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

What this blog is for:

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

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

Tuesday, January 7, 2025

New Biomarker Links Brain Waste Clearance to Vascular Dementia

 Your competent? doctor needs to measure this and provide EXACT PROTOCOLS to solve the problem!

New Biomarker Links Brain Waste Clearance to Vascular Dementia

New Biomarker Links Brain Waste Clearance to Vascular Dementia

Summary: A new study has identified a biomarker, DTI-ALPS, which connects glymphatic system dysfunction to vascular dementia. By analyzing over 3,750 participants, researchers found that lower DTI-ALPS scores correlated with worse executive function, highlighting the glymphatic system’s role in clearing brain waste.

The study also uncovered a potential pathway linking impaired waste clearance to cognitive decline, mediated by free water accumulation in white matter. These findings provide a robust tool for clinical trials and potential interventions, including lifestyle changes and medications, to enhance glymphatic function and treat vascular dementia.

3 Key Facts:

  • DTI-ALPS Role: DTI-ALPS scores measure glymphatic system health, with lower scores linked to cognitive impairment.
  • Pathway Identified: Impaired glymphatic function may lead to free water accumulation, white matter damage, and cognitive decline.
  • Diverse Validation: The biomarker was independently validated across four cohorts with diverse demographics.

Source: USC

A new study from the Keck School of Medicine of USC has tested a biomarker linked to vascular dementia across four separate groups and proposed an explanation for how cognitive impairment arises.

The findings were just published in Alzheimer’s & Dementia®: The Journal of the Alzheimer’s Association.

Vascular dementia is the second most common form of dementia following Alzheimer’s disease. It has similar symptoms, including problems with memory, decision-making and language, and represents a significant public health problem as the global population continues to age.

> This shows a brain.
The researchers found that lower DTI-ALPS scores, which indicated damage to the glymphatic system, were associated with worse executive function. Credit: Neuroscience News

The condition is usually caused by cerebral small vessel disease (cSVD), which damages the brain’s small blood vessels—but researchers don’t yet know the exact mechanism linking cSVD to dementia.

One theory involves problems with the glymphatic system, which helps clear waste from the brain.

A team of researchers from the Mark and Mary Stevens Neuroimaging and Informatics Institute (Stevens INI), part of the Keck School of Medicine, as well as researchers from the Biomarkers for Vascular Contributions to Cognitive Impairment and Dementia (MarkVCID) consortium, have found new evidence in support of that theory.

With funding from the National Institutes of Health, the group analyzed brain scans and cognitive tests from a total of 3750 people.

The researchers then used technique known Diffusion Tensor Image Analysis along the Perivascular Space – or DTI-ALPS – to determine how well the glymphatic system was functioning in each person based on their brain scans.

The researchers compared the DTI-ALPS results with the cognitive test results and found that people with lower DTI-ALPS scores also performed lower on cognitive tests.

The study confirmed that a low DTI-ALPS score is a biomarker for cSVD and suggests that glymphatic damage may be driving cognitive decline.

“The most significant finding is that we found a clear link between DTI-ALPS and cognitive function in all four cohorts, with ages ranging from middle-age through older adulthood,” said Danny J. J. Wang, PhD, the study’s senior author and a professor of neurology and radiology and director of imaging technology innovation at the Keck School of Medicine’s Stevens INI.

Wang and his team also analyzed the progression of symptoms across study participants, finding a possible pathway to explain how glymphatic problems lead to cognitive impairment.

Their results provide a target for clinical researchers seeking to develop treatments for vascular dementia, Wang said, and may also prove useful for treating symptoms of Alzheimer’s disease.

Validating the biomarker

The DTI-ALPS biomarker relies on magnetic resonance imaging (MRI) to measure water movement along perivascular spaces, fluid-filled regions around the brain’s blood vessels that are a key part of the glymphatic system.

If researchers detect changes in DTI-ALPS score, that can indicate damage and suggest that the waste clearance system is not functioning as it should.

In the present study, Wang and his team analyzed MRI scans to collect a measure of DTI-ALPS for each participant. They compared those measurements to each person’s level of executive function, a composite score of cognition that includes memory, attention, planning, emotion regulation and other abilities that tend to suffer as dementia progresses.  

The researchers found that lower DTI-ALPS scores, which indicated damage to the glymphatic system, were associated with worse executive function.

That link was verified independently in four separate participant groups—from the MarkVCID consortium; the University of California, Davis; the University of California, San Francisco; and the Framingham Heart Study—with a total of 3750 participants.

Independently validating the DTI-ALPS biomarker in each of the four cohorts provides strong evidence for the glymphatic system’s role in cSVD and vascular dementia, Wang said.

The racial and ethnic diversity of the participant groups, as well as the range of ages included (averaging between 56 and 76 years of age across cohorts) also suggests that the findings are robust and can be generalized to a broader patient population.

Treatments for vascular dementia

Once the team linked problems with glymphatic function to declines in executive function, they moved on to the next question — why?

To find out more, the researchers conducted a mediation analysis, which studies the process or mechanism connecting two or more variables. In this case, they found that another biomarker—”free water” or excess water in the brain’s white matter—helped explain the link between glymphatic problems and cognitive decline.

In this potential pathway, “first waste clearance is impaired, which causes accumulation of free water in the brain’s white matter. That leads to tissue damage and eventually to cognitive impairment,” said the paper’s first author, Xiaodan Liu, MD, PhD, a former postdoctoral researcher at the USC Stevens INI, now an assistant researcher in radiology at the University of California, San Francisco.

More research, including longitudinal work, is needed to confirm whether each step in that pathway is causal. But the team’s findings indicate that the DTI-ALPS score biomarker for vascular dementia is robust and ready to be used in clinical trials, Wang said.

Those studies could explore enhancing glymphatic function as a way to treat vascular dementia. Lifestyle changes such as exercising more and improving sleep quality are one way to do that, Wang said, and future studies may also reveal medications that can help.

The findings could also provide clues for how to treat Alzheimer’s disease, which has been linked to low DTI-ALPS scores in other studies.

About this research

In addition to Wang, the study’s other authors are Xiaodan Liu, Xingfeng Shao and Kay Jann from the Laboratory of fMRI Technology, Mark and Mary Stevens Neuroimaging and Informatics Institute, Keck School of Medicine of USC, University of Southern California; Steven Cen and John M. Ringman from the Department of Neurology, Keck School of Medicine of USC, University of Southern California; Pauline Maillard and Charles S. DeCarli from the University of California, Davis; Giuseppe Barisano from Stanford University; Arvind Caprihan from the Mind Research Network, Albuquerque, New Mexico; Hanzhang Lu from Johns Hopkins University School of Medicine; Konstantinos Arfanakis from the Illinois Institute of Technology and Rush University Medical Center, Chicago, Illinois; Brian T. Gold from the University of Kentucky; Sudha Seshadri, Claudia L. Satizabal and Mohamad Habes from the University of Texas Health Science Center at San Antonio, San Antonio, Texas; Alexa S. Beiser from Boston University; Joel H. Kramer and Lara Stables from the University of California, San Francisco; Herpreet Singh, Kristin Schwab and Steven M. Greenberg from Massachusetts General Hospital, Boston, Massachusetts; and Karl G. Helmer from Harvard Medical School, Massachusetts General Hospital and the Massachusetts Institute of Technology.

Funding: This work was supported by the National Institute of Neurological Disorders and Stroke and the National Institute on Aging, part of the National Institutes of Health [U24NS100591, UH3NS100599, UH3NS100605, UH3NS100588, UH3NS100608, UH3NS100606, UH3NS100598 and UH3NS100614]

About this neurology research news

Author: Laura LeBlanc
Source: USC
Contact: Laura LeBlanc – USC
Image: The image is credited to Neuroscience News

Original Research: Open access.
MRI free water mediates the association between diffusion tensor image analysis along the perivascular space and executive function in four independent middle to aged cohorts” by Danny J. J. Wang et al. Alzheimer’s & Dementia



Monday, December 30, 2024

Vascular dementia: A look at dementia caused by strokes

 

With your chances of getting dementia post stroke, your competent? doctor needs to be monitoring this and provide dementia prevention solutions. Over a decade to accomplish that! Was it done? NO? So, you DON'T have a functioning stroke doctor, do you? 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:

Vascular dementia: A look at dementia caused by strokes

About the Author

photo of Jennifer Fisher, MMSc, PA-C

Jennifer Fisher, MMSc, PA-C, Health Writer

Jennifer is a board-certified physician assistant. She earned her bachelor of science in kinesiology at James Madison University, then went on to obtain her master of medical science at Tufts University School of Medicine, where she … See Full Bio
View all posts by Jennifer Fisher, MMSc, PA-C

Wednesday, April 28, 2021

Glial enriched stem cell progenitors repair functional deficits due to white matter stroke and vascular dementia

Since this is in mice your doctor and hospital will need to ensure human testing. Or you could let them just be incompetent as usual and do nothing, but this impacts you and you might want a solution.

 

Wednesday, November 13, 2019

Prevent Stroke to Prevent Dementia?

You're missing the whole fucking point. WHAT NEEDS TO BE DONE TO PREVENT VASCULAR DEMENTIA POST STROKE?  This shows extreme laziness and NO STROKE LEADERSHIP.  I would have all these stroke 'experts' fired. Once again describing a problem but offering NO useful solution. 

Prevent Stroke to Prevent Dementia?

DUBAI, United Arab Emirates — To reduce the incidence of dementia, societies will need to reduce the incidence of strokes, a multinational panel of experts concluded here at the XXIV World Congress of Neurology.
Because there are modifiable risk factors for stroke, it should be possible to lessen the occurrence and impact of dementia, they say.
Disability-adjusted life years (DALYs) from stroke begin to increase in midlife for both women and men, followed approximately at ages 65 to 69 years by a rising trend in DALYs from Alzheimer's disease and other dementias for both sexes — but more so for men.
Given increasing populations, "the age-standardized rates of dementia have not changed even though… the absolute numbers of people with dementia has increased quite sharply," said William Carroll, MBBS, MD, president of the World Federation of Neurology (WFN) and consultant neurologist at the University of Western Australia in Perth.
Estimates are that the number of people living with dementias in the Americas in 2050 will increase by 248% (9 million recently to 31 million people), in Africa by 300% (3 million to 12 million), in Europe by 90% (11 million to 21 million), and in Southeast Asia by 226% (22 million to 72 million).
"The problem is about how countries and people and nations are going to manage this increased number of people suffering from dementia," he said, given that the human, financial, and societal burdens of dementia are already very large.
Because stroke is a risk factor for dementia, one logical approach to prevent dementia is to address hypertension, a major cause of stroke, as well as smoking, diabetes, and lifestyle. Climate change and air pollution have also become risk factors.
"If we reduce the rate of stroke, the argument goes, we may be able to reduce the face of dementia; if not stop it then at least reduce the severity of the dementia," Carroll predicted.
The Alzheimer's Disease International 2018 report gives a figure of 50 million people worldwide living with dementia in 2018. A new case occurs every 3 seconds. By 2050 the prevalence is expected to triple to 152 million people – two thirds of whom will live in developing countries.
During the news conference, Najeeb Qadi, MD, of King Faisal Specialist Hospital and Research Centre in Riyadh, Saudi Arabia, illustrated the link between stroke and dementia. He said the top three types of dementia are Alzheimer's disease (47%), mixed dementia (34%), and vascular dementia (9%).
The prevalence of vascular dementia doubles every 5 to 10 years after age 65, and it surpasses Alzheimer's disease after age 85 years. Qadi said dementia occurs in 20% to 30% of people within about 3 months of a stroke, with an additional 25% developing dementia over the next 3 years.

 

Saturday, October 26, 2019

Esteemed Panel of World's Leading Stroke Experts Share Breakthrough Research on Relationship Between Stroke Risk and Vascular Dementia During Press Conference Broadcast via Facebook Live from XXIV World Congress of Neurology, Dubai, UAE, Monday, Oct. 28, 3:15 p.m. GST

You're missing the whole fucking point. WHAT NEEDS TO BE DONE TO PREVENT VASCULAR DEMENTIA POST STROKE?  This shows extreme laziness and NO STROKE LEADERSHIP.  I would have all these stroke 'experts' fired. Once again describing a problem but offering NO useful solution.

Esteemed Panel of World's Leading Stroke Experts Share Breakthrough Research on Relationship Between Stroke Risk and Vascular Dementia During Press Conference Broadcast via Facebook Live from XXIV World Congress of Neurology, Dubai, UAE, Monday, Oct. 28, 3:15 p.m. GST 

News provided by
World Federation of Neurology
Oct 25, 2019, 16:48 ET

DUBAI, United Arab Emirates, Oct. 25, 2019 /PRNewswire/ -- What if by reducing your risk for stroke, you could also reduce the risk of dementia? Breakthrough research suggests that there is a connection. During the XXIV World Congress of Neurology (WCN 2019), join a panel of the world's leading experts on stroke as they discuss this breakthrough research during a live press conference. The press conference will take place at the World Trade Centre in Dubai and will be live-streamed via the World Federation of Neurology Facebook Page (www.facebook.com/wfneurology) on Monday, Oct. 28, 2019, at 3:15 pm. GST.
Global incidence of stroke is increasing at alarming rates, with new risk factors such as climate change and air pollution coming to the forefront. As the global burden of stroke becomes more evident, especially in developing countries, the need for a consistent approach to stroke prevention is more evident than ever.
The elite panel of experts will discuss breaking news in stroke and vascular dementia, including the following key insights:
  • Groundbreaking research revealing that measures of stroke prevention may also work to reduce the risk of dementia
  • Climate change, air pollution and other new risk factors for stroke
  • Challenges of managing stroke and dementia in Africa and developing countries
  • New designation of stroke by the World Health Organization(This occurred 13 years ago, keep up with the program. Incompetence in full display. )
  • All over the world, incidents of dementia are increasing at alarming rates
PRESS CONFERENCE PARTICIPANTS
  • Prof. William Carroll, MB, BS, MD, President of World Federation of Neurology
  • Prof. Michael Brainin MD PhD Dr (hons) FESO FAHA FEAN FWSO, President, World Stroke Organisation
  • Prof. Adesola Ogunniyi, MD
  • Prof. Najeeb Qadi, MD
  • Prof. Vladimir Hachinski, MD
Media are invited to join the WCN 2019 Live Stream at www.facebook.com/wfneurology, and can attend the World Congress of Neurology in person by obtaining complimentary passes upon arrival at the World Trade Centre Dubai.
About the World Federation of NeurologyThe World Federation of Neurology represents 120 member neurological societies around the globe whose mission is to foster quality neurology and brain health worldwide by promoting neurological education and training with an emphasis on under-resourced areas of the world. The WFN supports the spread of accurate research and clinical information in the pursuit of improvements in the field of neurology. With support from member organizations, the WFN unifies the world to give patients better access to brain health.
For more information, please visit www.wfneurology.org. Review all WCN 2019 News on our Virtual Press Office at http://wfneurology.vporoom.com/about. Like us on Facebook at https://www.facebook.com/wfneurology/, and follow us on Twitter at https://twitter.com/wfneurology or by searching using the tag #WCN2019.
Media Contact
Yakkety Yak Contact:

Ashley Logan
Yakkety Yak LLC
press@yakketyyak.com
SOURCE World Federation of Neurology

Thursday, July 5, 2018

Brain study paves way for therapy for common cause of dementia

Now our researchers need to find out whether this is the cause of most stroke related dementia. But since we have NO leadership to go to and NO strategy to update nothing will be done.  Without naming the drug you are totally reliant on your doctor figuring out if this can possibly be treated off label. 

Brain study paves way for therapy for common cause of dementia


July 4, 2018, University of Edinburgh

The authors discovered more proliferating dysfunctional endothelial cells (red arrows) in diseased human brains compared to controls. Credit: R.M. Rajani et al., Science Translational Medicine (2018)
Scientists have uncovered a potential approach to treat one of the commonest causes of dementia and stroke in older people.
Studies with rats found the treatment can reverse changes in blood vessels in the associated with the condition, called disease.
Treatment also prevents damage to caused by these blood vessel changes, raising hope that it could offer a therapy for .
Small vessel disease, or SVD, is a major cause of dementia and can also worsen the symptoms of Alzheimer's disease. It is responsible for almost half of all dementia cases in the UK and is a major cause of stroke, accounting for around one in five cases.
Patients with SVD are diagnosed from brain scans, which detect damage to white matter—a key component of the brain's wiring.
Until now, it was not known how changes in small blood vessels in the brain associated with SVD can cause damage to brain cells.
A team led by the University of Edinburgh found that SVD occurs when cells that line the small blood vessels in the brain become dysfunctional. This causes them to secrete a molecule into the brain.
The molecule stops production of the protective layer that surrounds brain cells—called myelin—which leads to brain damage.
Treating rats with drugs that stop from becoming dysfunctional reversed the symptoms of SVD and prevented , tests found.
Researchers say that further studies will need to test whether the treatment also works when the disease is firmly established. They will also need to check if the treatment can reverse the symptoms of dementia.
Dementia is one of the biggest problems facing society, as people live longer and the population ages. Estimates indicate there are almost 47 million people living with dementia worldwide and the numbers affected are expected to double every 20 years, rising to more than 115 million by 2050.
The research, published in Science Translational Medicine, was carried out at the Medical Research Council Centre for Regenerative Medicine and the UK Dementia Research Institute at the University of Edinburgh. It was funded by the MRC, Alzheimer's Research UK and Fondation Leducq.
Professor Anna Williams, Group Leader at the University of Edinburgh's MRC Centre for Regenerative Medicine, said: "This important research helps us understand why small vessel disease happens, providing a direct link between small blood vessels and changes in the brain that are linked to dementia. It also shows that these changes may be reversible, which paves the way for potential treatments."
Dr. Sara Imarisio, Head of Research at Alzheimer's Research UK said: "Changes to the blood supply in the brain play an important role in Alzheimer's disease as well as being a direct cause of . This pioneering research highlights a molecular link between changes to small blood vessels in the brain and damage to the insulating 'white matter' that helps nerve cells to send signals around the brain.
"The findings highlight a promising direction for research into treatments that could limit the damaging effects of blood vessel changes and help keep nerve cells functioning for longer. There are currently no drugs that slow down or stop Alzheimer's disease and no treatments to help people living with vascular dementia. Alzheimer's Research UK is very pleased to have helped fund this innovative research, which is only possible thanks to the work of our dedicated supporters."
Dr. Nathan Richardson, the MRC's Head of Molecular and Cellular Medicine, commented: "This study is a great example of how innovative discovery science into regenerative mechanisms can be applied to improve our understanding of how vascular changes contribute to dementia. This research in rats opens up new possibilities for developing therapies for cerebral small vessel disease."
More information: R.M. Rajani el al., "Reversal of endothelial dysfunction reduces white matter vulnerability in cerebral small vessel disease in rats," Science Translational Medicine (2018). stm.sciencemag.org/lookup/doi/ … scitranslmed.aam9507

Journal reference: Science Translational Medicine search and more info website
Provided by: University of Edinburgh search and more info website

Tuesday, May 23, 2017

Diagnosing Dementia: Alzheimer's May Really Be Mini-Strokes

Hopefully your cognitive reserve is enough to prevent this from happening.
http://www.alzheimersweekly.com/2013/02/diagnosing-dementia-alzheimers-may.html
Memory problems are too quickly diagnosed as Alzheimer's. (In Alzheimer's, the culprit is amyloid-plaque in the brain.) New research shows a more common memory-culprit may be vascular dementia, caused by stroke, mini-stroke and high blood pressure. Learn the difference and why the right diagnosis effects therapy and treatment.




Alzheimer's is connected to sticky plaques made of beta-amyloid that choke brain cells, thereby causing dementia. People may act like they have Alzheimer's when they really have vascular dementia. Vascular dementia is caused by vascular events (related to blood vessels) such as strokes and mini-strokes, so treatment is different. (Mini-strokes occur in the brain when blood vessels clog up or burst. They can accumulate slowly and can go unnoticed for years.)

For example, the damage caused by plaque is typically treated with acetylcholinesterase inhibitors like Aricept®. These drugs target the nervous system. Vascular problems like mini-strokes are treated with blood-targeting medications and therapies.

Alzheimer's disease and vascular dementia are two types of dementia that are common in the elderly. A person's dementia can even be caused by a combination of the two, called "Mixed Dementia."

With today's technology, both vascular brain injury as well as beta-amyloid plaque can be detected in the brain. They both cause memory and thinking problems, called "cognitive impairment". If the cognitive impairment is strong and interferes with a typical person's day, it is called dementia. If it is mild, it is called MCI (Mild Cognitive Impairment).

Until now, doctors generally assumed that when they saw cognitive impairment, it was probably from plaque building up in the brain. Treatment and therapy were given accordingly. New research is showing that vascular brain injury from strokes or the mini-strokes often caused by high blood pressure may deserve the greater part of their attention.

A study at the Alzheimer’s Disease Research Center at UC Davis has found that vascular brain injury from conditions such as high blood pressure and stroke are greater risk factors for cognitive impairment among non-demented older people than is the deposition of the amyloid plaques in the brain that long have been implicated in conditions such as Alzheimer’s disease.
Bruce Reed
Bruce Reed

Published online early today in JAMA Neurology (formerly Archives of Neurology), the study found that vascular brain injury had by far the greatest influence across a range of cognitive domains, including higher-level thinking and the forgetfulness of mild cognitive decline.

The researchers also sought to determine whether there was a correlation between vascular brain injury and the deposition of beta amyloid (Αβ) plaques, thought to be an early and important marker of Alzheimer’s disease, said Bruce Reed, associate director of the UC Davis Alzheimer’s Disease Research Center in Martinez, Calif. They also sought to decipher what effect each has on memory and executive functioning.

“We looked at two questions,” said Reed, professor in the Department of Neurology at UC Davis. “The first question was whether those two pathologies correlate to each other, and the simple answer is ‘no.’ Earlier research, conducted in animals, has suggested that having a stroke causes more beta amyloid deposition in the brain. If that were the case, people who had more vascular brain injury should have higher levels of beta amyloid. We found no evidence to support that.”

"The second,” Reed continued, “was whether higher levels of cerebrovascular disease or amyloid plaques have a greater impact on cognitive function in older, non-demented adults. Half of the study participants had abnormal levels of beta amyloid and half vascular brain injury, or infarcts. It was really very clear that the amyloid had very little effect, but the vascular brain injury had distinctly negative effects.”

“The more vascular brain injury the participants had, the worse their memory and the worse their executive function – their ability to organize and problem solve,” Reed said.

The research was conducted in 61 male and female study participants who ranged in age from 65 to 90 years old, with an average age of 78. Thirty of the participants were clinically “normal,” 24 were cognitively impaired and seven were diagnosed with dementia, based on cognitive testing. The participants had been recruited from Northern California between 2007 to 2012.

The study participants underwent magnetic resonance imaging (MRI) ― to measure vascular brain injury ― and positron emission tomography (PET) scans to measure beta amyloid deposition: markers of the two most common pathologies that affect the aging brain. Vascular brain injury appears as brain infarcts and “white matter hyperintensities” in MRI scans, areas of the brain that appear bright white.

The study found that both memory and executive function correlated negatively with brain infarcts, especially infarcts in cortical and sub-cortical gray matter. Although infarcts were common in this group, the infarcts varied greatly in size and location, and many had been clinically silent. The level of amyloid in the brain did not correlate with either changes in memory or executive function, and there was no evidence that amyloid interacted with infarcts to impair thinking.

Reed said the study is important because there’s an enormous amount of interest in detecting Alzheimer’s disease at its earliest point, before an individual exhibits clinical symptoms. It’s possible to conduct a brain scan and detect beta amyloid in the brain, and that is a very new development, he said.

“The use of this diagnostic tool will become reasonably widely available within the next couple of years, so doctors will be able to detect whether an older person has abnormal levels of beta amyloid in the brain. So it’s very important to understand the meaning of a finding of beta amyloid deposition,” Reed said.

“What this study says is that doctors should think about this in a little more complicated way. They should not forget about cerebrovascular disease, which is also very common in this age group and could also cause cognitive problems. Even if a person has amyloid plaques, those plaques may not be the cause of their mild cognitive symptoms.”



Other study authors include Natalie Marchant of UC Berkeley and the Buck Institute for Research on Aging; Roxana Dhada and William Jagust of UC Berkeley; Charles DeCarli and Dan Mungas of UC Davis; Stephen Kriger and Micheal Weiner of UC San Francisco and Nerses Sanossian, Wendy Mack and Helena Chui of the University of Southern California.

The research was supported by grants number AG012435, AG00266 and AG10129 from the National Institutes of Health.


The UC Davis Alzheimer's Disease Center is one of only 27 research centers designated by the National Institutes of Health's National Institute on Aging. The center's goal is to translate research advances into improved diagnosis and treatment for patients while focusing on the long-term goal of finding a way to prevent or cure Alzheimer's disease. Also funded by the state of California, the center allows researchers to study the effects of the disease on a uniquely diverse population. For more information, visit alzheimer.ucdavis.edu.

Monday, April 10, 2017

Marijuana & Vascular Dementia

So rather than demonizing marijuana like this our researchers should come up with a solution to this  vascular squeezing ability. I bet the stroke and heart attack risk are from the smoking part rather than marijuana itself and people with these other health problems are using marijuana to self-treat themselves.   I plan on using marijuana short term after my next stroke.

My 13 reasons for marijuana use post-stroke.  

But don't listen to me, I have absolutely no medical training.



http://www.alzheimersweekly.com/2017/04/marijuana-vascular-dementia.html
As marijuana legalization spreads, new research is improving our understanding of side effects. Heart cells have cannabis receptors relevant to vascular squeezing ability. Learn about marijuana's link to vascular dementia.




WASHINGTON - Using marijuana raises the vascular risks of stroke and heart failure, major risk factors leading to vascular dementia. Even after accounting for demographic factors, other health conditions and lifestyle risk factors such as smoking and alcohol use, the data is compelling, according to research being presented at the American College of Cardiology’s 66th Annual Scientific Session.

Vascular Health

Coming at a time when marijuana, medically known as cannabis, is on track to become legal for medical or recreational use in more than half of U.S. states, this study sheds new light on how the drug affects vascular health. While previous marijuana research has focused mostly on pulmonary and psychiatric complications, the new study is one of only a handful to investigate cardiovascular outcomes.

“Like all other drugs, whether they’re prescribed or not prescribed, we want to know the effects and side effects of this drug,” said Aditi Kalla, MD, Cardiology Fellow at the Einstein Medical Center in Philadelphia and the study’s lead author. “It’s important for physicians to know these effects so we can better educate patients, such as those who are inquiring about the safety of cannabis or even asking for a prescription for cannabis.”

Nationwide Inpatient Sample

The study drew data from the Nationwide Inpatient Sample, which includes the health records of patients admitted at more than 1,000 hospitals comprising about 20 percent of U.S. medical centers. Researchers extracted records from young and middle-aged patients—age 18-55 years—who were discharged from hospitals in 2009 and 2010, when marijuana use was illegal in most states.

Marijuana use was diagnosed in about 1.5 percent (316,000) of more than 20 million health records included in the analysis. Comparing cardiovascular disease rates in these patients to disease rates in patients not reporting marijuana use, researchers found marijuana use was associated with a significantly increased risk for cardiovascular events such as stroke, heart failure, coronary artery disease and sudden cardiac death.

Marijuana - Independent Association

Marijuana use was also linked with a variety of factors known to increase cardiovascular risk, such as obesity, high blood pressure, smoking and alcohol use. After researchers adjusted the analysis to account for these factors, marijuana use was independently associated with a 26 percent increase in the risk of stroke and a 10 percent increase in the risk of developing heart failure. (Really?)

“Even when we corrected for known risk factors, we still found a higher rate of both stroke and heart failure in these patients, so that leads us to believe that there is something else going on besides just obesity or diet-related cardiovascular side effects,” Kalla said. “More research will be needed to understand the pathophysiology behind this effect.”

Heart Cells Have Canabis Receptors

Research in cell cultures shows that heart muscle cells have cannabis receptors relevant to contractility, or squeezing ability, suggesting that those receptors might be one mechanism through which marijuana use could affect the cardiovascular system. It is possible that other compounds could be developed to counteract that mechanism and reduce cardiovascular risk, Kalla said.

Because the study was based on hospital discharge records, the findings may not be reflective of the general population. The study was also limited by the researchers’ inability to account for quantity or frequency of marijuana use, purpose of use (recreational or medical), or delivery mechanism (smoking or ingestion).

Further Insights

Kalla suggested that the growing trend toward legalization of marijuana could mean that patients and doctors will become more comfortable speaking openly about marijuana use, which could allow for better data collection and further insights into the drug’s effects and side effects.


SOURCE:
  • The American College of Cardiology
    The American College of Cardiology is a 52,000-member medical society that is the professional home for the entire cardiovascular care team. The mission of the College is to transform cardiovascular care and to improve heart health. The ACC leads in the formation of health policy, standards and guidelines. The College operates national registries to measure and improve care, offers cardiovascular accreditation to hospitals and institutions, provides professional medical education, disseminates cardiovascular research and bestows credentials upon cardiovascular specialists who meet stringent qualifications.

Thursday, February 5, 2015

Vascular Dementia Caused by Plaque Build-Up in Arteries

You can compare this Mayo clinic explanation of atherosclerosis to an earlier one I pointed to.
Vascular dementia and artery plaque by Mayo Clinic
You can see a video of how plaque forms here:
Inflammation In Atherosclerotic Plaque Formation 

You can see from both of these that the real solution is to stop the original inflammation in the first place. Reducing cholesterol is a secondary solution and a poor one at that.