and manipulate information over short intervals.
• Processing Speed: Increased cognitive reaction time and task execution speed.
• Verbal Learning: Stronger retention and recall during verbal memory tasks.
• Emotional Well-Being: Reductions in mood disturbance and gains in self-reported daily quality of life.

Lasting Neuroplastic Improvements Beyond Treatment

Critically, the therapeutic gains did not diminish when patients took off the headset at the end of week four. During the subsequent four-week washout observation period, participants in the active cohort exhibited continued cognitive and mood improvements through week eight.

While the primary mechanisms remain under investigation, preclinical models of MMT indicate that low-amplitude magnetic oscillations can suppress chronic neuroinflammation, downregulate reactive microglial activation, and support mitochondrial bioenergetics, biological pathways known to be compromised in post-viral encephalopathies.

“According to the Centers for Disease Control and Prevention, roughly 7 percent of Americans are experiencing symptoms related to long COVID, and a majority of these people report cognitive symptoms as amongst their most troubling and disabling symptoms,” said co-senior author David Putrino, Ph.D., Nash Family Director of the Cohen Center for Recovery From Complex Chronic Illness at Icahn Mount Sinai.

“There is an urgent need to find answers and effective treatments for the hundreds of millions of people worldwide who are struggling with long COVID. This first-in-human study is a promising start for a completely novel therapy that is showing great potential.”

The researchers emphasize that while these initial pilot results are promising, MMT remains an investigational therapy that requires verification in larger multicenter cohorts to determine optimal dosage schedules, long-term durability, and the exact biological mechanisms restoring network function.

Editorial Notes:

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

About this neurotech and long COVID Research:

• Media Contact: Elizabeth Dowling
• Source: Mount Sinai Hospital
• Image Credit: Image credited to Neuroscience News
• Original Research is Open Access: Brain Communications (Sept 22, 2026). “Microtesla magnetic therapy for cognitive impairment in long COVID: a randomized pilot study.” Authors: Alexandra Canori, PhD , Eric Watson, PhD , Devanshi Patel, MA , Arianna Fiorentino, MSc , Christopher Santiago, BS , David Maltz, MSE , Blake Gurfein, PhD , David Putrino, PhD , Jacqueline Becker, PhD.
• DOI: 10.1093/braincomms/fcag364

Natural Peptide Counters Multiple Hallmarks of Alzheimer’s

 

Can your doctor rub a couple of neurons together and get human testing going? Or is sitting with heads up the ass the likely outcome?

Natural Peptide Counters Multiple Hallmarks of Alzheimer’s

Summary:

Researchers at UC San Diego have identified  (CST), a naturally occurring peptide fragment, that simultaneously reduces amyloid and tau buildup, quells neuroinflammation, and improves cognitive and motor performance in mouse models of neurodegenerative disease. Unlike single-target therapies, CST acts across several interconnected pathological pathways, pointing toward a versatile peptide-based treatment strategy for complex dementias.

Key Facts:

• Multi-Target Clearance: In preclinical mouse models, treatment with catestatin significantly reduced toxic accumulations of both tau and amyloid proteins while dialing down neuroinflammation.
• Functional Recovery: Beyond clearing hallmark neuropathology, the peptide led to measurable improvements in both cognitive performance and motor coordination in animal models.
• Derived from Chromogranin A: CST is an endogenous cleavage product of chromogranin A, a protein fundamental to neurotransmitter storage and cellular signaling, and is currently being explored for its ability to reprogram brain energy metabolism to shield vulnerable neurons against cellular stress.

Source: University of California San Diego School of Medicine

Alzheimer’s disease and related dementias present one of the most stubborn hurdles in modern neurology, primarily because their pathology is not driven by a single isolated defect. Instead, disease progression involves an entangled network of problems: aberrant protein aggregation, persistent neuroinflammation, metabolic dysfunction, and progressive synaptic failure.

While many experimental drugs focus narrowly on single targets, such as clearing amyloid plaques or blocking tau tangles, a research team at the University of California San Diego School of Medicine and the VA San Diego Healthcare System took a different approach. In a study published in Molecular Therapy, the scientists investigated whether an endogenous peptide could intervene across multiple disease mechanisms simultaneously.

Their focus fell on catestatin (CST), a naturally occurring peptide fragment derived from chromogranin A. In animal models, CST not only cleared pathological hallmarks but also protected functional neural circuits.

“Neurodegenerative diseases involve multiple interconnected problems — including misfolded proteins, neuroinflammation and progressive dysfunction of brain cells,” said senior author Sushil K. Mahata, PhD, professor of medicine at UC San Diego School of Medicine and research physiologist at the VA San Diego Healthcare System.

“Our findings show that CST can act across several of these disease-associated pathways and shift the brain toward a healthier state. More broadly, the study suggests that peptide-based therapies may offer a new approach to treating complex neurodegenerative diseases.”

Reducing Amyloid, Tau, and Neuroinflammation

To evaluate the peptide’s therapeutic potential, the investigators administered CST to mouse models displaying hallmark features of neurodegenerative decline. The treatment produced widespread structural and cellular benefits:

• Toxin Clearance: CST significantly blunted the accumulation of both amyloid and tau aggregates, the twin proteinopathies characteristic of Alzheimer’s disease.
• Anti-Inflammatory Modulation: The peptide suppressed chronic neuroinflammatory signaling, reducing destructive immune activation in brain tissue.
• Behavioral and Motor Gains: Mice receiving CST demonstrated meaningful improvements in memory, learning tasks, and motor performance compared to untreated controls.

Because chromogranin A is naturally involved in cellular communication and the packaging and release of hormones and neurotransmitters, its derivative CST already plays diverse roles across cardiovascular, metabolic, and immune regulation throughout the body. This native systemic versatility appears to translate to the central nervous system, where it orchestrates several defensive processes rather than engaging only one receptor.

Cellular Resilience and Metabolic Support

Beyond cleaning up cellular debris and cooling inflammatory fires, the researchers are examining how CST alters neuronal bioenergetics.

“One exciting aspect of our findings is that CST may do more than reduce the pathological features of neurodegeneration. We are also investigating whether CST can alter how the brain produces and uses energy, which may help neurons become more resilient to the cellular stress that occurs during neurodegeneration,” said lead author Suborno Jati, PhD, a postdoctoral scholar at UC San Diego School of Medicine.

By potentially stabilizing how distressed brain cells generate and utilize ATP, CST could give damaged neurons the energetic bandwidth required to maintain synaptic communication despite accumulating toxic stressors.

The Path Forward

The researchers emphasize that the current findings are strictly preclinical. Moving CST or related peptide analogues from laboratory animal models into human clinical trials will require comprehensive studies to determine long-term safety, optimal dosing regimens, blood-brain barrier delivery dynamics, and clinical efficacy.

Nevertheless, the discovery highlights the promise of peptide therapeutics as multi-system regulators capable of treating the multifaceted biology of neurodegenerative decline.

Funding: The research was supported in part by grants from the National Institutes of Health and the U.S. Department of Veterans Affairs.

Mahata is founder of CgA Therapeuticals, Inc. and co-founder of Siraj Therapeutics. Mahata and Jati are listed as co-inventors on intellectual property related to the findings.

Editorial Notes:

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

About this Genetics and Neuroregeneration Research:

• Media Contact: Miles Martin
• Source: UCSD
• Image Credit: Image credited to Neuroscience News
• Original Research is Open Access: Molecular Therapy (September 21, 2026). “Catestatin peptide ameliorates tauopathy and amyloidogenesis via adrenergic inhibition.” Authors: Suborno Jati, Satadeepa Kal, Daniel Munoz-Mayorga, Kechun Tang, Debashis Sahoo, Xu Chen, and Sushil K. Mahata.
• DOI: 10.1016/j.ymthe.2026.09.022

Natural Peptide Counters Multiple Hallmarks of Alzheimer’s

 Can your doctor rub a couple of neurons together and get human testing going? Or is sitting with heads up the ass the likely outcome?

Natural Peptide Counters Multiple Hallmarks of Alzheimer’s

Summary:

Researchers at UC San Diego have identified catestatin (CST), a naturally occurring peptide fragment, that simultaneously reduces amyloid and tau buildup, quells neuroinflammation, and improves cognitive and motor performance in mouse models of neurodegenerative disease. Unlike single-target therapies, CST acts across several interconnected pathological pathways, pointing toward a versatile peptide-based treatment strategy for complex dementias.

Key Facts:

• Multi-Target Clearance: In preclinical mouse models, treatment with catestatin significantly reduced toxic accumulations of both tau and amyloid proteins while dialing down neuroinflammation.
• Functional Recovery: Beyond clearing hallmark neuropathology, the peptide led to measurable improvements in both cognitive performance and motor coordination in animal models.
• Derived from Chromogranin A: CST is an endogenous cleavage product of chromogranin A, a protein fundamental to neurotransmitter storage and cellular signaling, and is currently being explored for its ability to reprogram brain energy metabolism to shield vulnerable neurons against cellular stress.

Source: University of California San Diego School of Medicine

Alzheimer’s disease and related dementias present one of the most stubborn hurdles in modern neurology, primarily because their pathology is not driven by a single isolated defect. Instead, disease progression involves an entangled network of problems: aberrant protein aggregation, persistent neuroinflammation, metabolic dysfunction, and progressive synaptic failure.

While many experimental drugs focus narrowly on single targets, such as clearing amyloid plaques or blocking tau tangles, a research team at the University of California San Diego School of Medicine and the VA San Diego Healthcare System took a different approach. In a study published in Molecular Therapy, the scientists investigated whether an endogenous peptide could intervene across multiple disease mechanisms simultaneously.

Their focus fell on catestatin (CST), a naturally occurring peptide fragment derived from chromogranin A. In animal models, CST not only cleared pathological hallmarks but also protected functional neural circuits.

“Neurodegenerative diseases involve multiple interconnected problems — including misfolded proteins, neuroinflammation and progressive dysfunction of brain cells,” said senior author Sushil K. Mahata, PhD, professor of medicine at UC San Diego School of Medicine and research physiologist at the VA San Diego Healthcare System.

“Our findings show that CST can act across several of these disease-associated pathways and shift the brain toward a healthier state. More broadly, the study suggests that peptide-based therapies may offer a new approach to treating complex neurodegenerative diseases.”

Reducing Amyloid, Tau, and Neuroinflammation

To evaluate the peptide’s therapeutic potential, the investigators administered CST to mouse models displaying hallmark features of neurodegenerative decline. The treatment produced widespread structural and cellular benefits:

• Toxin Clearance: CST significantly blunted the accumulation of both amyloid and tau aggregates, the twin proteinopathies characteristic of Alzheimer’s disease.
• Anti-Inflammatory Modulation: The peptide suppressed chronic neuroinflammatory signaling, reducing destructive immune activation in brain tissue.
• Behavioral and Motor Gains: Mice receiving CST demonstrated meaningful improvements in memory, learning tasks, and motor performance compared to untreated controls.

Because chromogranin A is naturally involved in cellular communication and the packaging and release of hormones and neurotransmitters, its derivative CST already plays diverse roles across cardiovascular, metabolic, and immune regulation throughout the body. This native systemic versatility appears to translate to the central nervous system, where it orchestrates several defensive processes rather than engaging only one receptor.

Cellular Resilience and Metabolic Support

Beyond cleaning up cellular debris and cooling inflammatory fires, the researchers are examining how CST alters neuronal bioenergetics.

“One exciting aspect of our findings is that CST may do more than reduce the pathological features of neurodegeneration. We are also investigating whether CST can alter how the brain produces and uses energy, which may help neurons become more resilient to the cellular stress that occurs during neurodegeneration,” said lead author Suborno Jati, PhD, a postdoctoral scholar at UC San Diego School of Medicine.

By potentially stabilizing how distressed brain cells generate and utilize ATP, CST could give damaged neurons the energetic bandwidth required to maintain synaptic communication despite accumulating toxic stressors.

The Path Forward

The researchers emphasize that the current findings are strictly preclinical. Moving CST or related peptide analogues from laboratory animal models into human clinical trials will require comprehensive studies to determine long-term safety, optimal dosing regimens, blood-brain barrier delivery dynamics, and clinical efficacy.

Nevertheless, the discovery highlights the promise of peptide therapeutics as multi-system regulators capable of treating the multifaceted biology of neurodegenerative decline.

Funding: The research was supported in part by grants from the National Institutes of Health and the U.S. Department of Veterans Affairs.

Mahata is founder of CgA Therapeuticals, Inc. and co-founder of Siraj Therapeutics. Mahata and Jati are listed as co-inventors on intellectual property related to the findings.

Editorial Notes:

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

About this Genetics and Neuroregeneration Research:

• Media Contact: Miles Martin
• Source: UCSD
• Image Credit: Image credited to Neuroscience News
• Original Research is Open Access: Molecular Therapy (September 21, 2026). “Catestatin peptide ameliorates tauopathy and amyloidogenesis via adrenergic inhibition.” Authors: Suborno Jati, Satadeepa Kal, Daniel Munoz-Mayorga, Kechun Tang, Debashis Sahoo, Xu Chen, and Sushil K. Mahata.
• DOI: 10.1016/j.ymthe.2026.09.022

The association between serum klotho protein and stroke: a cross-sectional study from NHANES 2007–2016

 

You probably want to ask your incompetent? doctor for the protocols that create proper levels in humans. Since they won't exist yet, your incompetent doctors can sit with heads up asses doing nothing OR get research done! I'm guessing head up ass is the preferred position! Why is your doctor not fired yet?

I'm sure your incompetent? doctor DID NOTHING WITH THIS RESEARCH!

Klotho protein levels linked to Alzheimer's, cognitive decline, amyloid and tau burden November 2022 

The latest here for your doctor to DO NOTHING!

The association between serum klotho protein and stroke: a cross-sectional study from NHANES 2007–2016

Hongjia Xu^1†Yiming Ding^2,3†Ye Zhang¹Jianwen Li¹Shiyue Zhou¹Dewei Wang¹Xinyue Xing¹Xiaoyu Ma¹Cunfu Wang^1*Shunliang Xu^1,4*

• ¹Department of Neurology, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China
• ²Department of Pediatric Surgery, Qilu Hospital of Shandong University, Jinan, China
• ³Cheeloo College of Medicine, Shandong University, Jinan, China
• ⁴Department of Human Genetics, School of Medicine, Emory University, Atlanta, GA, United States

Objective: Serum klotho protein is a protein with anti-aging effects. Since the relationship between serum klotho and Stroke remains rather ambiguous, this research probed into the potential correlation between serum klotho concentration and Stroke.

Methods: This study employed a cross-sectional design and incorporated population data from the NHANES from 2007 to 2016. Weighted univariate and multivariate logistic regression models were utilized to inspect the relationship between klotho and Stroke. Stratified analyses and interaction tests were carried out to explore the latent correlation between klotho and Stroke. Finally, a fitted smooth curve was adopted to depict the non-linear relationship.

Results: In this study, after excluding all the missing data, a total of 12,414 participants were encompassed, including 450 Stroke individuals. After adjusting for all covariates, higher klotho was associated with a lower prevalence of Stroke. According to the subgroup analyses and interaction tests, age, gender, race, BMI, hypertension, diabetes mellitus, family members, drinker and smoker were not significantly correlated with the influence of klotho and Stroke. After adjusting for all covariates, higher klotho was associated with a lower prevalence of stroke [OR: 0.68, 95% CI: 0.47–0.99].

Conclusion: This study disclosed the negative correlation between serum klotho protein levels and the prevalence of Stroke. Further prospective studies are requisite to investigate the impact of serum klotho protein levels on Stroke and determine the causal relationship.

1 Introduction

Stroke represents the second leading global cause of mortality, surpassed only by acute ischemic heart disease (1). This severe acute cerebrovascular disease not only threatens survival but frequently induces debilitating sequelae including motor deficits, cognitive impairment, and affective disorders, imposing substantial socioeconomic burdens and quality-of-life deterioration (2). With the current development of an aging population, the prevalence rate of stroke is continuously rising (3). Furthermore, stroke is currently emerging gradually among the young population (attributed to factors including patent foramen ovale, dyslipidemia, hormonal therapies, and genetic predisposition) (4, 5). Since stroke is a global public health problem, researchers have never stopped their research on the specific etiology, pathogenesis, predictive means and treatment measures of stroke. And they have been endeavoring to prevent the occurrence of stroke and handle it in a timely manner through some laboratory test indicators and other approaches.

The klotho gene, first identified through longevity studies in murine models (1997), has emerged as a pleiotropic regulator of aging processes. In mice, the overexpression of the klotho gene prolongs lifespan, while its mutation reduces it (6). The human klotho gene is situated at chromosome 13q12. It demonstrates effects such as anti-aging and anti-inflammation and is correlated with numerous age-related diseases (7, 8). The klotho protein encoded by the klotho gene is predominantly a single-channel transmembrane protein, and its soluble component can be cleaved to form α-klotho and dissolve in the blood, featuring three distinct functional types: membrane-bound α-klotho, truncated soluble α-klotho, and secreted α-klotho (6). Unless otherwise specified, the term “klotho” specifically refers to α-klotho. In previous studies, it has been found to be associated with kidney diseases (9), cardiovascular diseases (10, 11), and diabetes mellitus (12). Additionally, in the field of neurology, it has also been discovered that its reduction might be related to Alzheimer’s disease and other degenerative disorders (13). In 2014, Dubal and colleagues discovered that mice with higher serum klotho levels exhibited stronger cognitive function across all age groups, independent of the aging process (14). Subsequently, the team of Castner demonstrated through experiments in rodents and primates that klotho enhances synaptic plasticity and cognitive capacity. Notably, their research revealed that a single low-dose (but not high-dose) administration of klotho could improve memory function in aged non-human primates (15). Emerging evidence from animal studies has demonstrated that beyond its well-documented cardiovascular effects, klotho protein plays a significant role in mediating ischemic preconditioning mechanisms. This endogenous neuroprotective function not only reduces stroke prevalence but also exhibits therapeutic potential through multifaceted cerebroprotective actions, including attenuation of oxidative stress and modulation of apoptotic pathways (16, 17).

Despite these advances, critical knowledge gaps persist regarding klotho’s clinical relevance in cerebrovascular disease. Whether serum klotho levels demonstrate an independent association with stroke risk beyond traditional cardiovascular risk factors. The number of related clinical studies is limited, and the sample sizes therein are relatively small. We hypothesize that: Serum klotho concentration inversely correlates with stroke prevalence in adults. This association remains significant after comprehensive adjustment for confounders including lipid profiles and metabolic comorbidities. Hence, we carried out this research, conducting a large-sample study in the NHANES, which is representative of the national population, in the hope of testing these hypotheses between serum klotho and the prevalence of Stroke in the clinical setting.

More at link.

Boosting Klotho Protein Slows Aging and Enhances Health

 You probably want to ask your incompetent? doctor for the protocols that do this in humans. Since they won't exist yet, your incompetent doctors can sit with heads up asses doing nothing OR get research done! I'm guessing head up ass is the preferred position! Why is your doctor not fired yet?

I'm sure your incompetent? doctor DID NOTHING WITH THIS RESEARCH!

Klotho protein levels linked to Alzheimer's, cognitive decline, amyloid and tau burden November 2022 

The latest here for your doctor to DO NOTHING!

Boosting Klotho Protein Slows Aging and Enhances Health

Summary: Increasing levels of the Klotho protein can slow aging and improve health across multiple systems. Scientists showed that mice treated to produce more secreted Klotho (s-KL) had better muscle strength, bone density, cognitive function, and even lived 15–20% longer.

The treatment promoted neuron growth, reduced muscle fibrosis, and protected bones, especially in females, suggesting widespread benefits. While human applications are still being developed, the findings point to s-KL as a promising future therapy to enhance healthy aging.

Key Facts:

• Longer Lifespan: Mice producing more Klotho lived 15–20% longer.
• Stronger Body: Treated mice showed better muscle, bone, and cognitive health.
• Therapy Potential: Researchers aim to develop Klotho-based treatments for aging.

Source: UAB

As we grow older, it is natural to lose muscle and bone mass, leading to greater frailty and a higher risk of falls and serious injuries.

Cognitively, neurons progressively degenerate and lose connections, while diseases such as Alzheimer’s and Parkinson’s become more prevalent. In a society where the population is steadily aging, reducing these effects is one of the main challenges for research.

At 24 months of age, roughly equivalent to 70 years in humans, they found that the treatment had improved the animals’ muscle, bone, and cognitive health. Credit: Neuroscience News

Now, in an article published in Molecular Therapy, an international research team led by Professor Miguel Chillón, ICREA researcher at the INc-UAB, has shown that increasing levels of the secreted form of the Klotho protein (s-KL) improves aging in mice.

The team treated young animals with gene therapy vectors that caused their cells to secrete more s-KL. At 24 months of age, roughly equivalent to 70 years in humans, they found that the treatment had improved the animals’ muscle, bone, and cognitive health.

“We have been working with the Klotho protein for some time, due to its therapeutic potential for treating neurodegenerative diseases. In this study, we wanted to see whether s-KL could also be beneficial for healthy aging by examining a broad range of factors”, explains Miguel Chillón.

Mice treated with s-KL lived 15–20% longer, with better physical performance, larger muscle fibers, and less fibrosis, indicating better muscle health. Improvements in bone health were also observed, particularly in females, with greater preservation of the internal bone structure (trabeculae), suggesting a potential protective effect against osteoporosis.

Finally, in the brain, treatment with s-KL promoted the generation of new neurons and increased immune activity in the hippocampus, suggesting possible cognitive benefits.

The viral vector treatment works by introducing copies of the gene encoding the desired protein into the body’s cells, so that they can start producing it on their own. In the mice, these vectors were administered intravenously and directly into the brain to ensure that brain cells also produced s-KL.

“We now have viral vectors that can reach the brain after being administered intravenously, which would make it easier to safely transfer this therapy to humans.

“Another option would be to administer the protein directly as a drug instead of using viral vectors, but we still need to find an efficient way to deliver it and ensure it reaches the target organs,” explains Joan Roig-Soriano, INc-UAB researcher and first author of the article.

The research group had already patented the use of Klotho to treat cognitive deficits, and following this study, three new patents were filed. These patents protect the use of Klotho for treating bone and muscle deficits, as well as for developing therapies aimed at increasing longevity.

“If we can find a viable delivery method, s-KL could make a significant contribution to improving people’s quality of life and helping to build the healthiest society possible,” the researchers conclude.

About this genetics and aging research news

Author: Maria Jesus Delgado
Source: UAB
Contact: Maria Jesus Delgado – UAB
Image: The image is credited to Neuroscience News

Original Research: Open access.
“Long-term effects of s-KL treatment in wild-type mice: Enhancing longevity, physical well-being, and neurological resilience” by Miguel Chillón et al. Molecular Therapy

Gregg Popovich addresses stroke recovery and his new role with Spurs as 'El Jefe'

 The real story is that the HOSPITAL, DOCTORS AND THERAPISTS COMPLETELY FAILED at getting him 100% recovered! That should be the story for every survivor. 100% recovery or complete failure of their stroke medical 'professionals'.  I call it like it is; stroke is a complete fucking failure and that won't change until we get survivors in charge!  In my opinion, they should be sued for incompetence; they've had decades to solve stroke and did nothing! There is NO leadership anywhere in stroke; sitting with heads up asses for decades; NOT SOLVING STROKE!

Gregg Popovich addresses stroke recovery and his new role with Spurs as 'El Jefe'

Former San Antonio Spurs head coach Gregg Popovich is still the boss.

The team introduced Mitch Johnson as its new head coach during a press conference on May 5, during which time Popovich spoke in public for the first time since he had a stroke last November.

Before Johnson addressed the media, Popovich, who officially stepped down as head coach May 2, announced he had a new job, unzipping his jacket to reveal a T-shirt that said “El Jefe,” which is Spanish for “The Boss.”

“I’m no longer coach. I’m ‘El Jefe,’” he said while Spurs greats Tim Duncan and Manu Ginobili took off his jacket and those assembled at the press conference laughed.

Popovich, 76, then turned around to show off the back of his shirt.

Gregg Popovich (center) declares himself "El Jefe" as he addresses his stroke and welcomes new coach Mitch Johnson while flanked by former players Manu Ginobili (left) and Tim Duncan (right).@spurs via X

“Senor Popovich,” it said. “President of basketball ops.”

Popovich, who will serve as the team’s president of basketball operations, is the NBA’s all-time leader in coaching wins and won five championships as head coach of the Spurs, a position he had held since 1996. He spoke for about seven minutes, also noting that his health is improving but that now was the moment to have Johnson take over the franchise.

“Things are getting better by the day, but it’s not good enough for what we plan ahead, and so it’s time to make this change,” he said a few moments before also thanking his rehab team and all the other people who’ve helped him during his recovery.

Popovich (center) lets people know about his new role with the Spurs.@spurs via X

He also praised Johnson, while reminding people the team’s aim is to continue its excellence.

“That’s the goal, to make sure we keep it going,” he said.

Popovich initially missed games last November due to what the team described as an illness. A little more than a week later, the Spurs announced he had had a stroke, and in late February the team said he would not return to the sidelines this season.

Popovich will go down as one of the greatest coaches in NBA history.Alex Goodlett / @spurs via X

The last game he coached was on Oct. 31. Johnson had filled in as an interim coach in the meantime.

In addition to his five NBA championships, Popovich coached the U.S. men’s basketball team to a gold medal at the Summer Olympics in 2021 and coached Spurs legends such as Duncan, Ginobili, Tony Parker and David Robinson, all of whom are in the Naismith Basketball Hall of Fame. He also coached up-and-coming Spurs star Victor Wembanyama.

Popovich himself was inducted into the Naismith Basketball Hall of Fame in 2023.

New stroke treatment imitates the survival strategy of C. elegans

I don't expect anything to come out of this, there is NO stroke leadership to ensure human testing gets done and NO stroke strategy to update. If they are right about the 70% adjoining neurons dying then my calculation of 5.4 billion neurons dying my first week is wrong.  I'm going to keep using my 5.4 billion dead neurons the first week because it is shocking and the stroke world needs to be shocked into action, rather than twiddling around with their heads up their asses. But we do need an objective way to calculate brain cell deaths. 

New stroke treatment imitates the survival strategy of C. elegans

Each year, some 200,000 people in Germany and 1 million people in Europe suffer a stroke. This happens when blood clots obstruct major vessels and there is no longer sufficient supply of blood to the brain. If doctors manage to break down or mechanically remove the clot, further damage is prevented.

Nevertheless, 100 percent of the tissue originally affected and about 70 percent of the cells in adjacent areas die off. Scientists based at the LMU Medical Center, the Charité in Berlin and the University of Maryland, Baltimore (USA), led by Dr. Francisco Pan-Montojo (Clinic for Psychiatry and Psychotherapy at University of Munich Hospital) has now been able to demonstrate in several relevant animal models of stroke that glycolic acid can be successfully used to salvage threatened tissue. The experimental treatment imitates a survival strategy of the nematode Caenorhabditis elegans a worm present in the soil, as the researchers report in Advanced Science.

Survival strategies of C. elegans

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The nematode C. elegans can withstand even desiccation by entering a special larval stage called dauer. Its metabolism stops as the worm dries— and reactivates again on contact with water. Both situations lead to a stress response with a huge increase in the production of reactive molecules (radicals), increased calcium levels in nerve cells, and functional changes in mitochondria, the energy-generating cell organelles. The fact that C. elegans survives this is substantially due to its ability to increase the production of glycolic acid in its cells upon desiccation, as experimental studies have shown: When glycolic acid production is inhibited, then it dies, whereas externally supplied glycolic acid has a protective effect enabling the worms to survive.

Good protection in animal models

In strokes, we see processes similar to those that take place in the desiccation and rehydration of C. elegans."

Dr. Francisco Pan-Montojo, Clinic for Psychiatry and Psychotherapy, University of Munich Hospital

Therefore, the researchers investigated the hypothesis that glycolic acid could be used in mammals to reduce secondary damage resulting from a stroke. Indeed, experiments in various representative in-vitro and animal models of stroke showed that up to 100 percent of all nerve cells could be protected after administration of the molecule. The size of the affected region also decreased. "We were able to demonstrate that the protective effect of glycolic acid is mainly based on counteracting stroke-dependent calcium increases in the cells," explains Pan-Montojo. "Our results indicate that treatment with glycolic acid has the potential to reduce mortality and disability in stroke patients." Together with colleagues, Pan-Montojo has founded a start-up with the aim of advancing the step from research to application in patients.

Source:

Ludwig-Maximilians-Universitaet Muenchen (LMU)

Journal reference:

Chovsepian, A., et al. (2021) A Primeval Mechanism of Tolerance to Desiccation Based on Glycolic Acid Saves Neurons in Mammals from Ischemia by Reducing Intracellular Calcium-Mediated Excitotoxicity. Advanced Science. doi.org/10.1002/advs.202103265.

 

Inpatient rehabilitation facilities’ hospital readmission rates for medicare beneficiaries treated following a stroke

Ask your hospital what is their 100% recovery rate and their readmission rate. No knowledge, fire the board of directors. The heads up asses must be pulled out. 

Inpatient rehabilitation facilities’ hospital readmission rates for medicare beneficiaries treated following a stroke

Laura Coots Daras , Anne Deutsch , Melvin J. Ingber , Jennifer Gaudet Hefele & Jennifer Perloff

Received 08 Nov 2019, Accepted 25 Apr 2020, Published online: 11 Jul 2020

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• https://doi.org/10.1080/10749357.2020.1771927
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ABSTRACT

Background

Stroke is the leading cause for admission to the nearly 1,200 Inpatient Rehabilitation Facilities (IRFs) nationally in the US. For many patients, post-acute care is an important component of their rehabilitation. Several quality measures have been publicly reported for post-acute care providers, including hospital readmissions. However, to date none have focused on specific medical conditions, limiting the usability for patients and quality improvement.

Objective

To assess hospital readmission rates for Medicare patients receiving inpatient rehabilitation following stroke and to identify risk factors in order to evaluate the feasibility of a stroke-specific hospital readmission measure.

Methods

Observational study analyzing national Medicare inpatient claims and administrative data to assess hospital readmissions. Using logistic regression, we calculated unadjusted and risk-standardized readmission rates, which adjusted for patient characteristics, including type of stroke and admission function, to capture stroke severity.

Results

Our national study included 116,073 fee-for-service Medicare beneficiary discharged from IRFs in 2013–2014 following stroke from 1,162 IRFs nationally. The observed hospital readmission rate among IRF patients following stroke was 11.6% and varied by patients’ admission motor function. Patients with greater functional dependence had higher readmission rates on average. Lower admission function, hemorrhagic and other stroke types (relative to ischemic) were significantly associated with higher odds of hospital readmission.

Conclusion

Results suggest it is feasible to assess hospital readmission rates among a stroke-cohort treated in IRFs. Stroke-focused quality measures would be useful to patients in selecting a provider and for providers in evaluating their stroke rehabilitation program outcomes. Secondary results suggest that admission function (FIM) capture stroke severity, a limitation with other claims-based stroke measures.