Sleep Brainwaves Flush Brain of Waste

 Are these flushing neurons still working post stroke? Then, if not, is this the reason for heightened dementia risk post stroke? Ask your doctor EXACTLY  how they will be testing to see if these brainwaves are still functioning properly! Your doctor has had years of knowledge on this to competently come up with a solution, but I bet you don't have a functioning stroke doctor!

• brain waste removal (4 posts to February 2018)

Your risk of dementia, has your doctor told you of this?  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:

Sleep Brainwaves Flush Brain of Waste

Summary: A new study unveiled a crucial role of sleep: brainwaves facilitating the cleansing of the brain by flushing out waste. This discovery not only underscores the brain’s non-dormant state during sleep but also highlights a sophisticated system where neurons’ synchronized activity powers the flow of cerebrospinal fluid, effectively removing metabolic waste and potentially neurodegenerative disease-causing toxins.

This insight opens up possibilities for enhancing brain cleaning processes to combat neurological diseases and improve sleep efficiency, hinting at a future where optimized sleep could lead to better health outcomes.

Key Facts:

1. Brainwaves Propel Cleansing Fluids: During sleep, neurons coordinate to produce rhythmic waves that drive the movement of fluid through the brain, washing away waste.
2. Potential for Disease Prevention: Understanding and enhancing this cleansing process could delay or prevent diseases like Alzheimer’s and Parkinson’s by ensuring the effective removal of brain waste.
3. Implications for Sleep Quality: This research suggests that improving the brain’s waste removal efficiency could allow for healthier brains even with less sleep, offering new avenues for treating sleep disorders and enhancing overall well-being.

Source: Washington University

There lies a paradox in sleep. Its apparent tranquility juxtaposes with the brain’s bustling activity. The night is still, but the brain is far from dormant. During sleep, brain cells produce bursts of electrical pulses that cumulate into rhythmic waves – a sign of heightened brain cell function.

But why is the brain active when we are resting?

Slow brain waves are associated with restful, refreshing sleep. And now, scientists at Washington University School of Medicine in St. Louis have found that brain waves help flush waste out of the brain during sleep. Individual nerve cells coordinate to produce rhythmic waves that propel fluid through dense brain tissue, washing the tissue in the process.

Cerebrospinal fluid surrounding the brain enters and weaves through intricate cellular webs, collecting toxic waste as it travels. Credit: Neuroscience News

“These neurons are miniature pumps. Synchronized neural activity powers fluid flow and removal of debris from the brain,” explained first author Li-Feng Jiang-Xie, PhD, a postdoctoral research associate in the Department of Pathology & Immunology.

“If we can build on this process, there is the possibility of delaying or even preventing neurological diseases, including Alzheimer’s and Parkinson’s disease, in which excess waste – such as metabolic waste and junk proteins – accumulate in the brain and lead to neurodegeneration.”

The findings are published Feb. 28 in Nature.

Brain cells orchestrate thoughts, feelings and body movements, and form dynamic networks essential for memory formation and problem-solving. But to perform such energy-demanding tasks, brain cells require fuel. Their consumption of nutrients from the diet creates metabolic waste in the process.

“It is critical that the brain disposes of metabolic waste that can build up and contribute to neurodegenerative diseases,” said Jonathan Kipnis, PhD, the Alan A. and Edith L. Wolff Distinguished Professor of Pathology & Immunology and a BJC Investigator. Kipnis is the senior author on the paper.

“We knew that sleep is a time when the brain initiates a cleaning process to flush out waste and toxins it accumulates during wakefulness. But we didn’t know how that happens. These findings might be able to point us toward strategies and potential therapies to speed up the removal of damaging waste and to remove it before it can lead to dire consequences.”

But cleaning the dense brain is no simple task. Cerebrospinal fluid surrounding the brain enters and weaves through intricate cellular webs, collecting toxic waste as it travels. Upon exiting the brain, contaminated fluid must pass through a barrier before spilling into the lymphatic vessels in the dura mater – the outer tissue layer enveloping the brain underneath the skull. But what powers the movement of fluid into, through and out of the brain?

Studying the brains of sleeping mice, the researchers found that neurons drive cleaning efforts by firing electrical signals in a coordinated fashion to generate rhythmic waves in the brain, Jiang-Xie explained. They determined that such waves propel the fluid movement.

The research team silenced specific brain regions so that neurons in those regions didn’t create rhythmic waves. Without these waves, fresh cerebrospinal fluid could not flow through the silenced brain regions and trapped waste couldn’t leave the brain tissue.

“One of the reasons that we sleep is to cleanse the brain,” Kipnis said.

“And if we can enhance this cleansing process, perhaps it’s possible to sleep less and remain healthy. Not everyone has the benefit of eight hours of sleep each night, and loss of sleep has an impact on health.

“Other studies have shown that mice that are genetically wired to sleep less have healthy brains. Could it be because they clean waste from their brains more efficiently? Could we help people living with insomnia by enhancing their brain’s cleaning abilities so they can get by on less sleep?”

Brain wave patterns change throughout sleep cycles. Of note, taller brain waves with larger amplitude move fluid with more force. The researchers are now interested in understanding why neurons fire waves with varying rhythmicity during sleep and which regions of the brain are most vulnerable to waste accumulation.

“We think the brain-cleaning process is similar to washing dishes,” neurobiologist Jiang-Xie explained.

“You start, for example, with a large, slow, rhythmic wiping motion to clean soluble wastes splattered across the plate. Then you decrease the range of the motion and increase the speed of these movements to remove particularly sticky food waste on the plate.

“Despite the varying amplitude and rhythm of your hand movements, the overarching objective remains consistent: to remove different types of waste from dishes. Maybe the brain adjusts its cleaning method depending on the type and amount of waste.”

About this sleep and neuroscience research news

Author: Marta Wegorzewska
Source: Washington University
Contact: Marta Wegorzewska – Washington University
Image: The image is credited to Neuroscience News

Original Research: Closed access.
“Neuronal dynamics orchestrate cerebrospinal fluid perfusion and brain clearance” by Li-Feng Jiang-Xie et al. Nature

Muscle, skin and gastrointestinal problems cause a quarter of patients with heart disease and strokes to stop treatment in HPS2-THRIVE trial

I was in the earlier trial - (AIM-HIGH) study  - that just had the niacin, no flushing blocker, I quit the trial I was in because of the exacerbation of existing excema I had on my leg. I was scratching at it until it bled.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=128784&CultureCode=en
The largest randomised study of the vitamin niacin in patients with occlusive arterial disease (narrowing of the arteries) has shown a significant increase in adverse side-effects when it is combined with statin treatment.
Results from the HPS2-THRIVE study (Heart Protection Study 2 – Treatment of HDL to Reduce the Incidence of Vascular Events), including the reasons patients stopped the study treatment, are published online today (Wednesday) in the European Heart Journal [1].
Niacin has been used for decades to help increase levels of “good” HDL cholesterol and to decrease levels of “bad” LDL cholesterol and triglycerides (fats) in the blood in people at risk of cardiovascular problems such as heart disease and stroke. However, it has a number of side-effects including flushing of the skin. Another drug, laropiprant, can reduce the incidence of flushing by blocking the prostaglandin D2 receptor that is involved in the process. Therefore, the HPS2-THRIVE study investigated whether combining extended-release niacin with laropiprant (ERN/LRPT), given in addition to an LDL cholesterol-lowering statin, simvastatin, could reduce the risk of cardiovascular problems in people at high risk due to existing occlusive arterial disease.
A total of 25,673 patients from China, the UK and Scandinavia were randomised between April 2007 and July 2010 to receive either 2g of extended release niacin plus 40 mg of laropiprant or matching placebo. In addition, all participants received intensive LDL cholesterol-lowering therapy with simvastatin (with or without ezetimibe). Researchers from the Clinical Trial Service Unit & Epidemiological Studies Unit (CTSU) at the University of Oxford (UK), who were responsible for designing and conducting the trial and analysing the results, followed the patients for an average of 3.9 years.
By the end of the study, 25% of patients taking ERN/LRPT had stopped their treatment, compared with 17% of patients taking placebo.
Jane Armitage, Professor of Clinical Trials and Epidemiology & Honorary Consultant in Public Health Medicine at the CTSU, said: “The main reason for patients stopping the treatment was because of adverse side-effects, such as itching, rashes, flushing, indigestion, diarrhoea, diabetes and muscle problems. We found that patients allocated to the experimental treatment were four times more likely to stop for skin-related reasons, and twice as likely to stop because of gastrointestinal problems or diabetes-related problems.
“We found that, in the trial as a whole, participants in the experimental arm had a more than four-fold increased risk of myopathy (muscle pain or weakness with evidence of muscle damage) compared with the placebo group. This is highly significant. It appeared that this effect was about three times greater among participants in China than those in Europe, for reasons that are not clear. In the placebo arm (i.e. those on statin-based treatment alone), the statin-related myopathy was more common among participants in China than those in Europe. Therefore – in combination with the greater effect of ERN/LRPT on myopathy in China – the excess number of cases of myopathy caused by ERN/LRPT (though low in both regions) was over ten times greater among participants in China than those in Europe (0.53 percent per year compared to 0.03 percent per year).”
Dr Richard Haynes, Clinical Coordinator at the CTSU, said: “This is the largest randomised trial of extended release niacin treatment and it provides uniquely reliable results on adverse side-effects and the ability of patients to tolerate them. Although 25 percent of patients stopped the treatment early, 75 percent continued on it for approximately four years. Currently, we are analysing the final data on the cardiovascular outcomes from the trial, and once we have these we will know whether or not the benefits of the treatment outweigh the myopathy, skin and gastrointestinal problems.”
The researchers will be presenting full results on the cardiovascular outcomes at the annual meeting of the American College of Cardiology in March and these will be published in another paper afterwards [2].
The co-principal investigator of the study, Dr Martin Landray, Reader in Epidemiology and Honorary Consultant Physician at the CTSU, said: “Previous research had suggested that improving cholesterol levels in high-risk patients might translate into a 10-15 percent reduction in major vascular events such as heart attacks and strokes. In the HPS2-THRIVE study, 3,400 of the 25,673 participants suffered a major vascular event over an average of four years of follow-up. This means the study has excellent statistical power to discover the effectiveness or otherwise of the treatment.”
In an accompanying editorial [3], Professor Ulf Landmesser, of the University Hospital Zurich (Switzerland), points out that although the study showed an increase in myopathy, it also showed that the ERN/LRPT substantially lowered LDL cholesterol and triglycerides by nearly 20%. He writes that these observations “raise important questions as to why niacin/laropiprant did not reduce major cardiovascular events”, and he wonders whether laropiprant “is really biologically inert with respect to atherosclerosis and thrombosis”.
He concludes that “niacin has failed as a valuable ‘partner’ of statin therapy in lipid-targeted approaches to further reduce major cardiovascular events in high-risk patients”. He continues: “At present, statin therapy has been clearly shown to reduce vascular events effectively and is reasonable well tolerated in most patients. We will still have to wait for the results of … ongoing studies to see whether another lipid-targeted intervention can further reduce vascular events in addition to statin therapy.”

Notes:
[1] “HPS2-THRIVE randomized placebo-controlled trial in 25 673 high-risk patients of ER niacin/laropiprant: trial design, pre-specified muscle, and liver outcomes and reasons for stopping study treatment”, by Richard Haynes, Lixin Jiang, Jemma C. Hopewell, Jing Li, Fang Chen, Sarah Parish, Martin J. Landray, Rory Collins, and Jane Armitage, The HPS2-THRIVE Collaborative Group. European Heart Journal. doi:10.1093/eurheartj/eht055
[2] In December 2012 the pharmaceutical company Merck, which manufactures ERN/LRPT under the trade name Tredaptive and which funded the HSP2-THRIVE study, issued a statement saying the trial had failed to meet its primary endpoint and that “the combination of extended-release niacin and laropiprant to statin therapy did not significantly further reduce the risk of the combination of coronary deaths, non-fatal heart attacks, strokes or revascularizations compared to statin therapy.” ERN/LRPT is not approved for use in the USA, and on January 11, Merck announced that it was “taking steps to suspend the availability of TREDAPTIVE™ (extended-release niacin/laropiprant) tablets worldwide.”
[3] ”The difficult search for a ‘partner’ of statins in lipid-targeted prevention of vascular events: the re-emergence and fall of niacin”, by Ulf Landmesser. European Heart Journal. doi:10.1093/eurheartj/eht064