What Brain Imaging Reveals About The Effects Of Light Alcohol Use by mindbodygreen

 If you insist on drinking, as I do, to prevent dementia via social connections then you will need your doctor to give you protocols on increasing cerebral blood flow. You can't use mine, I'm not medically trained. 

cerebral blood flow (51 posts to December 2015)

What Brain Imaging Reveals About The Effects Of Light Alcohol Use

Alzheimer's Disease May Begin with Subtle Decline in Brain Blood Flow: Study Shows

 Your competent? doctor has ways to measure this AND PROTOCOLS TO FIX IT, RIGHT?

Oh no, NOTHING EXISTS because your doctor is fucking incompetent for at least 10 years!

Knowledge of none of the following is grounds for screaming at your incompetents!

• cerebral blood flow (54 posts to December 2015)

Alzheimer's Disease May Begin with Subtle Decline in Brain Blood Flow: Study Shows

The U.S. POINTER Structured Healthy Lifestyle Program — Previously Shown to Improve Cognition — May Also Improve Sleep Apnea, Blood Pressure Regulation, and Cognitive Resilience

 How long will it take for your competent? doctor to set this up as an EXACT  PROTOCOL for you? Or doesn't your doctor even know of your increased dementia risk post stroke?  Or does know and DOES NOTHING! 

DOES YOUR DOCTOR HAVE EXACT DEMENTIA PREVENTION PROTOCOLS? NO? So, your doctor is incompetent? 

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 U.S. POINTER Structured Healthy Lifestyle Program — Previously Shown to Improve Cognition — May Also Improve Sleep Apnea, Blood Pressure Regulation, and Cognitive Resilience

Key Takeaways

• Findings from three NIA-funded ancillary studies to the U.S. POINTER trial described beneficial effects as measured by brain imaging, sleep health, and blood pressure regulation.

• The U.S. POINTER recipe, a 2-year multicomponent healthy lifestyle intervention with regular structured support, improved blood pressure regulation of blood flow to the brain, reduced sleep apnea respiratory events, and increased cognitive resilience for adults with certain Alzheimer’s-related brain changes.

SAN DIEGO, Dec. 2, 2025 — A two-year multicomponent healthy lifestyle intervention with regular, structured support — which has already shown that it can improve cognition in adults at risk for cognitive decline — may also improve blood pressure regulation and reduce hourly sleep apnea respiratory events, according to new data reported today at CTAD 2025 in San Diego. The intervention may also protect against the negative cognitive effects of certain Alzheimer’s disease-related brain changes.

The healthy lifestyle recipe was created for the Alzheimer’s Association’s U.S. POINTER trial, which published its initial results in JAMA last July and reported them at AAIC 2025. The evidence-based multicomponent lifestyle intervention adapted for the U.S. population consists of regular physical exercise, the MIND diet, cognitive challenge through computerized training and other intellectual and social activities, and regular review of health metrics and goal-setting with a study clinician.

“These studies tell us that the U.S. POINTER lifestyle intervention with structured support has substantial and significant health benefits beyond improving cognition — and the benefits are in areas known to lower risk of cognitive decline and dementia,” said Maria C. Carrillo, Ph.D., Alzheimer’s Association chief science officer and medical affairs lead. “This positive relationship may multiply the beneficial impact of closely adhering to the structured U.S. POINTER ‘recipe.’”

“Bottom line, we now have a more comprehensive picture of how the U.S. POINTER intervention affects brain health, and overall health, too,” Dr. Carrillo added.

There were two versions of the intervention — structured and self-guided — that differed in intensity, structure, accountability and support provided. Trial participants in the structured intervention showed greater improvement on global cognition compared to the self-guided intervention, a benefit that likely reflects slowing of cognitive aging by one to two years.

Poor regulation of blood flow to the brain and sleep problems/irregular sleep patterns are known risk factors for cognitive decline and dementia, including Alzheimer’s disease, so these new results describe additional benefits of the U.S. POINTER structured intervention.

The new data reports came from a series of U.S. POINTER ancillary studies funded by the NIH’s National Institute on Aging (NIA):

• The U.S. POINTER Sleep Ancillary Study: POINTER-zzz
• The U.S. POINTER Neurovascular Ancillary Study: POINTER-NV
• The U.S. POINTER Neuroimaging Ancillary Study: POINTER-Neuroimaging

A fourth ancillary study, The POINTER-Microbiome Study, which presented a poster at CTAD 2025, will report more fully at a later date.

NIA Director, Dr. Richard Hodes said, “I am very encouraged by these early findings from the U.S. POINTER ancillary studies, which offer valuable insights into the physiological mechanisms that may have contributed to the positive results of the U.S. POINTER trial. The forthcoming publications and continued analysis of this rich dataset will deepen our understanding of how multimodal interventions can support brain health.”

“These studies provide an unprecedented opportunity to better understand the impact that healthy lifestyle changes can have on overall health and risk for cognitive decline and dementia,” said Dr. Kristina McLinden, Program Officer at NIA.

POINTER-zzz
In older adults, sleep disorders are highly prevalent, frequently undetected or untreated, and associated with poor brain health outcomes, including cognitive decline. This highlights sleep as a modifiable risk factor for Alzheimer’s and other diseases that cause dementia. Interventions that improve sleep may also improve cognitive function in older adults. Two components of the U.S. POINTER’s structured intervention are physical activity and healthy diet, both of which have been shown to improve overall sleep health.

The POINTER-zzz study examined whether the lifestyle changes might improve sleep quality in a subset of 780 adults who participated in the U.S. POINTER clinical trial. Nearly 65% of the study group had at least mild sleep apnea when they started the study. POINTER-zzz used simple sleep tests that were completed at home. The tests involve wearing watch-like devices overnight to measure sleep apnea, restlessness and other sleep disruptions.

Respiratory disturbances from sleep apnea declined by 1 to 2 events per hour of sleep for study participants in the structured intervention versus those in the self-guided group.

“We are excited about this finding, as it shows that the structured intervention improves not only cognition but also other behaviors that affect brain health, which may increase protection against dementia,” said Laura D. Baker, Ph.D., Professor, Internal Medicine and Public Health Sciences; and Associate Director, Wake Forest Alzheimer’s Disease Research Center at the Wake Forest University School of Medicine, Winston Salem, NC. “The positive effect of the structured intervention on sleep deepens the significance of the U.S. POINTER trial results for older Americans.” Dr. Baker is one of the Principal Investigators of the parent trial and Principal Investigator of the sleep ancillary study.

POINTER-NV
Adequate blood flow to the brain is necessary to maintain a constant supply of oxygen and nutrients. While the relevance of reduced blood flow to the brain in Alzheimer’s disease and related dementias is well documented, few studies have investigated how vascular health is essential for regulation of blood flow in the brain; this was the primary focus of the neurovascular ancillary study.

POINTER-NV enrolled 491 parent trial participants who completed comprehensive testing of vascular health at baseline, month 12, and month 24. Several types of procedures, such as ultrasound and continuous blood pressure monitoring, were used to measure the structure and function of the blood vessels in the body and in the brain.

Many POINTER-NV participants have issues that strain the heart and blood vessels, like clogged arteries, stiff arteries, or drops in blood pressure when they stand up. The researchers found significant benefits from the structured intervention on the cardiovascular system and its ability to respond to sudden changes in blood pressure, indicating improved blood pressure regulation, compared to the self-guided group. The structured intervention also improved several measures of blood-vessel health in the body’s largest artery and the main arteries supplying the brain.

“Our findings indicate that a structured multidomain lifestyle intervention can improve the body’s ability to regulate blood pressure, which is crucial for proper brain blood flow to the brain. Improved blood pressure regulation can also reduce aging-related vascular changes that allow harmful, pulsing flow of blood — too fast and too much — into the brain. These benefits may help to support cognitive function and overall brain health in U.S. POINTER participants,” said ancillary study Principal Investigators, Drs. Brinkley and Shaltout.

POINTER-Neuroimaging
POINTER-Neuroimaging is the first large-scale investigation of how lifestyle interventions affect biological markers of Alzheimer’s and dementia in the brain. Trial participants from all five main study sites were invited to receive MRI and Aβ and tau positron emission tomography (PET) imaging to assess the effects of the U.S. POINTER intervention on brain health, including (1) brain imaging biomarkers of Alzheimer’s and cerebrovascular disease and (2) cognitive benefits that were influenced by these biomarkers.

POINTER-Neuroimaging enrolled roughly 50% of the parent trial participants. The researchers found that people in the study with certain Alzheimer's-related brain changes — lower hippocampal volume or higher tau protein build up — had greater cognitive benefits from the structured lifestyle intervention than those with these brain changes in the self-guided group. However, the presence, absence or level of amyloid in the brain did not impact the amount of cognitive benefit.

“Participating in the U.S. POINTER study’s structured intervention protected against the negative effects of tau tangle build up or smaller baseline hippocampal volume,” said Dr. Susan Landau, Principal Investigator of the ancillary study. “In other words, people with certain at-risk brain characteristics saw greater cognitive benefits following the intervention, but amyloid build up — the primary biomarker that defines Alzheimer’s disease — was not one of those at-risk characteristics. This means that people with amyloid build up experience the same benefits from the intervention as those without amyloid.”

The U.S. POINTER ancillary studies are supported by the following NIH grants:
 

• POINTER-zzz: R01AG064440

• POINTER-NV: R01AG066910

• POINTER-Neuroimaging: R01AG062689

• POINTER-Microbiome: U19AG063744

About the Alzheimer's Association

Research suggests a new strategy to improve blood flow to the brain to battle Alzheimer's

Of course, your competent? doctor decreased your initial brain damage by employing all these interventions! NO? So, you DON'T have a functioning stroke doctor, do you? Almost a decade of incompetence!

cerebral blood flow (36 posts to July 2016)

oxygen delivery (31 posts to January 2020)

 Research suggests a new strategy to improve blood flow to the brain to battle Alzheimer's

New University of Virginia School of Medicine research suggests an unexpected way doctors may be able to improve blood flow to the brain to battle Alzheimer's and other neurodegenerative diseases.

Scientists led by Ukpong B. Eyo, PhD, of UVA's Department of Neuroscience, found that immune cells called microglia play an essential role in determining how well tiny capillaries deliver blood and essential nourishment to our brains. The scientists believe problems with these microglia could be contributing to failing brain health, and targeting them could help us prevent or reverse memory-stealing diseases caused or worsened by lack of adequate blood flow. This could include Alzheimer's, vascular dementia and even some cases of Parkinson's.

For some time now, microglia have been suggested to play important roles in regulating vessel function. With this study, we have provided the most definitive evidence that they do regulate blood flow to the brain, specified the location of this function to the brain's small vessels or capillaries and identified an enzyme that they use to do this. Although microglia are dysfunctional in neurodegenerative diseases, our work now raises the possibility of improving blood flow deficits by targeting microglia."

Ukpong B. Eyo, PhD, UVA's Center for Brain Immunology and Glia (BIG Center) and the UVA Brain Institute

The brain's big demands

Our brains require a tremendous amount of sustenance. Even though they make up only 2% of our body weight, they use 20% of our total energy. To provide this, the brain is surrounded by a 400-mile-long network of blood vessels that branch most extensively into tiny capillaries. Proper function of these vessels and capillaries is essential to good brain health.

Scientists have known that problems with myeloid cells can contribute to excess carbon dioxide in the blood, robbing our brains of life-giving oxygen. But Eyo and his team wanted to understand more specifically which cells were responsible and to see what would happen if those cells weren't working properly.

The researchers determined that microglia are responsible for ensuring proper capillary "tone," which determines how well the tiny vessels can feed blood to the brain. Eliminating microglia significantly reduced the capillaries' diameter and reduced their ability to transport blood, the scientists found. Restoring the microglia fixed this problem.

"The microglial enzyme identified in this study has been targeted heretofore in patients with Alzheimer's disease, albeit with mixed results. Our study suggests that these therapeutics would have maximal benefit if prescribed according to the therapeutic window of microglia in Alzheimer's – a focus in our ongoing research," said UVA researcher William A. Mills III, PhD, the first author of a new scientific paper outlining the findings. "We have determined that all microglia are capable of regulating basal capillary tone as opposed to a subset of them, thus revealing their importance to meeting energy demands in the brain."

eBook: Advancing neurodegenerative research with iPSC-derived microglia models eBook Discover how iPSC-derived microglia are advancing neuroinflammation research and neurodegenerative disease modeling.Download the latest edition

The researchers say additional research will be needed to better understand the complex cellular communication network responsible for maintaining proper capillary function. But by better understanding how the immune system maintains capillary health, scientists may be able to boost blood flow to ensure the brain is properly nourished.

"Now that we have identified a novel role for microglia in blood vessel structure and function as well as a specific enzyme involved, we are poised to examine how this enzyme and microglial functions change, and to subsequently develop therapies to reduce these changes during neurodegenerative diseases broadly and in Alzhiemer's disease especially," Eyo said. "However, questions abound that our group will pursue – e.g. do the microglia regulate the small capillaries independently or in concert with other brain cells? When during development do microglia begin to play this role, and is this role also important in neurodevelopmental disorders where vascular function is also compromised? Can microglial replacement facilitate blood flow rejuvenation in neurodegenerative diseases? These are exciting questions we hope to answer in the near future."

UVA recently established the Harrison Family Translational Research Center in Alzheimer's and Neurodegenerative Diseases specifically to pioneer new treatments for Alzheimer's and other brain disorders. The center is part of UVA's Paul and Diane Manning Institute for Biotechnology. The institute will be housed in a four-story, 350,000-square-foot facility under construction at UVA's Fontaine Research Park that is expected to bring hundreds and potentially thousands of jobs to Virginia as part of a new "ecosystem of innovation."

Alzheimer's findings published

Eyo and his collaborators have published their findings in the scientific journal Nature Communications. The research team consisted of Mills III, Niesha A. Savory, Aida Oryza Lopez-Ortiz, Dennis H. Lentferink, Fernando González Ibáñez, Praise Agochi, Elina Rastegar, Arnav Gupta, Deetya Gupta, Arya Suram, Brant E. Isakson, Marie-ÈveTremblay and Eyo.

The research was supported by the National Institutes of Health's National Institute of Neurological Disorders and Stroke, grants NS122782 and NS119243; the NIH's National Heart, Lung and Blood Institute, grants HL007284, HL137112 and HL171997; the Owens Family Foundation; a UVA Brain Institute Postdoctoral Fellowship; and an American Heart Association Postdoctoral Fellowship, 25POST1376070.

Source:

University of Virginia Health System

Journal reference:

Mills, W. A., et al. (2025). Microglial cyclooxygenase-1 modulates cerebral capillary basal tone in vivo in mice. Nature Communications. doi.org/10.1038/s41467-025-60753-x.

Visceral Fat May Indicate Alzheimer’s Risk Decades Before Symptoms

 Your competent? doctor needs to first prevent this visceral fat and then if it occurs, remove it! You need excellent brain blood flow for recovery, so don't let your doctor weasel out of this requirement!

In case your doctor is incompetent in this matter, use this to train them:

Visceral Fat: What It is & How to Get Rid of It

With your chances of getting dementia post stroke, you need prevention solutions. YOUR DOCTOR IS RESPONSIBLE FOR PREVENTING THIS!

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:

Visceral Fat May Indicate Alzheimer’s Risk Decades Before Symptoms

Summary: A new study links visceral fat, a deep layer of abdominal fat, to increased brain amyloid and tau proteins—key markers of Alzheimer’s disease—decades before dementia symptoms arise. Researchers found that visceral fat accounted for 77% of the relationship between high BMI and amyloid accumulation, while other fat types showed no similar impact.

The study highlights how managing visceral fat through lifestyle changes or medication could reduce Alzheimer’s risk. Midlife interventions are especially critical, as participants in their 40s and 50s exhibited these pathologies early on. The findings further reveal that metabolic factors like insulin resistance and cholesterol levels amplify obesity-related brain damage. This research emphasizes the urgent need for targeted prevention strategies against obesity-related Alzheimer’s risk.

Key Facts:

• Visceral fat is strongly associated with amyloid and tau protein buildup in the brain.
• Insulin resistance and low HDL cholesterol worsen obesity-related Alzheimer’s pathology.
• Managing visceral fat through weight loss or metabolic treatments may reduce dementia risk.

Source: RSNA

Researchers have linked a specific type of body fat to the abnormal proteins in the brain that are hallmarks of Alzheimer’s disease up to 20 years before the earliest symptoms of dementia  appear, according to a study being presented today at the annual meeting of the Radiological Society of North America (RSNA).

The researchers emphasized that lifestyle modifications targeted at reducing this fat could influence the development of Alzheimer’s disease.

The effects of visceral fat on amyloid pathology were partially reduced in people with higher HDL. Credit: Neuroscience News

“This crucial result was discovered because we investigated Alzheimer’s disease pathology as early as midlife—in the 40s and 50s—when the disease pathology is at its earliest stages, and potential modifications like weight loss and reducing visceral fat are more effective as a means of preventing or delaying the onset of the disease,” said lead study author Mahsa Dolatshahi, M.D., M.P.H., post-doctoral research associate at Mallinckrodt Institute of Radiology (MIR) at Washington University School of Medicine in St. Louis, Missouri.

An estimated 6.9 million Americans, aged 65 and older, are living with Alzheimer’s disease, according to the Alzheimer’s Association. The association estimates this number could grow to 13 million by 2050, barring the development of medical breakthroughs to prevent or cure the disease.

For the study, the researchers focused on the link between modifiable lifestyle-related factors, such as obesity, body fat distribution and metabolic aspects, and Alzheimer’s disease pathology.

A total of 80 cognitively normal midlife individuals (average age: 49.4 years, female: 62.5%,) were included in the study. Approximately 57.5% of participants were obese, and the average body mass index (BMI) of the participants was 32.31.

The participants underwent brain positron emission tomography (PET), body MRI and metabolic assessment (glucose and insulin measurements), as well as a lipid (cholesterol) panel.

MRI scans of the abdomen were performed to measure the volume of the subcutaneous fat (the fat under skin) and visceral fat (deep hidden fat surrounding the organs).

“We investigated the association of BMI, visceral fat, subcutaneous fat, liver fat fraction, thigh fat and muscle, as well as insulin resistance and HDL (good cholesterol), with amyloid and tau deposition in Alzheimer’s disease,” said Dr. Dolatshahi, a member of the Raji Lab at MIR’s Neuroimaging Labs Research Center.

Thigh muscle scans were used to measure volume of muscle and fat. Alzheimer’s disease pathology was measured using PET scans with tracers that bind to amyloid plaques and tau tangles that accumulate in the brains of people with Alzheimer’s disease.

The findings revealed that higher levels of visceral fat were related to increased amyloid, accounting for 77% of the effect of high BMI on amyloid accumulation. Other types of fat did not explain obesity-related increased Alzheimer’s pathology.

“Our study showed that higher visceral fat was associated with higher PET levels of the two hallmark pathologic proteins of Alzheimer’s disease—amyloid and tau,” Dr. Dolatshahi said.

“To our knowledge, our study is the only one to demonstrate these findings at midlife where our participants are decades out from developing the earliest symptoms of the dementia that results from Alzheimer’s disease.”

The study also showed that higher insulin resistance and lower HDL were associated with high amyloid in the brain. The effects of visceral fat on amyloid pathology were partially reduced in people with higher HDL.

“A key implication of our work is that managing Alzheimer’s risk in obesity will need to involve targeting the related metabolic and lipid issues that often arise with higher body fat,” said senior study author Cyrus A. Raji, M.D., Ph.D., associate professor of radiology at MIR.

Although previous studies have shown the role of high BMI in damaging the cells of the brain, no similar study has investigated the differential role of visceral and subcutaneous fat or metabolic profile, especially in terms of Alzheimer’s amyloid pathology as early as midlife, Dr. Dolatshahi pointed out.

“This study goes beyond using BMI to characterize body fat more accurately with MRI and, in so doing, reveals key insights about why obesity can increase risk for Alzheimer’s disease,” Dr. Dolatshahi said.

Drs. Raji, Dolatshahi and colleagues are also presenting a study at RSNA 2024 that shows how obesity and visceral fat reduce blood flow in the brain.

In that study, the researchers performed brain and abdominal MRI on cognitively normal midlife individuals with a wide range of BMI and compared whole-brain and regional cerebral blood flow on brain MRI in individuals with high vs. low visceral and subcutaneous fat. 

The high visceral fat group showed lower whole-brain blood flow. No significant difference was observed in cerebral blood flow in the groups with high vs. low subcutaneous fat.

“This work will have a considerable impact on public health because nearly three out of four Americans are overweight or obese,” Dr. Raji said.

“Knowing that visceral obesity negatively affects the brain opens up the possibility that treatment with lifestyle modifications or appropriate weight-loss drugs could improve cerebral blood flow and potentially lower the burden of and reduce the risk for Alzheimer’s disease.”

Other co-authors are Paul K. Commean, B.E.E., Mahshid Naghashzadeh, M.S., Sara Hosseinzadeh Kassani, Ph.D., Jake Weeks, B.S., Caitlyn Nguyen, B.S., Abby McBee-Kemper, B.S., Nancy Hantler, B.S., LaKisha Lloyd, M.Sc., Shaney Flores, M.S., Yifei Xu, M.S., Jingxia Liu, Ph.D., Claude B. Sirlin, M.D., Bettina Mittendorfer, Ph.D., Joseph E. Ippolito, M.D., Ph.D., John C. Morris, M.D., and Tammie L.S. Benzinger, M.D., Ph.D.

This study was awarded the RSNA Trainee Research Prize.

About this Alzheimer’s disease research news

Author: Linda Brooks
Source: RSNA
Contact: Linda Brooks – RSNA
Image: The image is credited to Neuroscience News

Original Research: The findings will be presented at the 110th Scientific Assembly and Annual Meeting of the Radiological Society of North America

Brain Blood Flow Issues Linked to Mild Cognitive Impairment

 And I bet your competent? doctor DID NOTHING immediately post stroke to improve your cerebral blood flow and oxygen delivery to try and save those neurons about to die from the neuronal cascade of death in the first week.  

Maybe these, why isn't your incompetent doctor already delivering these to you?

cerebral blood flow (36 posts to July 2016)

oxygen delivery (31 posts to January 2020)

I'd suggest charging your doctor $1000 a neuron that died in the first week. 

Here are the calculations I put together:

My calculation is that my doctors let 

5.4 billion neurons die. 

21,600 miles dead myelinated fibers 

2.8 trillion dead synapses 

All in the first week!

Day 1: first 90 minutes:
171 million dead neurons 
1.260 trillion dead synapses
675 miles of dead myelinated fibers
Brain aged 5.4 years

----------------------------------------------------------------------------
Days 2-3:
So 1440 minutes a day * 2days * 950000 = 2,736,000,000  or 2.7 billion  dead neurons
  1440 minutes a day *2days * 7,000,000,000syn = 20,160,000,000,000     20.2 trillion        dead synapses
1440 * 2days * 3.75mi = 10800 mi  dead myelinated fibers
Brain aged - 2 years, a guess
------------------------------------------------------------------------------
Days 4-7:
So 1440 minutes a day * 4days * 475000 = 2,736,000,000  or 2.7 billion dead neurons
  1440 minutes a day *4days * 3,500,000,000syn = 20,160,000,000,000 20.2 trillion    dead synapses
1440 * 4days * 1.875mi = 10800 mi  dead myelinated fibers
Brain aged - 2 years, a guess 

-------------------------------------------------------------------------
This is one hell of a lot of damage to recover from. Especially since we don't know how to move functions from dead locations to new ones.  Or know how to usefully get neurogenesis to work.

-----------------------------------------------------------------------------
Totals:
5.571 billion dead neurons
4.041260 trillion dead synapses
 22,275 miles dead myelinated fibers
Brain aged -  9.4 years

---------------------------------------------------------------------------------

The brain contains 80 billion neurons, I only lost 6.96375% of my brain.  
My charge would be $5.57100000E+15, whatever that is in real terms, beyond my calculators capacity. 

Damn hard to recover from all that with no stroke protocols.    

Brain Blood Flow Issues Linked to Mild Cognitive Impairment

Summary: Older adults with mild cognitive impairment (MCI) face higher cerebrovascular impedance, or resistance in brain blood flow, according to a new study. Researchers found this increased resistance leads to hypoperfusion, or reduced blood flow in the brain, which may contribute to cognitive difficulties in aging adults.

By using ultrasound and blood pressure tools, scientists analyzed brain blood flow in 58 older adults with MCI and 25 without, discovering a significant difference in cerebrovascular health between the two groups.

This finding suggests vascular function plays a vital role in maintaining cognitive health. The study opens new avenues for exploring interventions to improve blood flow and support cognitive function in older adults at risk of Alzheimer’s.

Key Facts

• Increased cerebrovascular impedance in MCI patients lowers brain blood flow.
• Hypoperfusion from blood flow resistance may worsen cognitive symptoms.
• The study suggests vascular health is crucial for cognitive function in aging.

Source: American Physiological Society

Older adults with mild cognitive impairment showed greater resistance to brain blood flow compared to those without cognitive impediments.

The first-of-its-kind study is published in the Journal of Applied Physiology and has been chosen as an APSselect article for October.  

The research team found the volunteers with mild cognitive impairment had higher cerebrovascular impedance and, in turn, decreased blood flow (hypoperfusion) through the brain. Credit: Neuroscience News

Brain blood flow resistance (also called cerebrovascular impedance) is linked to cognitive problems, which can manifest in several ways, including:

• Difficulty remembering recent events.
• Difficulty finding the right word or remembering a name.
• Difficulty focusing on a task.
• Disorientation in time and space. 

The purpose of the study was to determine if mild cognitive impairment affects the brain’s blood vessels’ ability to transport blood.

Using blood pressure instruments and ultrasonogram imaging to measure impedance in the brain’s blood vessels, the research team studied 58 older adults with mild cognitive impairment who have a higher risk for developing Alzheimer’s disease.

The researchers compared these participants to 25 age-matched volunteers with normal cognition.

The research team found the volunteers with mild cognitive impairment had higher cerebrovascular impedance and, in turn, decreased blood flow (hypoperfusion) through the brain.

Hypoperfusion can lead to cognitive problems in older adults.

“These findings shed light on the pathophysiological mechanisms of brain hypoperfusion in older adults who have a high risk of [Alzheimer’s disease],” the researchers wrote.

“This study highlights the importance of brain vascular function in brain health in older adults,” said Rong Zhang, PhD, a professor of neurology and senior author of the study.

About this cognition and aging research news

Author: Erica Roth
Source: American Physiological Society
Contact: Erica Roth – American Physiological Society
Image: The image is credited to Neuroscience News

Original Research: Open access.
“Patients with amnestic mild cognitive impairment have higher cerebrovascular impedance than cognitively normal older adults” by Rong Zhang et al. Journal of Applied Physiology

New laser device offers hope for non-invasive stroke risk monitoring

 You just might want your competent? doctor to be up-to-date on this technology.

New laser device offers hope for non-invasive stroke risk monitoring

Researchers have developed a laser-based device that can be placed on the head to non-invasively monitor changes in brain blood flow and volume. The new device could one day help save lives by offering a direct and simple way to assess stroke risk based on physiological markers rather than indirect markers like lifestyle factors.

Strokes occur when blood flow to the brain is blocked or reduced, causing debilitating brain cell damage. With about 15 million people worldwide affected by strokes each year, it is the second leading cause of death and a leading cause of long-term disability.

"The lack of a cost-effective and scalable stroke risk assessment system complicates long-term stroke prevention because a physician can't tell whether a patient's risk is stable or worsening," said research team member Simon Mahler, a postdoctoral scholar in Changhuei Yang's laboratory at the California Institute of Technology. "This new method could help catch early signs of increased stroke risk, which is key to lowering the chances of having a stroke and reducing stroke severity."

In the Optica Publishing Group journal Biomedical Optics Express, the researchers describe their approach, which uses speckle contrast optical spectroscopy (SCOS) to track changes in blood flow and volume during a breath-holding exercise. They report that the portable system was able to differentiate between low and high stroke risk in a group of 50 volunteers. The work is part of a larger collaboration led by Yang and Charles Liu from the University of Southern California.

This approach could one day be incorporated into the regular testing performed during annual physical examinations, providing physicians with crucial information about the patient's health. It could be particularly beneficial for communities with limited access to advanced medical facilities and has the potential to lead to personalized strategies for reducing stroke risk."

Charles Liu, University of Southern California

Spectroscopy on the go

For the past 40 years, researchers have been experimenting with various methods to measure blood flow in the brain and changes associated with stroke risk. Measuring blood flow when the brain is stressed, such as during breath holding, can be used to assess the risk of stroke.

Although imaging techniques like PET, SPECT and CT can reveal changes in blood flow, they are expensive and aren't easy to use in clinics or for widespread community screening. To solve this challenge, the researchers turned to SCOS as a more practical way to access changes in blood flow and volume in the brain. They built a simple, portable spectroscopy system that consists of a laser diode and a CMOS-based camera that can be placed on the head with no external optical elements.

SCOS works by shining an infrared laser or light onto the brain and analyzing the patterns of scattered light. The infrared light can penetrate the skull and brain, producing a back-scattered speckle pattern that varies with changes in blood flow and tissue oxygenation. Using a coherent laser makes it possible to determine brain blood flow rate by calculating how fast the captured laser speckle field fluctuates, which speeds up with faster blood flow.

Simplified blood flow assessment

"As people age their blood vessels get stiffer, making them more prone to stroke," said Yang. "By asking a person to hold their breath, we can use SCOS to measure how much the blood vessels expand and how much faster blood is flowing within the vessels in response. These reactive measurements are indicative of vessel stiffness, and such measurement capabilities are unique to transcranial optical methods."

The researchers tested the SCOS method with 50 people who were divided into low- and high-risk stroke groups based on a stroke risk assessment performed with the Cleveland Stroke Risk Calculator. The researchers found that blood flow and blood volume changes were significantly different between the two groups and, therefore, have the potential to serve as physiological markers for stroke risk.

"While the current study is very promising, we are planning additional studies to further understand the clinical implications of the laser SCOS recordings in larger patient groups over longer time periods," said Liu. They are also working to incorporate machine learning to improve data analysis and further validate the method's effectiveness.

Source:

Optica

Journal reference:

Huang, Y. X., et al. (2024). Correlating Stroke Risk with Non-Invasive Cerebrovascular Perfusion Dynamics using a Portable Speckle Contrast Optical Spectroscopy Laser Device. Biomedical Optics Express. doi.org/10.1364/boe.534796.

Brain Vasculature Changes Important for Predicting Cognitive Impairment

Once your doctor has predicted this problem, WHAT EXACT PROTOCOLS ARE GIVEN YOU TO PREVENT IT FROM HAPPENING? Don't have any do you? 

Your competent? doctor started working on neurovascular coupling 8 years ago, RIGHT?

Neurovascular coupling in humans: Physiology, methodological advances and clinical implications April 2016

The latest here:

Brain Vasculature Changes Important for Predicting Cognitive Impairment

Several measurements of the brain, including blood flow and the brain’s ability to compensate for the lack of it, are better predictors of mild cognitive impairment (MCI) than risk factors like hypertension and high cholesterol.

The findings, published in the journal Alzheimer’s & Dementia, further the prospects of preventing or treating memory problems early before they progress to dementia. 

“People with mild cognitive impairment are at highest risk for the next step, which is dementia,” said Calin Prodan, MD, Oklahoma University College of Medicine, Oklahoma City, Oklahoma. “We’re trying to decipher the ‘fingerprints’ of mild cognitive impairment. What happens to the brain when a person moves from healthy ageing to mild cognitive impairment, and is there something we can do to intervene and prevent the decline to dementia?”

The researchers team took several types of brain measurements in people at 3 stages of life: young adults, older adults with ageing but healthy brains, and older adults with MCI. Each group played a short memory challenge game during functional near-infrared spectroscopy recording, and changes in plasma levels of extracellular vesicles (EVs) were assessed using small-particle flow cytometry. The game consisted of trying to memorise increasingly larger sequences of letters.

In the brains of young adults, blood flow increased, giving their brains the energy they needed to meet the demands of the game, a process called neurovascular coupling. In people with healthy ageing brains, the blood flow did not increase as much, but to compensate, their brains engaged other regions of the brain to help with the challenge, a process known as functional connectivity. In the brains of older adults with MCI, the blood flow was greatly reduced, and they lost the ability to compensate by recruiting other parts of the brain to help.

“People with mild cognitive impairment have lost that compensation mechanism,” said lead author Cameron Owens, PhD, Oklahoma University College of Medicine. “There is a drastic change in brain activity in those with mild cognitive impairment.”

Another type of assessment using a blood test gave researchers an additional window into the brains of people with cognitive impairment. This blood analysis measured the amount of cerebrovascular endothelial extracellular vesicles (CEEVs), which are tiny particles released from the cells lining the brain’s blood vessels. Existing research shows that when the inner lining of blood vessels is damaged, it secretes CEEVs. People with MCI  had more CEEVs in their brains than those with healthy ageing brains. Furthermore, MRI images confirmed that people with higher levels of CEEVs also had more ischaemic damage. The researchers believe this is the first time that CEEVs have been measured in a cognitive condition.

“Every brain is different, and there may be differing reasons for cognitive impairment, but having these predictors -- measuring neurovascular coupling, functional connectivity, and CEEVs -- potentially opens opportunities to develop individualised interventions, whether it’s a pharmacological therapy or non-invasive brain stimulation, or something as simple as cognitive behavioural therapy,” said coauthor Andriy Yabluchanskiy, PhD, Oklahoma University College of Medicine.

Reference: https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.14072

SOURCE: University of Oklahoma

Viagra Shows Promise in Boosting Brain Blood Flow for Dementia Prevention

 My doctor a year ago said it wasn't proven enough to do this. Is it now totally proven? Was this tested in women also?

Isn't your competent? doctor already doing these? If not, you don't have a functioning stroke doctor! Why are you seeing them?

• brain blood flow (6 posts to April 2019)

 

But this for the negative view: Does Viagra really help prevent Alzheimer’s? Not so fast

The latest here:

Viagra Shows Promise in Boosting Brain Blood Flow for Dementia Prevention

Summary: A new study reveals that sildenafil (Viagra) enhances brain blood flow and improves blood vessel function in patients at risk of vascular dementia. This study marks a significant advancement in addressing this condition.

The team found that sildenafil increased blood flow in the brain’s small and large vessels, potentially preventing dementia. These findings highlight the drug’s promise for larger-scale trials to confirm its effectiveness.

Key Facts:

1. Sildenafil improved blood flow and cerebrovascular function in at-risk patients.
2. The trial involved 75 participants with minor stroke and small vessel disease signs.
3. Sildenafil had fewer side effects compared to cilostazol, another similar drug tested.

Source: Oxford University

A new trial conducted by the University of Oxford reveals that sildenafil, commonly known as Viagra, enhances blood flow to the brain and improves the function of brain blood vessels in patients at a heightened risk of vascular dementia.

This study, published in Circulation Research, marks a potentially pivotal step in the fight against this debilitating condition.

Dr. Alastair Webb, as Associate Professor at the Wolfson Center for Prevention of Stroke and Dementia at Oxford University said, “This is the first trial to show that sildenafil gets into the blood vessels in the brain in people with this condition, improving blood flow and how responsive these blood vessels are.

Sildenafil enhanced the blood flow response to carbon dioxide, indicating improved cerebrovascular function. Credit: Neuroscience News

“These two key factors are associated with chronic damage to the small blood vessels in the brain, which is the commonest cause of vascular dementia. This demonstrates the potential of this well-tolerated, widely-available drug to prevent dementia, which needs testing in larger trials.”

The significance of this research lies in its potential to transform the treatment and prevention of vascular dementia, which currently lacks specific therapies.

Chronic damage to the small blood vessels in the brain is not only the leading cause of vascular dementia but also contributes to 30% of strokes and 80% of brain bleeds. High blood pressure, reduced blood flow to the brain, and impaired blood vessel function exacerbate these conditions, making the findings of this trial particularly crucial.

The OxHARP trial was a meticulously designed double-blind, placebo-controlled study involving 75 participants who had experienced a minor stroke and showed signs of mild to moderate small vessel disease.

Each participant received sildenafil, a placebo, and cilostazol (a similar drug) over three-week periods in a randomized order. The study employed cardiovascular physiology tests, ultrasound, and functional MRI scans to evaluate the drugs’ effects.

Key findings include:

• Sildenafil increased blood flow in both large and small brain vessels as measured by ultrasound and MRI scans.
• Sildenafil enhanced the blood flow response to carbon dioxide, indicating improved cerebrovascular function.
• Both sildenafil and cilostazol lowered blood vessel resistance in the brain.
• Sildenafil caused fewer side effects compared to cilostazol, particularly with less incidence of diarrhea.

Looking ahead, the next steps involve larger-scale trials to confirm these findings and explore sildenafil’s potential in preventing vascular dementia on a broader scale.

Professor Peter Rothwell, Founding Director of the Wolfson Center for Prevention of Stroke and Dementia said, “Professor Webb’s findings are very encouraging and highlight the potential for preventing vascular dementia using existing drugs that target the underlying reduction in flow in the small blood vessels in the brain.”

About this dementia and neuropharmacology research news

Author: Alastair Webb
Source: Oxford University
Contact: Alastair Webb – Oxford University
Image: The image is credited to Neuroscience News

Original Research: Open access.
“Cerebrovascular Effects of Sildenafil in Small Vessel Disease: The OxHARP Trial” by Alastair Webb et al. Circulation Research

Impact of orally administered cannabidiol (CBD) on fitness and health among healthy adult individuals

If you have a functioning stroke doctor and hospital research on this will be initiated by them to test this on stroke survivors.  But I doubt that will occur.

Impact of orally administered cannabidiol (CBD) on fitness and health among healthy adult individuals

By Pooja Toshniwal PahariaJun 9 2023Reviewed by Lily Ramsey, LLM

In a recent study published in the Nutrients Journal, researchers evaluated the effects of oral cannabidiol (CBD) administration on the health and fitness of healthy adults.

Study: Effects of Oral Cannabidiol on Health and Fitness in Healthy Adults: An 8-Week Randomized Trial. Image Credit: KimberlyBoyles/Shutterstock.com

Background

CBD, a non-intoxicating phytocannabinoid extracted from Cannabis sativa L., has shown significant therapeutic benefits in managing neuroinflammatory disorders, including anxiety, depression, Alzheimer's disease, and Parkinson's disease.

Regular CBD usage has been encouraged to improve fitness. Studies have reported that CBD may alter body composition by impacting glucose metabolism and can increase maximal oxygen consumption (VO₂ max) with no impact on other parameters of cardiovascular health.

CBD use has also improved learning and memory and increased blood flow in the cerebrum of individuals with cognitive decay.(This sounds very useful to us.) CBD can also reduce interleukin-6 (IL-6) levels among adults with cocaine usage disorders and lower pro-inflammatory gene expression and C-reactive protein (CRP) levels among individuals infected with the human immunodeficiency virus (HIV).

However, contradictory findings have been reported, warranting further research, including randomized controlled trials (RCTs).

About the study

In the present double-blinded, placebo-controlled RCT, researchers investigated the impact of oral CBD use over eight weeks on the health of adult individuals, particularly on health-associated fitness, cognitive health, body composition, physical exercise patterns, psychological well-being, and C-reactive protein (CRP) levels.

The trial included 48 individuals aged 18 to 50 years, who were randomly allocated to receive oral capsules of 50.0 milligrams of CBD (n=23) or 225.0 milligrams of medium-chain triglyceride (MCT) as a placebo (n=25) daily over eight weeks post-dinner and before sleeping.

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The individuals completed four visits before and after the intervention, and assessments, including eight-hour fasted blood draws, fitness, body composition, physical exercise, and self-documented surveys, were performed.

All individuals were provided wearable activity trackers (Fitbits) to assess physical activity. The peak value for uptake of oxygen (VO₂ peak) in relative terms was calculated on the second visit to evaluate aerobic fitness; a 30.0-second Wingate test was performed to assess power output and evaluate anaerobic fitness on the third visit; and bench press and back squat one-repetition maximums (1RMs) were performed during the fourth visit to assess muscle strength.

Adverse events (AEs) were documented. Primary study outcomes included relative VO₂ peak, body fat percentage (BF%), body mass (BM) and lean BM (LBM), peak power (PP) and relative PP (RPP), anaerobic fatigue (AF), mean power (MP), relative MP (RMP), bench press and back squat 1RM, a one-week mean daily step count, self-documented psychological well-being and cognitive function scores, and serological CRP concentrations.

Individuals who abstained from cannabis [CBD and/or tetrahydrocannabinol (THC)] use for six weeks before study initiation and had no history of chronic alcohol consumption or drug usage were included.

Individuals diagnosed with metabolic, neurological, cardiovascular, or mood disorders; pregnant or lactating mothers; and individuals who could not adhere to the intervention for eight weeks were excluded from the analysis.

Cognitive function was evaluated using the National Institute of Health (NIH) Patient-Reported Outcomes Measurement Information System (PROMIS) Cognitive Function-Abilities-Short Form 8a.

Serological CRP levels were determined using enzyme-linked immunosorbent assays (ELISA). Muscular strength was assessed using the National Strength and Conditioning Association (NSCA) guidelines.

Results

The mean values for participant age, height, and BM were 25 years, 171 cm, and 73 kg, respectively. No significant differences were observed between groups regarding body composition, aerobic fitness, muscular strength, physical activity, cognitive health, psychological well-being, or serological resting CRP concentrations.

However, the placebo group experienced a 9.6% reduction in PP and a 6.6% reduction in RPP compared to the intervention group participants.

In contrast, CBD recipients experienced no changes in PP or RPP. No severe adverse events were reported. Combining both groups showed LBM ranging between 37 and 84 kg, BF% ranging between 8.2% and 40%, relative VO₂ peak ranging between 28 and 62 mL/kg/min, bench press 1RM ranging between 25 and 161 kg, and back squat 1RM ranging between 39 and 166 kg.

Further, PP ranged between 372 and 1148 W, RPP ranged between 6.0 and 13 W/kg, MP ranged between 288 and 804 W, RMP ranged between 4.2 and 8.3 W/kg, and AF ranged between 43 and 71%. The one-week mean daily step count was 11,415 steps. Cognitive function T-scores ranged between 30 and 64, and cognitive function ability T-scores ranged between 37 and 67.

Concerning psychological well-being, autonomy scores ranged between 8.0 and 21.0; environmental mastery scores ranged between 7.0 and 21.0; personal growth scores ranged between 15.0 and 21.0; scores for positive relations with others ranged between 10.0 and 21.0; purpose in life scores ranged between 11.0 and 21.0; and self-acceptance scores ranged between 8.0 and 21.0. The mean CRP level in serum was 1.40 mg per liter, ranging between 0.10 and 8.8 mg per liter.

Conclusions

Overall, the study findings showed that the regular intake of 50.0 mg of CBD for eight weeks may prevent reductions in anaerobic power with time, likely due to an increase in the levels of antioxidants such as glutathione peroxidase and superoxide dismutase and a decrease in free radicals such as reactive oxygen species (ROS).

However, long-term CBD use did not improve aerobic fitness, body composition, mental health, physical activity, inflammation, or psychological well-being among adults.

Journal reference:

• Flores, V. et al. (2023) "Effects of Oral Cannabidiol on Health and Fitness in Healthy Adults: An 8-Week Randomized Trial", Nutrients, 15(12), p. 2664. doi: 10.3390/nu15122664. https://www.mdpi.com/2072-6643/15/12/2664

Researchers reveal surprising findings on how salt affects blood flow in the brain

 Your doctor needs to understand this so your diet doesn't inadvertently reduce your brain blood flow. YOUR DOCTOR'S RESPONSIBILITY IS TO GET EXACT DIET PROTOCOLS CREATED. No protocols s/he needs to be fired. I take no prisoners in trying to get stroke solved by those who are responsible for solving it. In fact I would have the board of directors fired for incompetency also.

Researchers reveal surprising findings on how salt affects blood flow in the brain

A first-of-its-kind study led by researchers at Georgia State reveals surprising new information about the relationship between neuron activity and blood flow deep in the brain, as well as how the brain is affected by salt consumption.

When neurons are activated, this typically produces a rapid increase of blood flow to the area. This relationship is known as neurovascular coupling, or functional hyperemia, and it occurs via dilation of blood vessels in the brain called arterioles. Functional magnetic resource imaging (fMRI) is based on the concept of neurovascular coupling: Experts look for areas of weak blood flow to diagnose brain disorders.

However, previous studies of neurovascular coupling have been limited to superficial areas of the brain (such as the cerebral cortex) and scientists have mostly examined how blood flow changes in response to sensory stimuli coming from the environment (such as visual or auditory stimuli). Little is known about whether the same principles apply to deeper brain regions attuned to stimuli produced by the body itself, known as interoceptive signals.

To study this relationship in deep brain regions, an interdisciplinary team of scientists led by Dr. Javier Stern, professor of neuroscience at Georgia State and director of the university's Center for Neuroinflammation and Cardiometabolic Diseases, developed a novel approach that combines surgical techniques and state-of-the-art neuroimaging. The team focused on the hypothalamus, a deep brain region involved in critical body functions including drinking, eating, body temperature regulation and reproduction. The study, published in the journal Cell Reports, examined how blood flow to the hypothalamus changed in response to salt intake.

"We chose salt because the body needs to control sodium levels very precisely. We even have specific cells that detect how much salt is in your blood," said Stern. "When you ingest salty food, the brain senses it and activates a series of compensatory mechanisms to bring sodium levels back down."

The body does this in part by activating neurons that trigger the release of vasopressin, an antidiuretic hormone that plays a key role in maintaining the proper concentration of salt. In contrast to previous studies that have observed a positive link between neuron activity and increased blood flow, the researchers found a decrease in blood flow as the neurons became activated in the hypothalamus.

"The findings took us by surprise because we saw vasoconstriction, which is the opposite of what most people described in the cortex in response to a sensory stimulus," said Stern. "Reduced blood flow is normally observed in the cortex in the case of diseases like Alzheimer's or after a stroke or ischemia."

The team dubbed the phenomenon "inverse neurovascular coupling," or a decrease in blood flow that produces hypoxia. They also observed other differences: In the cortex, vascular responses to stimuli are very localized and the dilation occurs rapidly. In the hypothalamus, the response was diffuse and took place slowly, over a long period of time.

"When we eat a lot of salt, our sodium levels stay elevated for a long time," said Stern. "We believe the hypoxia is a mechanism that strengthens the neurons' ability to respond to the sustained salt stimulation, allowing them to remain active for a prolonged period."

The findings raise interesting questions about how hypertension may affect the brain. Between 50 and 60% of hypertension is believed to be salt-dependent—triggered by excess salt consumption. The research team plans to study this inverse neurovascular coupling mechanism in animal models to determine whether it contributes to the pathology of salt-dependent hypertension. In addition, they hope to use their approach to study other brain regions and diseases, including depression, obesity and neurodegenerative conditions.

"If you chronically ingest a lot of salt, you'll have hyperactivation of vasopressin neurons. This mechanism can then induce excessive hypoxia, which could lead to tissue damage in the brain," said Stern. "If we can better understand this process, we can devise novel targets to stop this hypoxia-dependent activation and perhaps improve the outcomes of people with salt-dependent high blood pressure."

The study authors include Ranjan Roy and Ferdinand Althammer, postdoctoral researchers in the Center for Neuroinflammation and Cardiometabolic Diseases, Jordan Hamm, assistant professor of neuroscience at Georgia State, and colleagues at the University of Otago in New Zealand, Augusta University and Auburn University. The research was supported by the National Institute of Neurological Disorders and Stroke.

To read more, click here

 

 

Dose Escalation and Safety of Capsaicin for Cerebral Perfusion Augmentation

 I think this means you're getting higher blood velocity in your brain. Sounds like a winner to get more oxygen to your brain and maybe save a few neurons from dying. But since this was tested in healthy volunteers your doctor and hospital have the responsibility to initiate research in this on stroke subjects with the objective being to see how many neurons can be saved. 

No initiation of research you need to fire the board of directors, they are not setting correct goals for the hospital and staff.  But since this is not yet proven useful for stroke survivors don't start bringing in ghost peppers(Scoville of 855,000 to 1,041,427). I don't know how to translate Scoville units to μMol(A micromole is a unit of measure defined as 10^-6 (one-millionth) of a mole. The symbol for micromole is commonly umol or μmol.)

Dose Escalation and Safety of Capsaicin for Cerebral Perfusion Augmentation

 

Juan Manuel Marquez-Romero

,

María Raquel Huerta-Franco

,

Miguel Vargas-Luna

,

César Abraham Madrigal-Gutiérrez

,

José Martín Esparza-Hernández

,

María Guadalupe Velázquez-Barcena

Originally published10 May 2021https://doi.org/10.1161/STROKEAHA.120.032773Stroke. 2021;52:2203–2209

Abstract

• Download figure
• Download PowerPoint

Background and Purpose:

Sphenopalatine ganglion (SPG) electrical stimulation has been studied in the setting of acute ischemic stroke to enhance collateral flow. Capsaicin poses an alternative to chemically stimulate the sphenopalatine ganglion. Therefore, the objective of this study was to determine the safety and effect of increasing doses of capsaicin upon serial transcranial Doppler markers of cerebral blood flow.

Methods:

We performed serial transcranial Doppler testing in 30 healthy volunteers divided into 5 equal groups. Capsaicin doses ranged from 33 to 165 μMol. We recorded peak systolic and end-diastolic velocities in the middle cerebral artery, arterial pressure, and perceived pungency in 5-minute intervals up to 20 minutes. We then calculated the mean velocity, the pulsatility index, and the cerebral blood flow index.

Results:

The participants’ median age was 21 years (range, 5 years); all reported consumption of capsaicin in their diets. After and during the study, none reported side effects. Perceived pungency peaked at 5 minutes, and by the 20-minute mark, none perceived any pungency. All the tested doses produced the same pattern, consisting of augmentation of the middle cerebral artery mean velocity with the pulsatility index’s diminution. The effects peaked between the 5- and the 10-minute measurements and then returned to basal levels except for the 66-μMol doses, which produced a sustained effect. We found no correlation between perceived pungency and dose, but the middle cerebral artery mean velocity was strongly correlated with the dose administered.

Conclusions:

This study provides evidence supporting the safety and tolerability of oral capsaicin in a population of healthy volunteers. Capsaicin appears to produce effects similar to those of sphenopalatine ganglion electrical stimulation.

Registration:

URL: https://www.clinicaltrials.gov; Unique identifier: NCT04545892.