Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 34,370 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.
What this blog is for:
My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
Showing posts with label brain blood flow. Show all posts
Showing posts with label brain blood flow. Show all posts
Meredith Hay, PhD (center), has been hard at work on this research for more than a decade now. Image courtesy of The University of Arizona.
Researchers with the University of Arizona College of Medicine – Tucson are hoping a small peptide born in a laboratory can be a game-changer for the treatment of patients presenting with vascular dementia.
There are currently no real treatments for vascular dementia other than making lifestyle changes. The group behind this research hopes they can change that forever.
“Patients are in desperate need of an effective treatment, and we are doing everything we can to help find that treatment,” Meredith Hay, PhD, a professor of physiology with the college and co-inventor of this peptide, said in a statement. “The greatest reward would be to see a safe and effective treatment for people who currently have very few options.”
Hay and her team have been examining the potential of this peptide , PNA5, for more than a decade at this point. When it enters the brain, it triggers chemical reactions that increase oxygenation(This would seem very important in stroke to try to save as many neurons as possible in the hyperacute stage! If your doctor doesn't even know about this; PURE INCOMPETENCE!) and decrease inflammation. PNA5 has already been shown to improve blood flow and target inflammation in a way that improves cognitive performance—now the goal is to see if this can help treat vascular dementia.
“Inflammation is part of the body's natural repair system,” Hay explained. “If you have an injury, inflammation helps the healing process. The problem occurs when inflammation does not switch off. In vascular dementia, the brain's resident immune signals can remain activated.”
Hay’s team is currently planning to kick off a new clinical trial funded by a $9 million grant from the National Institute on Aging. For this study, 60 healthy volunteers will receive injections of PNA5 at different doses to evaluate the peptide’s safety. If that trial is a success, additional research could be underway by late 2027.
After helping invent PNA5, Hay co-founded a startup, ProNeurogen, focused on the development and potential commercialization of the small peptide. In the same statement, she shared the satisfaction she has felt seeing PNA5 continue to gain more momentum in recent years.
“The most rewarding part is seeing a basic scientific observation move toward something that could eventually help patients and families—that's what gets me up every day," she said. "It's exciting, but also very humbling.”
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.
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?
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:
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!
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 eBookDiscover 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.
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.
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:
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
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?
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.
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
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.
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.
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:
Sildenafil improved blood flow and cerebrovascular function in at-risk patients.
The trial involved 75 participants with minor stroke and small vessel disease signs.
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
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.
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.
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.
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.
