Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Showing posts with label brain blood vessels. Show all posts
Showing posts with label brain blood vessels. Show all posts

Wednesday, July 31, 2024

Brain Blood Vessels Key to Combating Cognitive Decline

 Is your competent? doctor checking this out and addressing any needs you might have? NO? So you don't have a functioning stroke doctor, do you?

Brain Blood Vessels Key to Combating Cognitive Decline

Summary: New research highlights the critical role of healthy blood vessels in maintaining brain health and addressing age-related cognitive decline. The study reveals that vascular degradation in the brain can lead to neurodegenerative disorders like Alzheimer’s disease.

Advanced imaging of mice brains showed significant vascular changes with aging, particularly in areas vital for memory and cognitive function. These findings suggest that preserving vascular health could be crucial for preventing cognitive decline.

Key Facts:

  1. Healthy brain blood vessels are essential for preventing cognitive decline.
  2. Vascular degradation can lead to neurodegenerative disorders like Alzheimer’s.
  3. Study used advanced imaging to map brain vascular changes in aging mice.

Source: Penn State

Healthy blood vessels matter for more than just heart health. Vascular well-being is critical for brain health and potentially in addressing age-related cognitive decline and neurodegenerative disorders, like Alzheimer’s disease, according to new study led by Penn State researchers.

The findings point to an understudied but possible key role the brain’s vascular network — or energy infrastructure — plays in the onset of neurodegenerative disease.

They published their work today (July 30) in Nature Communications.

Using advanced imaging techniques, the team developed maps of a mouse brain that illustrate how vascular cells and structures like blood vessels change with age and identified areas that are vulnerable to deterioration.

When blood vessels degrade, nerve cells in the brain, called neurons, are starved of energy, causing them to malfunction or die. It can lead to a condition called vascular dementia, the second leading cause of cognitive impairment in older adults, and symptoms like sleep disturbance.

“With something like Alzheimer’s disease, by the time you can see vascular changes and significant brain shrinkage on a MRI, cell death has already occurred. We need to understand how these cells and structures change before a major catastrophe happens,” said Yongsoo Kim, associate professor of neural and behavioral sciences at Penn State College of Medicine and senior author of the study.

“This study provides early signs of neurodegenerative disorders, potentially leading to earlier diagnosis, and clues for how we can slow down the aging process and cognitive changes.”

According to Kim, aging is one of the primary factors involved in neurodegenerative disorders.

“Yet, we really don’t have a good baseline understanding of how normal aging itself changes the brain, particularly the brain’s vasculature,” Kim said. And with the aging population in the United States growing, he said it’s critical to understand these changes, especially within the network of blood vessels.

Blood vessels, especially micro-vessels, regulate oxygen and energy supply and waste removal to and from neurons. Despite their importance, Kim said, most existing research focuses on how neuron structure and function degenerates over time, rather than the vasculature.

When researchers do study the brain’s vasculature, they’ve primarily examined larger blood vessels or focused on a single, easy-to-access region of the brain, the somatosensory cortex.

More importantly, typical neuroimaging techniques, like MRI, don’t provide high enough resolution to see what’s happening in the tiny blood vessels, which make up 80% to 85% of the brain’s vasculature, according to Kim.

Kim and the research team produced a detailed map of the vascular network of the whole mouse brain using two high-resolution 3D mapping techniques: serial two-photon tomography — a technique that creates a series of stacked 2D images — and light sheet fluorescence microscopy, which images intact 3D samples to visualize the whole brain at a single cell-resolution.

They imaged the brains of young and old mice to chart vasculature changes across the brain with normal aging.

“Because we’re doing high-resolution mapping with the sufficient resolution, we can reconstruct the whole vascular structure and scan the entire brain to pinpoint areas that undergo selective degeneration with age,” Kim said.

“What we found is that the area that most people study showed the least amount of change, whereas profound change happens in areas in the deep areas of the brain. This suggests that we’ve been looking at the wrong area when it comes to aging studies.”

The images showed that changes in the vascular network don’t occur equally across the brain. Rather, they were concentrated in the basal forebrain, deep cortical layers and hippocampal network, suggesting these areas are more vulnerable to vascular degeneration. These regions play a role in attention, sleep, memory processing and storage, among other functions.

As brains age, vascular length and branching density decreases approximately 10%, indicating that there’s a sparser network to distribute blood. Arteries in older brains also appear more twisted compared to those in younger brains, which can impede blood flow, especially to areas further away from the main arteries like the deep cortical layers, Kim explained.

The team also examined functional changes of vasculature and found that the system responds more slowly in older brains. That means that it can’t provide the neurons with energy as quickly and readily as the cells may need.

There’s also a loss of pericytes, a type of cell that regulates blood supply and blood vessel permeability, too. As a result, the blood vessels become “leaky,” compromising the blood-brain barrier.

This study builds on the group’s previous research, where they mapped the vasculature of a young mouse brain. Next, they are studying how Alzheimer’s disease-induced changes in the brain influences vascular health and neuronal function. Ultimately, they said they hope their work will lead to treatments for neurodegenerative disorders.

Hannah Bennett, dual medical degree and doctoral degree student, and Steffy Manjila, postdoctoral scholar, co-led the study along with Quingguang Zhang, who was assistant research professor at Penn State at the time of the research and is currently assistant professor at Michigan State University, and Yuan-ting Wu, who was previously research scientist at Penn State and currently project scientist at Cedars-Sinai Medical Center. Other Penn State authors on the paper include: Patrick Drew, professor of engineering science and mechanics, of neurosurgery, of biology and of biomedical engineering and interim director of the Huck Institutes of the Life Sciences; Uree Chon, research technician; Donghui Shin, research technologist; Daniel Vanselow, research project manager; Hyun-Jae Pi, data scientist.

Funding: The National Institutes of Health and the American Heart Association funded this work. 

About this neuroscience research news

Author: Christine Yu
Source: Penn State
Contact: Christine Yu – Penn State
Image: The image is credited to Neuroscience News

Original Research: Open access.
“Aging drives cerebrovascular network remodeling and functional changes in the mouse brain” by Yongsoo Kim et al. Nature Communications

Tuesday, April 12, 2022

Thinning, Leaky Brain Blood Vessels Seen in COVID-19

 You don't want this or the other findings on brain damage post COVID-19.  So get vaccinated and mask up.

Earlier has these reports:

1. The researchers observed that, in slices of hamster brain, SARS-CoV-2 blocks the functioning of receptors on pericytes, causing capillaries in the tissue to constrict. “It turns out this is a big effect,” says Attwell.

2. Evidence has also accumulated that SARS-CoV-2 can affect the brain by reducing blood flow to it — impairing neurons’ function and ultimately killing them.

3. A new study offers the first clear evidence that, in some people, the coronavirus invades brain cells, hijacking them to make copies of itself. The virus also seems to suck up all of the oxygen nearby, starving neighboring cells to death.

Thinning, Leaky Brain Blood Vessels Seen in COVID-19

High-resolution MRI shows injury and inflammation, but no direct viral attack

Three MRI images showing the brain blood vessels displayed on a computer monitor.

Microvascular brain injury was seen in COVID-19 patients who died, but no evidence of a direct viral attack on the brain was detected, a pathology report showed.

Damage caused by thinning and leaky brain blood vessels consistently appeared on high-resolution MRI, but there were no signs of SARS-CoV-2 infection in tissue samples, reported Avindra Nath, MD, clinical director of the National Institute of Neurological Disorders and Stroke (NINDS), and co-authors in a New England Journal of Medicine letter.

"We found there were many foci of small blood vessel damage from which there was leakage of blood products into the brain tissue," Nath said. "The cause of this was not clear but is most likely due to damage from the immune cells or lymphocytes. We found some lymphocytes attached to the endothelial cells in the blood vessels and in the perivascular regions," he told MedPage Today.

"The inflammatory response is key to the neuropathogenesis of this syndrome, since we were unable to find virus in the brain," Nath added. "The study potentially has important implications for long-term damage to several structures in the brain, particularly the olfactory bulb and the brainstem."

Other researchers have found SARS-CoV-2 RNA and protein in the brain and nasopharynx of patients who died with COVID-19, with highest levels of viral RNA found in the olfactory mucous membrane.

In this study, Nath and colleagues looked at brain tissue samples of COVID-19 patients -- 16 cases from the New York City chief medical examiner's office and three from the University of Iowa in Iowa City -- who died between March and July 2020. Their analysis included 11.7T MRI images of 13 patients at resolutions of 25 μm for the olfactory bulb and 100 μm for the brain, plus conventional histopathological brain exams of 18 patients.

Ages ranged from 5 to 73, with a median of 50. Fourteen patients had chronic illnesses, including diabetes and hypertension, and 11 had been found dead or had died suddenly. Of 16 patients with available medical histories, one had delirium, five had mild respiratory symptoms, four had acute respiratory distress syndrome, two had pulmonary embolism, and symptoms were unknown in three.

Magnetic resonance microscopy showed punctate hyperintensities representing areas of microvascular injury and fibrinogen leakage in nine patients that correlated with histopathological exam, which showed thinning of the basal lamina of endothelial cells.

In contrast, punctate hypointensities in 10 patients corresponded to congested blood vessels with areas of fibrinogen leakage and "relatively intact vasculature," the researchers said. They also observed minimal perivascular inflammation but no vascular occlusion, consistent with other studies.

Perivascular-activated microglia, macrophage infiltrates, and hypertrophic astrocytes were seen in 13 patients. In eight patients, T cells were observed in perivascular spaces and in lumens adjacent to endothelial cells.

"We were completely surprised," Nath said. "Originally, we expected to see damage that is caused by a lack of oxygen. Instead, we saw multifocal areas of damage that is usually associated with stroke and neuroinflammatory disease."

SARS-CoV-2 was not detected in brain tissue, but it's possible the virus was cleared by the time of death or viral copy numbers were below levels of detection by the assays used, the researchers noted.

So far, the findings suggest the damage was not caused by direct brain infection, Nath observed. With limited clinical information available in this study, no conclusions can be drawn about how these findings relate to neurologic features of COVID-19.

But studies are underway to "further characterize the inflammatory infiltrates and the pattern of neuronal injury in the autopsy material," Nath said. In addition, NINDS researchers are studying a cohort of COVID-19 patients with neurologic sequelae to determine whether they also have microvascular injury and whether inflammatory infiltrates are linked to persistent neurologic symptoms.

  • Judy George covers neurology and neuroscience news for MedPage Today, writing about brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy, autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep, pain, and more. Follow

Disclosures

This study was supported by the NIH Intramural Research Program at NINDS.

The researchers had no disclosures.