Study shows asthma drug salbutamol's potential as Alzheimer's treatment

You'll want your doctor to keep you informed of this, so ask her/him how they are keeping up with research that survivors need to know about.  The answer will tell you about your hospital's competence. If neither of the following never made it to your hospital you need to start the firings with the board of directors.

Can An Anti-Asthma Drug Rejuvenate the Brain? montelukast January 2016 

A Decades-Old Asthma Drug Has Reversed Brain Damage From Dementia in Mice - zileuton July 2018

Your chances of getting dementia.

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 

5. Parkinson’s Disease May Have Link to Stroke March 2017 

The latest here:

Study shows asthma drug salbutamol's potential as Alzheimer's treatment

MedicalXpress Breaking News-and-Events|July 2, 2020

A new study reveals that the common asthma drug salbutamol may offer potential as a treatment for Alzheimer's disease.

Alzheimer's disease is the most common form of dementia, affecting 47 million people worldwide and its prevalence is expected to triple to more than 130 million cases by 2050.

No effective treatments that cure the disease or slow down its progression have been discovered. However, this new early-stage study has revealed that repurposing an existing drug, salbutamol, offers significant potential as a low cost and rapid response option.

Extensive analytical in-vitro experiments conducted by the research team show that salbutamol is effective at reducing the accumulation of insoluble fibers of the tau protein—which is found in the brains of people with Alzheimer's disease. These microscopic fibers accumulate into neurofibrillary tangles and can cause neuron destabilization, brain cell death, and are a key characteristic of the disease's progression.

Much Alzheimer's disease research has focused on the build-up of amyloid plaques, caused by misfolding of the amyloid-β protein. However, because of disappointing results from numerous therapies targeting Aβ aggregation, more attention is shifting towards tau.

This study, led by researchers at Lancaster University, used a new automated 'high throughput' screening approach to study the structure of the misfolding tau protein with a special analytical technique called 'Synchrotron Radiation Circular Dichroism' (SRCD) at Diamond Light Source, the UK national synchrotron light source in Oxfordshire. With this powerful technique they were able to look at a selection of more than 80 existing compounds and drugs simultaneously to determine their effectiveness at preventing the formation of tau fibrils.

This method confirmed the compound epinephrine, more commonly known as adrenaline, was effective at stabilizing the tau proteins and preventing the formation of tau tangles. However, our bodies do not easily absorb epinephrine and it rapidly gets metabolized, so the scientists then looked at a range of readily available compounds with similar chemical structures. This search revealed four current drugs as possible candidates—etamivan, fenoterol, dobutamine and salbutamol.

Etaminvan and fenoterol were found to have little effect on the assembly of tau tangles. Dobutamine, which is used for the rapid treatment of heart attacks and heart failure, was found to have some benefit. However, because its effects are very short-lived, and because it needs to be administered intravenously, it is not ideal as a basis for treatment of Alzheimer's disease.

Further tests using a range of analytical techniques all revealed salbutamol could inhibit tau aggregation in vitro. Tests where salbutamol was added to solutions containing tau resulted in drastically reduced density of fibrous tau structures responsible for the tau neurofibrillary tangles.

The researchers believe that salbutamol interacts with an early stage of tau fibril formation, reducing their ability to form an initial nucleus which drives the aggregation process.

Because it is easily ingested, absorbed into the brain, and remains in the body for several hours, salbutamol has attractive properties as a research avenue for potential new treatment for Alzheimer's.

Dr. David Townsend, of Lancaster University and lead author of the research, said: "Our work highlights the potential impact of repurposing drugs for secondary medical uses, by discovering a novel therapeutic strategy that impedes the molecular pathology of Alzheimer's disease, and which may have otherwise gone unstudied.

"Salbutamol has already undergone extensive human safety reviews, and if follow up research reveals an ability to impede Alzheimer's disease progression in cellular and animal models, this drug could offer a step forward, whilst drastically reducing the cost and time associated with typical drug development."

Professor David Middleton, co-author of the research, said: "This work is in the very early stages and we are some way from knowing whether or not salbutamol will be effective at treating Alzheimer's disease in human patients. However, our results justify further testing of salbutamol, and similar drugs, in animal models of the disease and eventually, if successful, in clinical trials."

Dr. Rohanah Hussain, of Diamond Light Source, Senior Beamline Scientist and co-author said: "Diamond B23 beamline unique micro-collimated beam has made high throughput CD possible allowing the screening of many compounds through structural activity correlation crucial in drug discovery."

The researchers say that current asthma inhalers result in only a small amount of salbutamol reaching the brain and so, if further research is successful, a new delivery method would also need to be developed. They add that future research could also focus on other asthma drugs that are chemically similar to salbutamol, but which circulate in the bloodstream for much longer.

To read more, click here

A Decades-Old Asthma Drug Has Reversed Brain Damage From Dementia in Mice - zileuton

Did your stroke hospital do anything with this earlier one? If not you need to fire the whole staff.  They will do nothing with this new research.

Can An Anti-Asthma Drug Rejuvenate the Brain? Jan. 2016

A Decades-Old Asthma Drug Has Reversed Brain Damage From Dementia in Mice - zileuton 

Scientists have used a mice model to reverse some of the most severe damage done to the brain by dementia - and they did this with a surprisingly old medication typically used for asthma.
The discovery could open up the road for treatments that could restore memory and spatial impairment in people with conditions like Alzheimer's. While a human treatment is still some way off, the research shows one method we could use to retroactively treat the buildup of tau proteins, long thought to be a key factor in dementia.
Key to the improvement was an asthma drug called zileuton (or Zyflo) that's been in use for 22 years. The team from Temple University in Philadelphia is highly optimistic, claiming that their findings could eventually improve the lives of millions of people with dementia.
"We show that we can intervene after disease is established and pharmacologically rescue mice that have tau-induced memory deficits," says senior investigator Domenico Praticò.
There's still plenty we don't know about diseases like Alzheimer's, but the evidence points to tangles of tau proteins blocking connections between neurons. Another protein, amyloid precursor protein (APP), is also thought to be involved.
In this study the scientists targeted inflammatory molecules called leukotrienes. Having found that leukotrienes cause damage to nerve cells as dementia develops, the team wanted to try blocking the formation of these molecules.
That's where zileuton came in. It was given to one group of mice engineered to have similar dementia problems to 60-year-old humans with the condition, while another group of mice were given placebos instead.
After 16 weeks, treated mice were performing much better on maze tests than mice who hadn't received zileuton. The treated group was also found to have 90 percent fewer leukotrienes in their brains, and 50 percent fewer tau tangles.
"It's really dramatic what we observed," Praticò told Stacey Burling at The Inquirer. "For the first time, we are showing that we can do something after the disease is established."
In fact, the synapses of the mice given zileuton looked as healthy as normal mice after close analysis. It's almost as if this aspect of the dementia had been completely cleared up.
Before we get too excited, there are some limitations to consider. For example, these mice didn't have any beta-amyloid plaque build ups (caused by APP) in their brains, which are consistently found alongside tau plaques in human brains with dementia.
And while mice are often used in research for their genetic and biological similarity to humans, transferring treatments over from these animals can be difficult. Add to that the limits of our understanding about dementia, and there's still a lot of work to be done.
Nevertheless, the fact that researchers were able to actually reverse some of the damage of dementia after it had taken hold is cause for celebration, because the condition isn't usually diagnosed in humans until the effects have already started.
Another reason for optimism is that zileuton has already been approved as a safe drug, albeit with advisory warnings and potential side effects. But it should make it easier to set up a clinical trial, which the team of scientists wants to do next.
"This is an old drug for a new disease," says Praticò. "The research could soon be translated to the clinic, to human patients with Alzheimer's disease."
The research has been published in Molecular Neurobiology.

Asthma Medicine Halves Risk of Parkinson´s

This particular article is totally fucking worthless, doesn't name the asthma medicine, and doesn't name the blood pressure med that causes problems. Demand your doctor get that information.  A great stroke association would publicly publicize that to all stroke doctors, but instead we have fucking failures of stroke associations doing nothing useful for stroke survivors to get 100% recovered.  I need to know the blood pressure drug since I'm on one and I'm not sure I'm drinking the correct quantity of coffee to prevent Parkinsons.

Asthma Medicine Halves Risk of Parkinson´s

By Kim E. AndreassenPublished: 31.08.2017 (Last updated: 01.09.2017)

• By studying the effect of 1000 medicines, researchers discovered that medicine against asthma and blood pressure is linked to the risk of getting Parkinson´s disease.
• While the use of asthma medicine halves the risk of getting Parkinson´s, one type of medicine against high blood pressure doubles the risk.
• The researchers examined more than 100 million prescriptions ordered over the last 11 years in Norway.
• These discoveries could be the start of a radically new treatment of Parkinson´s patients.

Parkinson´s disease is a chronic disease with unknown causes. The disease destroys the brain cells that control body movements. Shivering, stiff arms and legs and poor coordination are typical symptoms of Parkinson´s. The symptoms may develop slowly, and it sometimes takes time to make a correct diagnosis.

Researchers at the Department of Global Public Health and Primary Care (IGS) at the University of Bergen (UiB) have completed a large study that included data from the Norwegian Prescription Database, in cooperation with researchers at Harvard University.

“Our analysis of data from the whole Norwegian population has been decisive for the conclusion in this study,” says Professor Trond Riise at IGS. He leads the registery study in Norway.

The study is published in Science.

100 million prescriptions

Together with colleagues Anders Engeland and Kjetil Bjørnevik, Riise has analysed more than 100 million Norwegian prescriptions registered since 2004.

In the study, the treatment of Parkinson´s was linked to prescriptions of asthma medicine and the medicine for high blood pressure. It enabled the researchers to see the connection between medicine use and illness.

The UiB-researchers were able to make these comparisons by using the prescription database. The Norwegian analysis was done after researchers at Harvard University found these effects of the medicines in animal tests and in experiments with brain cells in the lab. Their results showed that these different medicines had opposite effects on the risk of Parkinson´s.

Possible new treatment

To find out if these medicines had the same effect on humans, the researchers at Harvard University started to collaborate with the Norwegian research team, and their unique resource of having access to the unique and large Norwegian database, where all Norwegian prescriptions are registered.

“We analysed the whole Norwegian population and found the same results as in the animal testing at Harvard University. These medicines have never been studied in relation to Parkinson’s disease,” says Riise.

Trond Riise underlines the fact that “Our discoveries may be the start of a totally new possible treatment for this serious disease. We expect that clinical studies will follow these discoveries.”

Can An Anti-Asthma Drug Rejuvenate the Brain? montelukast

Your doctor should be vastly interested in how this can be applied to stroke survivors. But don't worry this will never be followed up on because we have NO stroke strategy or stroke leadership in any part of stroke and this will fall thru the cracks. Our fucking failures of stroke associations once again will lead the way to failure by not doing anything about this.

Can An Anti-Asthma Drug Rejuvenate the Brain?

A couple of paragraphs from there.

This group of researchers from Austria, Germany, Italy and Croatia presented a new therapy that, according to their own words, can “functionally rejuvenate the aged but otherwise healthy brain”. And the therapeutic agent is probably surprising: it’s an anti-asthmatic drug named montelukast.
The authors had previously identified a molecule involved in asthma pathology as being elevated in ageing, contributing to neuroinflammation and cognitive impairment. This led them to the hypothesis that other mechanisms originally related to peripheral inflammatory conditions such as asthma might affect the central nervous system, potentially contributing to degenerative processes.
Leukotrienes are a group of molecules that mediate inflammatory reactions associated with increased vascular permeability. Increased levels of leukotrienes have been reported in a number of neurological conditions, as well as in the aged brain. Although their role is mostly unclear, it is believed that they may mediate inflammatory responses in the brain and blood vessels. The drug they used, montelukast, acts by blocking leukotriene activity, being highly successful in asthma.
According to their data, montelukast seems to be able to reduce the levels of inflammatory molecules in the brain, restore the blood-brain barrier’s integrity and increase neurogenesis in the brain of aged rats. As a consequence, montelukast treatment also restores cognitive function in the old animals.
Montelukast seems to be able to cross the blood-brain barrier and it had previously been shown to have a protective effects in animal models of neurodegenerative diseases, including Huntintgon’s and Alzheimer’s disease, as well as in induced loss of memory function, spinal cord and brain injuries and stroke, decreasing cognitive and structural deficits.
Here, they showed that this anti-asthma drug can reduce age-associated changes, improving learning and memory in old rats, reducing the inflammation-induced activation of glial cells in the brain, and restoring neurogenesis in the hippocampus of old rats most likely by targeting leukotriene actions in the brain.

asthma drug, Xolair - Omalizumab May Elevate Risk of Cardiovascular, Cerebrovascular Adverse Events

Be careful out there.
http://www.docguide.com/omalizumab-may-elevate-risk-cardiovascular-cerebrovascular-adverse-events
A review of safety studies by the US Food and Drug Administration (FDA) suggests a slightly increased risk of cardiovascular and cerebrovascular adverse events among patients being treated with the asthma drug omalizumab (Xolair) than in those who were not treated with the drugs.
As a result, the FDA has added information about these potential risks to the drug label.
The review found no difference in the rates of cancer between those patients being treated with omalizumab and those who were not being treated with omalizumab. However, due to limitations in the 5-year study, the FDA cannot rule out a potential risk of cancer with omalizumab, so this information was added to the Warnings and Precautions section of the drug label.
Information for healthcare professionals:
• The FDA has added information about the findings of a slightly elevated risk of cardiovascular and cerebrovascular serious adverse events in omalizumab -treated patients to the Adverse Reactions section of the omalizumab label. The FDA has also added information about uncertain findings regarding a potential risk of cancer to the Warnings and Precautions section of the drug label.
• Periodically reassess the need for continued therapy with omalizumab based on the patient’s disease severity and level of asthma control.
• The appropriate duration of therapy for chronic idiopathic urticaria has not been evaluated. Periodically reassess the need for continued omalizumab therapy.
• Instruct patients receiving omalizumab not to decrease the dose or stop taking the drug or any other asthma medicines unless you instruct them to do otherwise.
• Provide and instruct patients to read the omalizumab patient Medication Guide before starting treatment and before starting each new prescription.
• Report adverse events involving omalizumab to the FDA MedWatch program.
Healthcare professionals and patients are encouraged to report adverse events or side effects related to the use of these products to the FDA's MedWatch Safety Information and Adverse Event Reporting Program: www.fda.gov/MedWatch/report.htm