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.

Showing posts with label vascular aging. Show all posts
Showing posts with label vascular aging. Show all posts

Friday, March 13, 2026

Spain’s Cardiovascular Risk Standards Introduce Vascular Age

 See if you have an incompetent doctor, one who knows nothing about this because s/he doesn't follow research! And then fire your board of directors since they don't know how to run a stroke hospital!

Arterial stiffness (32 posts to December 2014) The latest here:

Spain’s Cardiovascular Risk Standards Introduce Vascular Age

Cardiovascular disease (CV) remains the leading cause of death in Spain, contributing to disability and healthcare costs. The Spanish Society of Arteriosclerosis released the 2026 edition of its standards for global CV risk control, which is an updated clinical reference designed to guide prevention, diagnosis, and management.

The document, updated every 2 years, combines current evidence and incorporates recent advances in CV research and clinical practice. One of the most notable changes in the 2026 update is the replacement of the traditional concept of CV risk with the concept of vascular age, which is presented in a newly updated risk table intended to improve communication with patients.

These standards were first introduced in 2020 and have become important references for clinicians involved in vascular risk management.

More than 30 professionals from multiple specialties contributed to the latest update, including experts in internal medicine, endocrinology, primary care, clinical laboratory medicine, and cardiology.

Comprehensive Risk Assessment

Because atherosclerosis has a multifactorial origin, standards emphasize a comprehensive approach to CV risk assessment.

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This document reviews the full clinical pathway for patients with vascular disease, including the initial evaluation and diagnostic testing, criteria for diagnosis, methods for estimating vascular risk, recommendations for both lifestyle and pharmacologic management, and criteria for referral and discharge.

It also proposes organizational recommendations for dedicated vascular risk clinics to offer practical guidance to healthcare professionals in managing these patients in daily clinical practice.

Role of Family History

These standards highlight the importance of obtaining detailed family histories of first-degree relatives when evaluating CV risk.

This is particularly relevant for conditions linked to atherosclerotic vascular disease and major CV risk factors, such as suspected familial hypercholesterolemia or premature vascular disease.

Family history was more significant when events occurred at younger ages (< 55 years in men and < 65 years in women).

In addition to general medical history, such as allergies or earlier surgical procedures, clinicians are recommended to investigate the history of atherosclerotic vascular disease and major risk factors, including diabetes, hypertension, dyslipidemia, smoking, and obesity.

When present, the age of onset and details of current or earlier treatments should be recorded, regardless of their indication.

Diagnostic Evaluation

According to a consensus document developed by 15 Spanish scientific societies, the evaluation should include a basic lipid profile.

Clinicians should also conduct a targeted smoking history test, including the Fagerström test, to assess nicotine dependence in individuals who smoke.

Diagnostic evaluations may also include additional tests tailored to individual patient profiles.

For individuals without proven atherosclerotic vascular disease but with CV risk factors, calculating vascular risk is a key step. This estimation informs major clinical decisions, such as when to initiate lipid-lowering therapy and what treatment targets should be pursued.

Imaging for Subclinical Disease

José María Mostaza, MD, PhD, from the Hospital Carlos III, Madrid, Spain, and the first author of the document, noted that the section on imaging for subclinical CV disease has been substantially expanded.

The updated guidelines clarify how carotid ultrasound, femoral ultrasound, and coronary artery calcium scoring can improve CV risk estimation.

These imaging approaches may help detect early vascular changes before the development of a clinical disease.

Key Innovations in the 2026 Edition

Another new feature of the 2026 standards is the introduction of an updated table on vascular age.

Clinicians can estimate the age of a patient’s arteries based on their risk profiles instead of communicating abstract risk percentages.

According to Mostaza, many patients find CV risk percentages difficult to understand. Telling a 50-year-old patient that their arteries resemble those of a 70-year-old often makes the message clearer.

The new edition also incorporates updated recommendations from the Spanish Society of Arteriosclerosis on diet and CV prevention, as well as clinical practice recommendations derived from the society’s consensus on lipoprotein(a).

In addition, the standards integrate guidance from various international and national guidelines published in the past 2 years. These include the 2025 European update on dyslipidemia, American guidelines on hypertension, Spanish guidelines on obesity, the American Diabetes Association standards, Canadian guidelines on tobacco cessation, and European guidelines on atrial fibrillation.

Ferrer, part of Grupo Ferrer Internacional SA, provided support for the publication and administrative support for updating the Spanish Society of Arteriosclerosis 2026. However, the company had no role in drafting or deciding the content of the document.

This story was translated from El Medico Interactivo, part of the Medscape Professional Network.

Saturday, January 18, 2025

The pathobiology of neurovascular aging

 

What will your competent? doctor do with this to ensure you DON'T GET DEMENTIA from your extra risk from your stroke? NOTHING? So, you DON'T have a functioning stroke doctor, do you? Why the hell doesn't the board of directors' have policies to remove incompetent doctors? They also must be fucking incompetent!

Send me hate mail on this: oc1dean@gmail.com. I'll print your complete statement with your name and my response in my blog. Or are you afraid to engage with my stroke-addled mind? No excuses are allowed! You're medically trained; it should be simple to precisely refute all my points with NO EXCUSES!! And what is your definition of competence in stroke? Swearing at me is allowed, I'll return the favor. Don't even attempt to use the tyranny of low expectations as an answer.

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

The latest here:

The pathobiology of neurovascular aging

Cover Image - Neuron, Volume 113, Issue 1

Summary

As global life expectancy increases, age-related brain diseases such as stroke and dementia have become leading causes of death and disability. The aging of the neurovasculature is a critical determinant of brain aging and disease risk. Neurovascular cells are particularly vulnerable to aging, which induces significant structural and functional changes in arterial, venous, and lymphatic vessels. Consequently, neurovascular aging impairs oxygen and glucose delivery to active brain regions, disrupts endothelial transport mechanisms essential for blood-brain exchange, compromises proteostasis by reducing the clearance of potentially toxic proteins, weakens immune surveillance and privilege, and deprives the brain of key growth factors required for repair and renewal. In this review, we examine the effects of neurovascular aging on brain function and its role in stroke, vascular cognitive impairment, and Alzheimer’s disease. Finally, we discuss key unanswered questions that must be addressed to develop neurovascular strategies aimed at promoting healthy brain aging.

Keywords

  1. neurovasculome
  2. neurovascular unit
  3. blood-brain barrier
  4. vascular cognitive impairment
  5. Alzheimer’s disease
  6. rejuvenation strategies

Introduction

The world population is aging at an unprecedented rate, making it a public health priority to improve the quality of life by preventing or minimizing the impact of age-related diseases. Comprehensive global estimates of disease burden and mortality have shown that the increase in life expectancy has led to a shift from communicable to non-communicable diseases as the major causes of death and disability., Given the chronic course of non-communicable diseases, the world population lives longer but in poorer overall health. Neurovascular diseases, such as stroke and dementia, are major culprits of the deteriorating quality of life of the elderly. Every year, 15 million people have a new stroke worldwide, 30% of whom survive with long-term physical or cognitive disabilities that negatively impact activities of daily living (https://www.emro.who.int/health-topics/stroke-cerebrovascular-accident/index.html). In addition, 55 million people worldwide are living with dementia, mainly vascular cognitive impairment dementia (VCID) and Alzheimer’s disease (AD) (https://www.alzint.org/about/dementia-facts-figures/dementia-statistics/), conditions that often overlap and in which vascular factors play a pathogenic role., Therefore, it has become increasingly apparent that brain health critically depends on neurovascular health, and gaining a better understanding of how aging alters the neurovasculature may help develop new strategies to promote healthy brain aging and improve the quality of life in old age (“adding life to years”).
Aging induces profound alterations in all segments of the neurovasculature, from the large blood vessels in the neck to the intracranial, meningeal, and lymphatic vasculature. These alterations have long been known to play a critical role in brain diseases of old age and have been a topic of intense study for decades. Seminal advances in the biology of aging have provided a deeper understanding of the integrated drivers of organismal aging, such as genomic alterations, chronic inflammation, cellular senescence, extracellular matrix (ECM) remodeling, stem cell exhaustion, and others. These processes have a profound impact on the neurovasculature, and cerebrovascular aging has emerged as a key determinant of brain aging and associated diseases. At the same time, advances in brain imaging and the recent introduction of single-cell or single-nuclei transcriptomics have provided new insights into the intimate relationships between the brain and its vasculature in health and disease. These advances have shed new light on the influence of aging on neurovascular and neurodegenerative diseases.
Here, we seek to provide a critical appraisal of these new developments and their significance for brain health and for the risk for neurological diseases of old age. After briefly reviewing basic concepts on the structure and function of the neurovasculature and the biology of aging, the vascular changes induced by “healthy aging” will be examined. These findings will be integrated with data emerging from single-cell or single-nuclei molecular studies of aging vessels aimed at identifying the cell types and related signaling mechanisms driving age-related changes. Finally, the impact of the vascular changes on disease risk will be examined, focusing on highly prevalent conditions associated with cognitive decline and on rejuvenation strategies to support healthy brain aging by promoting neurovascular health.

More at link.

Wednesday, January 8, 2020

First-Time Marathoners Turn Back Clock on Vascular Aging

You'll want this reversal but your doctor will look at the healthy individuals recruited and be able to successfully say this doesn't apply to stroke survivors. That 'get out of jail free' card should be laughed at and DEMAND your doctor provide protocols to get you running again.  Since you will get no help from your doctor you are completely on your own to learn running again. I'd suggest 'Teaching Me to Run' by Tommye-K. Mayer

First-Time Marathoners Turn Back Clock on Vascular Aging

Arterial stiffening cannot be helped by available medications

  • by Staff Writer, MedPage Today
Healthy individuals training for their first marathon saw a reversal in age-related aortic stiffening, a known cardiovascular risk factor, researchers found in a prospective study.
After 6 months of unsupervised training for the London Marathon, 138 people demonstrated improved distensibility on cardiac MRI in two levels of the thoracic aorta: the proximal descending aorta (average 9% increase from baseline, P=0.009) and the diaphragmatic descending aorta (16% increase, P=0.002).
This correlates with 4 years regained in "aortic age" given the amount of distensibility known to be lost over time due to aging, reported Charlotte Manisty, MD, of Barts Heart Centre in London, and colleagues in the Journal of the American College of Cardiology.
"If the observed effects of exercise on LAS [large artery stiffening] can be sustained, they could have major effects on the myocardium, kidney, brain, and various other organs, with a potentially broad impact on age-related conditions," commented Julio Chirinos, MD, PhD, of the Hospital of the University of Pennsylvania in Philadelphia.
"Despite its benefits, exercise remains underutilized and challenging to implement on a large scale, both in the general public and in clinical populations. Therefore, there is a need for implementation research aimed at overcoming common barriers to exercise and physical activity," he wrote in an accompanying editorial.
Study participants had no previous marathon experience and were running less than 2 hours a week at baseline. Half of the enrolled cohort were men. Mean age was 37.
Their recommended exercise training regimen consisted of 6 to 13 miles of weekly running before the 2016 and 2017 London Marathons. They had central blood pressure and aortic stiffness evaluated roughly 176 days before and 16 days after finishing the marathon.
Greater reversals in aortic stiffening were observed in older individuals, men, slower runners, and those with higher blood pressure.
"This study emphasizes the importance of lifestyle to modify the aging process, particularly as it appears 'never too late' to gain the benefit as seen in older, slower runners," Manisty's group noted.
Not all thoracic aortic segments showed improved elasticity with marathon training, however, as no change was seen in the ascending aorta in the study.
Marathon training reduced both brachial and aortic systolic blood pressures by 4 mm Hg -- in line with the magnitude achievable on first-line antihypertensive drugs, the investigators reported.
"The improvement in aortic stiffness was both functional due to blood pressure lowering, as well as intrinsic due to structural changes in the descending aorta. This is supported by wave separation analysis, which showed that reflection magnitude was unchanged," they stated.
That the increase in distal descending aortic distensibility was at least partially independent of the change in distending pressure suggests intrinsic changes in the material properties of the aortic wall, rather than changes in loading conditions alone, Chirinos agreed.
Manisty's team acknowledged that the study of healthy marathon-finishers precludes the generalizability of their results to hypertensive individuals and those who didn't complete the marathon.
They also had no information on the intensity, frequency, and type of exercise training undertaken.
A lack of controls also limits the interpretation of the findings, Chirinos said, noting that the finding of a more pronounced reduction in aortic stiffness among certain subgroups appears to be at odds with previous data suggesting less pronounced effects of exercise training on aortic stiffness among hypertensive and older adults.
"As a consequence of its key role in health and disease, LAS imposes a large global burden of age-related morbidity and mortality, which will become increasingly important as competing causes of death (such as atherosclerosis, cancer, and transthyretin amyloidosis) are addressed with more effective prevention and treatment strategies," the editorialist said.
"LAS therefore represents a high-priority therapeutic target that is not addressed by our current pharmacological approaches," he stated.

Saturday, September 15, 2018

Fasting-induced anti-aging molecule keeps blood vessels young

I bet this is not enough for your doctor to establish a protocol on this for your better health.Or would a transfusion of young blood be better?
https://www.medicalnewstoday.com/articles/323039.php

New research has found that fasting triggers a molecule that can delay the aging of our arteries. The findings could help prevent age-related chronic diseases such as cancer, cardiovascular disease, and Alzheimer's.
blood vessels
Scientists have discovered a new role for a molecule produced during fasting: it can keep our vascular system supple and young.
The search for eternal youth has preoccupied the human imagination since the times of Ancient Greece.
In fact, a quick look at Greek mythology shows that youth was more prized than immortality, as some myths tell the story of how futile the latter is if it's not accompanied by the former.
In this regard, modern medicine has recently been catching up with ancient mythology.
Emerging scientific breakthroughs encourage us to hope that the myth of eternal youth will soon become a reality.
In a recent study, researchers were able to reverse signs of aging such as hair loss and wrinkles in mice; and, perhaps more impressively, another team of researchers managed to rejuvenate aging human cells.
Now, a new study adds to the evidence that aging can indeed be reversed. Scientists led by Dr. Ming-Hui Zou — the director of the Center for Molecular and Translational Medicine at Georgia State University in Atlanta — showed that fasting, or restricting calorie intake, can produce a molecule that delays vascular aging.
The findings were published in the journal Molecular Cell.

How a ketone molecule keeps cells young

Dr. Zou explains the motivation for this study, saying, "The most important part of aging is vascular aging. When people become older, the vessels that supply different organs are the most sensitive and more subject to aging damage, so studying vascular aging is very important."
So, the scientists set out to focus on vascular aging, on the changes that occur with senescence, and on ways to prevent them.
Specifically, the researchers looked at the link between calorie restriction and vascular aging. Dr. Zou used mouse models of atherosclerosis, studied their aortas post-mortem, and performed a series of cell culture experiments. They also induced starvation in the rodents and conducted similar tests.
They saw that, as expected, the starving mice produced the molecule beta-hydroxybutyrate. Surprisingly, however, this molecule also prevented vascular aging.
Beta-hydroxybutyrate is a ketone — that is, a molecule produced by the liver and used as an energy source when glucose is not available. The body produces ketones during fasting or starvation, on low-carb diets, and after prolonged exercise.
Interestingly, the research also revealed that beta-hydroxybutyrate promotes the division and multiplication of the cells that line the inside of blood vessels. Cellular division is a marker of cellular youth.
"We found [that beta-hydroxybutyrate] can delay vascular aging. That's actually providing a chemical link between calorie restriction and fasting and the anti-aging effect."
Dr. Ming-Hui Zou
"This compound can delay vascular aging through endothelial cells," Dr. Zou explains, "which line the interior surface of blood vessels and lymphatic vessels. It can prevent one type of cell aging called senescence, or cellular aging."