If your doctor can't summarize this into EXACT PROTCOLS FOR YOUR RECOVERY; COMPLETE INCOMPETENCE!
Why you need this in here:
vagus nerve (56 posts to July 2012)
Wednesday, February 25, 2026
Breakthrough Study Reprograms Obese Fat Cells to Boost Metabolism
Is this what you need to not gain weight post stroke? Or did your competent? doctor get you 100% recovered?
Breakthrough Study Reprograms Obese Fat Cells to Boost Metabolism
Sleep Apnea Increases In-Hospital Pneumonia Risk After Acute Stroke
Part of the reason for my extreme fatigue post stroke was sleep apnea which my doctors never found. Once found, the CPAP machine was useless, couldn't sleep with the need to forcibly exhale against the incoming air. Have no clue if I still have sleep apnea, no partner to tell me otherwise, my fatigue has lessened considerably so I'm guessing my sleeping habits are now preventing the problem. Didn't get pneumonia.
Sleep Apnea Increases In-Hospital Pneumonia Risk After Acute Stroke
Preexisting sleep apnea is an independent predictor for acquiring in-hospital pneumonia following an acute stroke.
Inpatients with stroke and comorbid sleep apnea are at higher risk for acquiring pneumonia, according to study results presented at the International Stroke Conference (ISC), held from February 4 to 6, 2026, in New Orleans, Louisiana.
After acute stroke, patients are at risk for in-hospital pneumonia and those who develop pneumonia have longer hospital stays, worse outcomes, and higher mortality. The subset of patients with preexisting sleep apnea may be at increased risk for pneumonia due to higher risk for aspiration, hypoxia, and impaired airway clearance and due to the associated systemic inflammation.
To investigate the relationship between sleep apnea and poststroke pneumonia risk, investigators evaluated data from the Florida Stroke Registry. Patients (N=189,757) who were discharged after acute stroke between 2010 and 2025 were evaluated for in-hospital pneumonia on the basis of sleep apnea status.
Sleep apnea was a preexisting condition among 2.1% of patients.
Given the challenges of formal screening in acute care, efforts should focus on recognizing pre-existing sleep apnea and supporting adherence to therapies (eg, CPAP/BiPAP [continuous or bilevel positive airway pressure]) alongside standard pneumonia prevention protocols.
The rate of in-hospital pneumonia in the study population was 4.6%.
The in-hospital pneumonia rate was higher among patients with sleep apnea (7.9%) than among those without sleep apnea (4.5%).
The independent predictors for in-hospital pneumonia included sleep apnea (adjusted odds ratio [aOR], 1.76; 95% CI, 1.55-2.00), higher stroke severity, subarachnoid or intracerebral hemorrhage relative to ischemic stroke, male gender, underweight body mass index (BMI), smoking, atrial fibrillation, diabetes, dyslipidemia, and depression. Conversely, in-hospital pneumonia risk was lower with transient ischemic attack relative to ischemic stroke, Hispanic ethnicity compared with White race, and in patients with overweight or obese BMI.
The study investigators concluded, “In acute stroke care, sleep apnea independently predicts in-hospital pneumonia, likely due to aspiration risk, respiratory compromise, and systemic inflammation. Given the challenges of formal screening in acute care, efforts should focus on recognizing pre-existing sleep apnea and supporting adherence to therapies (eg, CPAP/BiPAP [continuous or bilevel positive airway pressure]) alongside standard pneumonia prevention protocols.”
This article originally appeared on The Cardiology Advisor
Oklahoma City Rehabilitation Hospital Earns Center of Excellence Designation in Rehabilitation Services and Stroke Care
'Care' is NOT RECOVERY!
This is the whole problem in stroke enumerated in one word; 'care'; NOT RECOVERY!
Our non-existent stroke leadership should be demanding RECOVERY NOT 'CARE'! This is you, WSO!
My god, anyone in the business world would be fired immediately for managing or caring about something rather than delivering RESULTS. And this is why this is a complete fucking failure! This does nothing to guarantee recovery for survivors!
If your stroke medical 'professional'/hospital is touting 'care' it means they are a failure because they are delivering 'care'; NOT RECOVERY! I would never go to a failed hospital! Anytime I see the word 'care' associated with a stroke hospital; I immediately think fucking failure!
YOU have to get involved and change this failure mindset of 'care' to 100% RECOVERY! Survivors want RECOVERY, NOT 'CARE'!
I see nothing here that states going for 100% recovery! You need to create EXACT PROTOCOLS FOR THAT!
ASK SURVIVORS WHAT THEY WANT, THEY'LL NEVER RESPOND 'CARE'! This tyranny of low expectations has to be completely rooted out of any stroke conversation! I wouldn't go there because of such incompetency as not having 100% recovery protocols!
RECOVERY IS THE ONLY GOAL IN STROKE!
GET THERE!
Oklahoma City Rehabilitation Hospital Earns Center of Excellence Designation in Rehabilitation Services and Stroke Care
OKLAHOMA CITY, OK, UNITED STATES, February 10, 2026 /EINPresswire.com/ — Oklahoma City Rehabilitation Hospital, a Nobis-owned hospital, has been officially designated a Center of Excellence in Rehabilitation Services – Stroke Care by the Center for Improvement in Healthcare Quality (CIHQ). This dual certification recognizes exemplary performance in the clinical management of patients requiring rehabilitation after a disabling disease or injury, as well as specialized rehabilitation and medical treatment for patients who have suffered a stroke. Oklahoma City Rehabilitation Hospital successfully completed a comprehensive onsite survey to assess its adherence to evidence-based care(NOT RECOVERY!) standards established by leading healthcare experts and nationally recognized organizations. This thorough survey process involved an in-depth review of medical documentation, direct observation of patient care(NOT RECOVERY!), interviews with the hospital’s rehabilitation team and hospital leadership, and patient interviews at the rehabilitation hospital.
“We are extremely proud of Oklahoma City Rehabilitation Hospital for achieving these distinguished designations as a Center of Excellence in both medical rehabilitation services and stroke care(NOT RECOVERY!),” said Chris Bergh, COO of Nobis. “Our mission is to be the premier medical rehabilitation leader in every community we serve. Achieving this Center of Excellence designation affirms the outstanding work our hospital teams commit to every day.”
About Nobis
Nobis brings together healthcare providers, developers, and investment partners to develop, design, own, and manage inpatient rehabilitation hospitals. Nobis has opened 18 rehabilitation hospitals and has another nine hospitals under construction. Patients will receive exceptional care(NOT RECOVERY!) from highly experienced and inspired caregivers in the most uniquely designed and efficient hospital.
About Oklahoma City Rehabilitation Hospital
The Oklahoma City Rehabilitation Hospital, a 40-bed hospital, opened in September 2022 at 10240 Broadway Extension, Oklahoma City, OK. The inspired hospital rehab team has provided comprehensive rehab for people who have suffered a disabling disease or illness, such as a stroke, brain injury, major multi-trauma, and other complex neurological and orthopedic diseases or injuries, and return them to an optimal fulfilling life.
Contact them and tell them EXACTLY why they are a failed stroke hospital!
JILL WATSON
NOBIS
+1 469-640-6510
email us here
Visit us on social media:
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Immediate Effects of Walker-Assisted Gait Training at Higher Training Speeds Comparing Conditions With and Without Body Weight Support After Stroke: A Pilot Crossover Study
I tried this once, never worked. Body weight support was useless; I needed the weight over my legs to counteract my spasticity. The only thing that did that was the Lokomat which my doctor thought was worthless. Shows you how incompetent doctors are!
Immediate Effects of Walker-Assisted Gait Training at Higher Training Speeds Comparing Conditions With and Without Body Weight Support After Stroke: A Pilot Crossover Study
Hiroo Koshisaki • Shota Nagai
Published: February 01, 2026 DOI: 10.7759/cureus.102772 Peer-Reviewed Cite this article as: Koshisaki H, Nagai S (February 01, 2026) Immediate Effects of Walker-Assisted Gait Training at Higher Training Speeds Comparing Conditions With and Without Body Weight Support After Stroke: A Pilot Crossover Study. Cureus 18(2): e102772. doi:10.7759/cureus.102772 Abstract
Background: Body weight-supported treadmill training (BWSTT) permits patients with stroke to practice walking at higher speeds under safe conditions but is limited by cost and accessibility. A suspended body weight-supported (BWS) walker has been developed as a practical alternative, enabling higher training speeds during walker-assisted gait training. However, it is unclear whether high-speed BWS walker-assisted gait training leads to immediate improvements in gait performance and how training speed and body weight support contribute to these effects. Methods: Twenty patients with chronic stroke participated in a crossover study. Each participant underwent two gait training sessions using the same walker device: one without BWS and one with BWS activated. Gait performance was assessed before and after each session using the 10 m walk test. Training speed during each session was recorded to evaluate its relationship with pre-to-post changes in gait performance.Results: Training with BWS enabled higher training speeds and resulted in significant improvements in gait speed and affected side step time, with a significantly greater increase in gait speed than that during training without BWS. Of the participants, 70% demonstrated increased training speed accompanied by immediate improvements in gait speed during BWS walker-assisted training. Improvements in gait speed were associated with increased stride length and reduced affected side step time.
Conclusion: Walker-assisted gait training that enables higher training speeds, particularly when combined with BWS, may contribute to immediate improvements in gait speed in patients with stroke. Reductions in affected side step time may represent one mechanism underlying this training speed-related effect.
Introduction
Stroke patients often experience reduced gait speed due to functional impairments such as hemiplegia [1]. Improving gait speed is a critical rehabilitation goal, as it is directly associated with activities of daily living [2]. The efficacy of suspended body weight-supported (BWS) treadmill training (BWSTT) in enhancing gait speed in stroke patients has been well documented [3-5]. One of the major advantages of BWSTT is that the use of a safety harness allows precise control of walking speed while minimizing the risk of falls. This enables patients to practice walking at speeds higher than their self-selected walking speed under safe conditions. Gait training performed at higher walking speeds is associated with improvements in gait speed and spatiotemporal gait parameters in patients with stroke [6,7]. These speed-dependent training effects are considered an important mechanism underlying gait improvement. However, suspension-based BWS devices such as those used for BWSTT have notable limitations, including high cost, lack of portability, and restricted availability to specialized facilities. To address these drawbacks, a suspended BWS walker has been developed [8].
To prevent falls and make weight unloading during gait training easier, the BWS walker uses a harness fastened to the walker to support body weight. Recent studies on BWS walkers have shown that the use of a suspension system reduces the fear of falling and enables patients with stroke to walk at higher training speeds than those during usual walking [9]. Importantly, both walker-assisted walking without body weight support and walking with body weight support allowed patients to achieve faster walking speeds, suggesting that the presence of a safety suspension itself plays a key role in facilitating higher training speeds by enhancing postural confidence.
Although it has become clear that walker-assisted gait training enables patients to walk at higher training speeds under safe conditions, it remains unclear whether such high-speed gait training translates into improvements in actual walking performance. In addition, the relative contributions of training speed and body weight support to immediate gait improvements have not been fully elucidated.
In this study, we aimed to investigate the immediate effects of walker-assisted gait training at higher training speeds by comparing conditions with and without body weight support in patients with stroke.
Materials & Methods
Study design and experimental protocol
The immediate effects of gait training were assessed by comparing gait performance using the same suspended walker device with BWS activated (BWS walker condition) or without BWS (walker condition). The study design employed an open-label crossover design (Figure 1).
Participants were randomly assigned to one of two groups: group A first underwent walker gait training, followed by a one-week washout period, and then BWS walker gait training. Group B first underwent BWS walker gait training, followed by a one-week washout period, and then walker gait training. Walker gait training was performed without body weight support, whereas BWS walker gait training included 25% body weight support. Each training session lasted 10 minutes, including rest periods. The intervention was conducted under therapist supervision, and no falls, accidents, or other adverse events occurred during the study period. Pre- and post-training gait performance was assessed using a 10-meter walk test. The differences in gait parameters before and after each training session were analyzed, and the magnitude of change was compared between walker and BWS walker gait training. Additionally, gait speed during each training session was calculated for both conditions.
Tai Chi Interventions for Slowing Cognitive Decline in Mild Cognitive Impairment: A Review of Randomized Controlled Trials
Will your competent? doctor get you recovered enough to do this or are OTHER EXACT METHODS AVAILABLE TO PREVENT THE PROBLEM?
I tried Tai chi once but had to adjust all the moves to fit my limitations.
Tai Chi Interventions for Slowing Cognitive Decline in Mild Cognitive Impairment: A Review of Randomized Controlled Trials
Abstract
The objective of this review was to compile randomized controlled trials that examined the effectiveness of tai chi in slowing cognitive decline among individuals with mild cognitive impairment (MCI). We limited our review to studies with interventions that lasted at least six months (≥ 24 weeks).Three databases were searched using similar search terms and inclusion/exclusion criteria to identify studies for review. In total, eight randomized controlled trials were included. The inclusion criteria limited the selected articles to RCTs whose patients all had MCI and were at risk for developing cognitive decline. All eight studies revealed that tai chi slows cognitive decline among patients with MCI across various domains, including memory, attention, and global cognition, compared to the control groups.Notably, improvements in patient cognition were consistently observed across studies. Three studies using the Montreal Cognitive Assessment revealed a greater increase in MoCA scores from baseline to follow-up (≥24 weeks) among the tai chi intervention group compared to the non-tai chi control group (0.84, 1.3, and 2.9). Similarly, two studies using the Mini-Mental State Examination found greater cognitive improvements among the tai chi group than in the control group from baseline to follow-up (0.60 and 0.48). In conclusion, this review supports tai chi as a promising intervention for slowing cognitive decline in individuals with MCI. Positive effects were observed across various cognitive assessments. Thus, these findings may help guide patient care strategies and inform clinical models for MCI management.Introduction & Background
As accessibility to medical care continues to improve globally, longer life expectancies continue to be observed. By 2030, 1 in 6 individuals will be 60 years or older, and the global elderly population is expected to double from 1 billion in 2030 to 2.1 billion in 2050 [1]. Mild cognitive impairment (MCI) refers to impaired cognition without impairment of social and daily activities, and it is mostly observed among the aging population. An estimated 15.6% of the global population of community-dwelling adults aged 50 years and older have MCI [2]. MCI has been described to affect one or more cognitive domains in learning and memory, language, complex attention, executive function, social cognition, and visuospatial function. The histopathology is heterogeneous, with some studies reporting MCI being associated with the buildup of amyloid plaques (identified via the Bielschowsky silver method) and others noting neuronal loss [3]. Since many presentations of MCI develop into dementia [4], prevention efforts are increasingly important in mitigating the incidence of dementia in elderly populations.Tai chi, also known as tai chi chuan/quan or taiji, was developed in China by martial artist Chen Wangting at the end of the Ming dynasty (17th century) [5]. Tai chi is a mind-body exercise that incorporates physical, cognitive, and psychosocial components [6]. While the practice of tai chi is extremely popular in the East and is even cited as the most common regular form of exercise in Shanghai, China, it remains an emerging activity in the West whose popularity is gradually increasing [7-9]. From 2007 to 2017, a 64% increase in tai chi engagement was observed among individuals in the United States who participated in the National Health Interview Survey [10]. Tai chi is a highly recommended exercise for older adults due to its low-intensity movements that promote participant safety and its benefits for balance, muscle flexibility, and muscle endurance [11]. Current clinical guidelines recommend that patients with MCI conduct both physical and mental exercise routines to help mitigate further cognitive decline, with some studies investigating tai chi’s use in MCI specifically [12-13]. Learning choreography for tai chi enhances visuospatial processing, processing speed, and episodic memory [14]. Additionally, the sustained attention and multitasking behaviors required for tai chi improve executive functioning while the meditative components reduce susceptibility to anxiety and depression [15].
The aim of conducting this review is to compile available research that meets rigorous criteria and assess the efficacy of tai chi as an intervention for the longitudinal prevention of cognitive decline and dementia. While there are existing review papers on the effects of tai chi on MCI, they are limited in size [16], are not specific to MCI and include other types of cognitive deficits [17], and/or are not exclusively examining long-term interventions and follow-up periods (≥24 weeks) [18-19]. This review adds new knowledge to the literature because of our rigorously defined inclusion criteria, most notably limiting included studies to RCTs whose patients all had MCI and were at risk for developing cognitive decline, and those intervention periods lasting at least six months (≥24 weeks). Since individuals with MCI are at risk of cognitive decline throughout the rest of their lives [3], it is necessary to focus exclusively on longitudinal effects. Thus, this review offers novel insight that can inform researchers and clinicians involved with treating patients with MCI about the role of complementary therapies like tai chi.
Review
Methods
Search Strategy
Covidence was used to compile the results from the searches across three separate databases. From a total of 348 studies, an automated screening was conducted to reduce the number of studies to n=218 (Figure 1).
The search strategy we conducted was in consultation with a research librarian in our field. We conducted a comprehensive search across three databases: PubMed, Scopus, and APA PsycINFO (Table 1). We automatically filtered only for papers written in the English language, along with an additional filter for middle-aged patient populations. We then found search terms using the National Library of Medicine’s Medical Subject Headings (MeSH) online tool.
Angiotensin II-Stimulating vs Inhibiting BP Drugs: Stimulating Class Linked to Lower Dementia Pathology Risk, JAMA
Have your competent? doctor figure out if you are on the right class of blood pressure drugs.
Here's info to bring to your doctor:
Angiotensin
II–stimulating antihypertensives are a class of blood pressure
medications that, while lowering systemic blood pressure, are thought to
increase the stimulation of protective
and
receptors, potentially offering cognitive benefits. These include Angiotensin II Receptor Blockers (ARBs) (e.g., losartan), dihydropyridine Calcium Channel Blockers (CCBs) (e.g., amlodipine), and thiazide diuretics.
Common Angiotensin II Antagonist Drugs (Sartans)
The following are major ARBs approved for clinical use, often identified by the suffix "-sartan":
- Azilsartan (Edarbi): Used for hypertension.
- Candesartan (Atacand): Used for hypertension and heart failure.
- Eprosartan(Teveten):Used for hypertension.
- Irbesartan (Avapro): Used for hypertension and diabetic nephropathy.
- Losartan (Cozaar): Commonly used for hypertension and stroke reduction.
- Olmesartan (Benicar): Used for hypertension.
- Telmisartan (Micardis): Used for hypertension and cardiovascular risk reduction.
- Valsartan (Diovan): Used for hypertension and heart failure.
Mechanism of Action and Clinical
Angiotensin II-Stimulating vs Inhibiting BP Drugs: Stimulating Class Linked to Lower Dementia Pathology Risk, JAMA
Gut-Brain-Heart Axis: How Microbes Control Your Blood Pressure
Will your competent? doctor figure how to use this and stop your blood pressure meds. NO? So, incompetently will DO NOTHING? Won't get human testing going?
Gut-Brain-Heart Axis: How Microbes Control Your Blood Pressure
Sumary: High blood pressure and heart failure might be managed through the gut. New research has identified a direct communication line between gut bacteria, the brain, and the heart. The study reveals that a specific bacterial metabolite called indole-3 acetic acid (IAA) acts as a brake on “stress” neurons in the brain’s hypothalamus.
When IAA levels are low, these neurons become overactive, causing the heart muscle to stiffen—a condition known as diastolic dysfunction. This discovery suggests that diet, probiotics, or IAA supplementation could become powerful new tools for preventing hypertension and heart failure.
Key Facts
- The IAA Brake: Gut microbes produce indole-3 acetic acid (IAA) from the amino acid tryptophan. IAA travels to the brain to regulate hypocretin (Hcrt) neurons.
- Brain as a Hub: Hcrt neurons in the hypothalamus act as the central switch. Without enough IAA, these neurons overfire, sending sympathetic nerve signals that stiffen the heart.
- Diastolic Dysfunction: This research helps explain why the heart struggles to relax in millions of patients—a key driver of heart failure with preserved ejection fraction (HFpEF).
- Human Connection: A study of human patients showed that those with hypertension have lower IAA levels, with a particularly strong effect seen in hypertensive women.
- Biomarker Potential: IAA levels in the blood could serve as an early warning signal for people at high risk of heart failure, allowing for preventative dietary changes.
Source: MDC
Hypertension and heart failure affect millions worldwide. Yet in many patients, doctors cannot fully explain why the heart becomes stiff and struggles to relax – a condition known as diastolic dysfunction.
Researchers in the lab of Dr. Suphansa Sawamiphak, Group Leader of Cardiovascular-Hematopoietic Interaction at the Max Delbrück Center, have identified a direct communication line between gut bacteria, the brain, and the heart.
Using zebrafish as a model, the team discovered that certain gut microbes produce a small molecule called indole-3 acetic acid (IAA) from the dietary amino acid tryptophan. IAA acts on neurons in the brain, which in turn, control the heart. The study was published in “Circulation Research.”
“We were surprised that a single bacterial metabolite could influence the central nervous system, the heart, and major hormonal systems at the same time,” says Bhakti Zakarauskas-Seth, lead author of the paper. “It shows that the brain can act as a central hub in gut-heart communication.”
Tracking a signal from gut to brain
To understand how gut bacteria might influence the heart, the researchers focused on a distinct group of neurons in the hypothalamus known as hypocretin (Hcrt) in zebrafish larvae. These cells produce Hcrt neuropeptides, also known as orexins, regulate many involuntary functions in the body, such as sleep and eating patterns, but also heart activity.
When IAA levels dropped, Hcrt neurons became overactive. This increased sympathetic nerve signals to the heart, causing the heart muscle to stiffen, impairing its ability to relax properly.
When the researchers supplemented the larvae with IAA, neuronal activity normalized, heart function and blood pressure improved, and even related hormones such as renin and angiotensinogen returned to healthier levels.
They then examined data from a cohort of patients – humans also have Hcrt neurons – and found that IAA levels were reduced in patients with hypertension. Notably, they observed a sex-specific effect, with hypertensive women showing significantly lower levels of IAA in their serum samples than men.
Implications for patients and prevention
Diastolic dysfunction very common – up to half of all people over age 70 have some level of impairment. It is also is the underlying functional mechanism of heart failure with preserved ejection fraction (HFpEF), which accounts for over 50% of all heart failure cases.
For these patients, the findings open several potential avenues for better care, says Zakarauskas-Seth.
“IAA levels could serve as a biomarker to identify patients at high risk of hypertension or heart failure. Therapeutically, boosting IAA production – for example through diet, probiotics, or supplementation – could become a new strategy to prevent or treat cardiovascular disease.”
That a single bacterial metabolite can influence the central nervous system, the heart, and major hormonal system also underscores a broader message, she adds.
“The body does not operate in isolated compartments. Gut health, microbial balance, and diet directly shape how well the heart functions.”
The researchers will need to validate their findings in other animal models and clinical studies will be needed to determine whether restoring IAA can benefit patients.
Key Questions Answered:
Q: How does my gut talk to my heart?
A: It uses the brain as a middleman! Your gut bacteria produce a chemical called IAA from the food you eat. This chemical tells your brain to stay calm. If your gut doesn’t produce enough IAA, your brain gets “stressed” and sends signals that make your heart stiff and your blood pressure rise.
Q: Can I eat my way to a healthier heart?
A: The study suggests that foods rich in tryptophan (like turkey, eggs, and cheese) might help, as gut bacteria turn tryptophan into IAA. However, the key is having the right microbes to do the work. Probiotics or IAA supplements could be the future of heart care.
Q: Why is this especially important for women?
A: The researchers found that hypertensive women had significantly lower levels of IAA than men. This suggests that the gut-brain-heart connection might play a particularly crucial role in cardiovascular health for women.
Editorial Notes:
- This article was edited by a Neuroscience News editor.
- Journal paper reviewed in full.
- Additional context added by our staff.
About this neuroscience research news
Author: Gunjan Sinha
Source: MDC
Contact: Gunjan Sinha – MDC
Image: The image is credited to Neuroscience News
Original Research: Open access.
“Indole-3 acetate limits dysbiosis-driven diastolic failure via Hcrt neurons” by Bhakti I. Zakarauskas-Seth, Giovanni Forcari, Harithaa Anandakumar, Ilan Kotlar-Goldaper, Clara Barraud, Nina Jovanovic, Ulrike Brüning, Jennifer Kirwan, Nicola Wilck, Sofia K. Forslund, Dominik N. Müller, Alessandro Filosa, and Suphansa Sawamiphak. Circulation Research
DOI:10.1161/CIRCRESAHA.125.326990
Alzheimer’s may begin with a silent drop in brain blood flow
Does your doctor have ANY PROTOCOLS TO ENSURE YOUR CERBRAL BLOOD FLOW IS CORRECT? I thought not, so incompetence is standard for your doctor!
Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand action!
Alzheimer’s may begin with a silent drop in brain blood flow
- February 24, 2026
- Keck School of Medicine of USC
- Subtle changes in brain blood flow and oxygen use are closely linked to hallmark signs of Alzheimer’s, including amyloid plaques and memory-related brain shrinkage. Simple, noninvasive scans may one day help spot risk earlier—by looking at the brain’s vascular health, not just its plaques.
Amyloid PET imaging was used in the study to measure plaque buildup in the brain, a hallmark of Alzheimer's disease. Warmer colors indicate higher amyloid levels. Participants with healthier patterns of brain blood flow and oxygen regulation had lower amyloid burden, reinforcing the idea that vascular function may be linked to Alzheimer's-related changes. Credit: Stevens INISmall shifts in how blood moves through the brain and how brain cells receive oxygen may be closely connected to the risk of Alzheimer's disease. That is the conclusion of new research from the Mark and Mary Stevens Neuroimaging and Informatics Institute (Stevens INI) at the Keck School of Medicine of USC.
The study, published in Alzheimer's and Dementia: The Journal of the Alzheimer's Association, examined older adults both with and without cognitive impairment. Researchers found that simple, noninvasive measures of brain blood flow and oxygen levels were linked to well known signs of Alzheimer's, including amyloid plaque buildup and shrinkage of the hippocampus, the part of the brain that plays a central role in memory. The results suggest that the health of the brain's blood vessels may influence the disease process early on and could help flag people at risk before noticeable symptoms develop.
"Amyloid and tau are often considered the primary players in Alzheimer's disease, but blood flow and oxygen delivery are also critical," said Amaryllis A. Tsiknia, lead author of the study and USC PhD candidate. "Our results show that when the brain's vascular system functions more like it does in healthy aging, we also see brain features that are linked to better cognitive health."
Noninvasive Tools to Measure Brain Circulation
To study these changes, the team relied on two painless techniques that can be used while a person rests quietly. Transcranial Doppler ultrasound tracks how quickly blood travels through the brain's major arteries. Near infrared spectroscopy evaluates how effectively oxygen reaches brain tissue near the surface of the cortex.
Researchers then applied advanced mathematical modeling to combine these readings into overall indicators of cerebrovascular function. These indicators reflect how well the brain adjusts blood flow and oxygen delivery in response to natural fluctuations in blood pressure and carbon dioxide.
Vascular Health Linked to Amyloid and Memory Centers
Participants whose vascular indicators more closely resembled those of cognitively healthy adults tended to have lower amyloid levels and a larger hippocampus. Both features are associated with reduced Alzheimer's risk.
"These vascular measures are capturing something meaningful about brain health," said Meredith N. Braskie, PhD, senior author of the study and assistant professor of neurology at the Keck School of Medicine. "They appear to align with what we see on MRI and PET scans that are commonly used to study Alzheimer's disease, providing important information about how vascular health and standard brain measures of Alzheimer's disease risk may be related."
The researchers also observed that people diagnosed with mild cognitive impairment or dementia showed weaker vascular function compared to cognitively normal participants. This finding supports the view that declining blood vessel health in the brain is part of the broader Alzheimer's disease continuum.
"These findings add to growing evidence that Alzheimer's involves meaningful vascular contributions in addition to classic neurodegenerative changes," said Arthur W. Toga, PhD, director of the Stevens INI. "Understanding how blood flow and oxygen regulation interact with amyloid and brain structure opens new doors for early detection and potentially prevention."
Potential for Earlier and Broader Screening
Compared with MRI and PET imaging, these methods are less costly and easier to perform. They do not involve injections, radiation exposure, or demanding tasks for patients. That simplicity could make them useful for large scale screening or for individuals who are unable to undergo more intensive brain imaging.
The authors caution that the findings represent a single snapshot in time and do not establish cause and effect. Ongoing long term studies are tracking participants to see whether shifts in these vascular measures can predict future cognitive decline or response to treatment.
"If we can track these signals over time, we may be able to identify people at higher risk earlier and test whether improving vascular health can slow or reduce Alzheimer's-related brain changes," Tsiknia said.
About the Study
In addition to Tsiknia and Braskie, the study's other authors are Peter S. Conti, Rebecca J. Lepping, Brendan J. Kelley, Rong Zhang, Sandra A. Billinger, Helena C. Chui and Vasilis Z. Marmarelis.
This work was supported by the Office of The Director, National Institutes of Health, under Award Number S10OD032285, and by the National Institute on Aging [R01AG058162].
Tuesday, February 24, 2026
Researchers Link Pneumonia-Causing Bacterium to Alzheimer's Disease Risk
Your competent? doctor immediately gave you the pneumonia vaccine post stroke, right!
Researchers Link Pneumonia-Causing Bacterium to Alzheimer's Disease Risk
Study Highlights Immune Differences Between Coffee and Caffeine
Your competent? doctor is already familiar with regular coffee vs. decaf, right! Oh no, your doctor knows nothing and has no plans on ever learning anything past medical school!
How Coffee May Protect Brain Health: A New Study Suggests The Benefits Aren't Just From Caffeine December 2018
The latest here:
Study Highlights Immune Differences Between Coffee and Caffeine
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