Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:

Monday, October 16, 2017

Only 1 in 4 survivors feels confident in preventing another stroke

What do you expect when you get fucking generalities? By leaving it at generalities instead of specifics you can continue to blame the patient rather than have the problem fall back on the stroke medical world to solve.
Take care of blood pressure, cholesterol, exercise.
Like maybe a 307%  stroke risk reduction from these 11 possibilities? They also are not specific enough to do any good.

American Heart Association News
Results from a new survey conducted by the American Heart Association/American Stroke Association (AHA/ASA), the world’s leading voluntary health organization devoted to fighting cardiovascular disease and stroke, found that stroke survivors have low confidence in their ability to prevent another stroke.

Nearly 800,000 people in the U.S. have a stroke every year, with about one in four being recurrent strokes. Fortunately, stroke is largely preventable through physical activity, healthy eating and medication adherence.

The survey, which included 1,129 adult participants (survivors, caregivers and healthcare professionals) nationwide, was conducted as part of the American Stroke Association’s Together to End Stroke® second stroke awareness campaign, nationally sponsored by Bayer® Aspirin.

The newly launched, four-year campaign, aims to raise greater awareness among stroke survivors of their heightened risk of having another stroke and to provide them with guidance to help with behaviors like exercising regularly and staying motivated, as these were major challenges reported by the survey participants. Specific campaign goals include:
  • Reducing stroke reoccurrence
  • Reducing 30-day hospital readmission
  • Increasing stroke patient knowledge of risk factors
  • Educating about healthy lifestyle changes and medication adherence
  • Educating about rehabilitation options and benefits
“We are working diligently to provide stroke survivors and caregivers with the awareness, education and tools needed to feel highly confident in taking control of their health to significantly reduce their risk of experiencing another stroke,” said Dr. Joseph Hanna, Chairman of Neurology at The MetroHealth System, Inc., in Cleveland and AHA/ASA Spokesperson.

Frequent doctor recommended interventions such as medications to manage known stroke risk factors, following an aspirin regimen, if prescribed, and stroke rehabilitation, are key elements that can contribute to preventing another stroke.

Additional survey findings:
  • Exercising regularly is the biggest challenge reported by Survivors (23%).
  • The most common changes that survivors made to their lifestyle since their stroke are taking recommended medication (83%) and taking aspirin daily (63%).
  • Half of Survivors and Caregivers (49%) have heard of F.A.S.T.
  • Both Survivors and Caregivers view high blood pressure as the most important factor putting someone at risk for a second stroke (58% and 59%, respectively).
  • Survivors consistently rate their overall health and sociability as much better than do Caregivers.

Fat Cells Converted Into Stem Cells Can Repair Any Damaged Tissues

Personally I still think handing your doctor a pee cup and asking for stem cells is much better, but to each her own.  Or course stem cells are probably decades off before becoming useful in stroke.

Turning urine into brain cells could help fight Alzheimer’s, Parkinson’s and it is only 5 years old, plenty of time for your doctor to contact researchers and get something done. But I bet absolutely NOTHING was done by your doctor, incompetence in action once again.

Fat Cells Converted Into Stem Cells Can Repair Any Damaged Tissues

Stem cell therapies capable of regenerating any human tissue damaged by injury, disease or ageing could be available within a few years, following landmark research led by UNSW Australia researchers. Watch the video below for more details.
The repair system, similar to the method used by salamanders to regenerate limbs, could be used to repair everything from spinal discs to bone fractures, and has the potential to transform current treatment approaches to regenerative medicine. The findings were published in the Proceedings of the National Academy of Sciences journal.
“This technique is a significant advance on many of the current unproven stem cell therapies, which have shown little or no objective evidence they contribute directly to new tissue formation,” study lead author, haematologist and UNSW Associate Professor John Pimanda said.
The technique developed by UNSW researchers involves extracting adult human fat cells and treating them with the compound 5-Azacytidine (AZA), along with platelet-derived growth factor-AB (PDGF-AB) for approximately two days. The cells are then treated with the growth factor alone for a further two-three weeks.
AZA is known to induce cell plasticity, which is crucial for reprogramming cells. The AZA compound relaxes the hard-wiring of the cell, which is expanded by the growth factor, transforming the bone and fat cells into iMS cells. When the stem cells are inserted into the damaged tissue site, they multiply, promoting growth and healing.
The technique is similar to salamander limb regeneration, which is also dependent on the plasticity of differentiated cells, which can repair multiple tissue types, depending on which body part needs replacing.
Along with confirming that human adult fat cells reprogrammed into iMS stem cells can safely repair damaged tissue in mice, the researchers said further work is required to establish whether iMS cells remain dormant at the sites of transplantation and retain their capacity to proliferate on demand.
“We are currently assessing whether adult human fat cells reprogrammed into iMS cells can safely repair damaged tissue in mice, with human trials expected to begin in late 2017.” Associate Professor Pimanda said.

New study examines full range of post-stroke visual impairments

And the next study should be how to cure these. But that won't occur since we have NO stroke leadership and NO stroke strategy.  You're screwed if you have a stroke. NO one in the world knows how to get you to 100% recovery. I had minor left neglect which spontaneously recovered.
A new University of Liverpool study, published today in Wiley Brain and Behaviour, examines the wide range of visual impairments developed by stroke survivors.
Approximately 65% of acute stroke survivors have visual impairment which typically relates to impaired central or peripheral vision, eye movement abnormalities, or visual perceptual defects.
Symptoms can include blurred or altered vision, double or jumbled vision, loss of visual field, reading difficulty, inability to recognize familiar objects or people and glare.
Post stroke visual impairment (PSVI) is currently an under researched area. However the full range of impairments is currently unknown.
915 post-stroke patients
In order to profile the full range of visual disorders researchers from the University’s Department of Health Services Research, led by Dr Fiona Rowe, examined the visual impairment screening/referral forms from 915 post-stroke patients from 20 NHS hospital trusts.
The researchers found that the average number of days post-stroke onset before a visual assessment was conducted was 22.
Once assessed 92% were confirmed to have a visual impairment, of these:
•         24% had reduced clarity of vision (central visual acuity)
•         16% percent of those with a visual impairment had developed a squint (strabismus)
•         68% had impairments to the way their eye or eyes moved (ocular motility disorders)
•         Peripheral visual field loss was present in 52%
•         15% had developed a condition causing them to ignore everything on one side of their visual world. The condition, known as visual inattention, usually affects people who have had a right sided stroke and they ignore things on their left side
Overall 84% were visually symptomatic with visual field loss the most common complaint followed by blurred vision, reading difficulty, and diplopia.
Wide range of disorders
Treatment options were provided to all with confirmed visual impairment. Targeted advice was most commonly provided along with refraction, prisms, and occlusion.
Of the research Dr Rowe, said: “There are a wide range of visual disorders that occur following stroke and, frequently, with visual symptoms. There are equally a wide variety of treatment options available for these individuals.
“Our research highlights the fact that ALL stroke survivors require early screening for visual impairment and warrant referral for specialist assessment and targeted treatment specific to the type of visual impairment.”
The full paper, entitled ‘Vision In Stroke cohort: Profile overview of visual impairment’, can be found here.
DOI: 10.1002/brb3.771

Warrington South MP Faisal Rashid raises 'serious concerns' over future of stroke care in letter to Jeremy Hunt

YOU have to scream at this guy for the totally wrong focus. RESULTS not 'care'. 
WARRINGTON South MP Faisal Rashid has expressed ‘serious concerns’ over the future of stroke care.
The national 10-year stroke strategy will end in December, with Mr Rashid recently meeting with stroke survivors and carers – who expressed the need for a new place for the next decade.
Mr Rashid has now written a letter to the secretary of state for health Jeremy Hunt, in which he raises ‘serious concerns’ over the future of stroke care across the UK.
In the letter, he said: “I am sure you will be aware that there are over 1.2m stroke survivors in the UK, and that 45 per cent of stroke survivors in England feel abandoned after they leave hospital.
“This is a deeply troubling statistic that highlights the need for improvements to stroke care across the UK.
“I represent 1,800 stroke survivors in Warrington South and recently met with my local Stroke Action Group, made up of stroke carers and survivors who shared their experiences and concerns with me.
“Many of these people acknowledged the improvements in stroke care since the implementation of the national stroke strategy, but remain concerned about the variation in stroke care across the country and have serious concerns about the future of stroke care – especially when the national stroke strategy comes to an end in December.
“I would therefore like to ask for your assurances for my constituents – and the 1.2m other stroke survivors in the UK – that ministers in your department are taking action to replace the national stroke strategy and ask what conversations have been had between the department of health and the NHS in regards to the future of stroke care in the UK.”

Magic Mushrooms “Reset” Key Brain Circuits in Depressed People

Well, nothing has come of these earlier reports on magic mushrooms. If we can't even legalize marijuana mushrooms will never get there either. Don't do this, there is NO proof it works or any amount or purity available.

Eat more mushrooms if you want to avoid dementia  Jan. 2017 

Edible and medicinal mushrooms show potential to mitigate neurodegenerative diseases  Feb. 2017 

How Magic Mushrooms Affect Your Brain: From Higher Levels Of Awareness To Hallucinations   March 2015
Psychedelics like lysergic acid diethylamide (LSD) and psilocybin are popular for their use as party drugs, but less so for what researchers claim to be their therapeutic effects — which has been a major focus for a number of clinical trials in the last decade. Magic mushrooms, for example, have been the focus of some recent work that saw how it could help with treating some of the symptoms of clinical depression. For instance, a study from the U.S. last year showed how a single does of psilocybin can lift anxiety and depression felt by cancer patients.
Now, scientists from the Imperial College London have found how psilocybin, which is the active psychedelic compound that occurs naturally in magic mushrooms, can “reset” brain activity in patients suffering from depression. Their study, which was published in the journal Scientific Reports on Friday, highlights how psilocybin gave patients a “kick start” in fighting clinical depression.
psychadelics magic mushrooms psilocybin mental health
Image credit: Robin Carhart-Harris/Imperial College London
The researchers at Imperial gave two doses (10 mg and 25 mg) of psilocybin, with a week in between each dose, to 20 patients with a treatment-resistant form of depression. Immediately after receiving the doses, the patients said they felt a decrease in depressive symptoms, which MRI scans of their brains revealed to have been due to a reduce in blood flow to areas involved in handling emotional responses, stress, and fear.

Rebooting Through Depression with Magic Mushrooms

In short, the patients experienced a sort of reboot. “We have shown for the first time clear changes in brain activity in depressed people treated with psilocybin after failing to respond to conventional treatments,” Robin Carhart-Harris, head of Psychedelic Research — there’s such a thing — at Imperial, said in a press release. “Several of our patients described feeling ‘reset’ after the treatment and often used computer analogies. For example, one said he felt like his brain had been ‘defragged’ like a computer hard drive, and another said he felt ‘rebooted’.”

It would seem that during the drug “trip,” brain networks went through an initial disintegration that was followed by a re-integration afterwards, when the patients “come down” from the psychedelic. “Psilocybin may be giving these individuals the temporary ‘kick start’ they need to break out of their depressive states and these imaging results do tentatively support a ‘reset’ analogy. Similar brain effects to these have been seen with electroconvulsive therapy,” Carhart-Harris added.
The researchers acknowledged, however, that while their study provides a new window into the brains of people who’ve taken psychedelics, the small number of patients tested and the absence of a control/placebo group limits the significance of their study. “Larger studies are needed to see if this positive effect can be reproduced in more patients,” said senior author David Nutt, director of the Neuropsychopharmacology unit of the Brain Sciences division at Imperial. “But these initial findings are exciting and provide another treatment avenue to explore.” The researchers also warned against self-medicating using such psychedelics.

Clinician’s Guide to Aerobic Exercise after Stroke - Canadian Partnership for Stroke Recovery

Fairly useless since it is still only guidelines NOT protocols with efficacy ratings/. I expect exact numbers of exercises needed for various types of recovery. These guidelines still allow doctors to blame the survivors for not recovering. When if we don't recover that doctor would then update the stroke protocol for that particular objective damage diagnosis. This is so fucking simple to solve. Why can'r Drs. and Ph.Ds. get this?
Clinician’s Guide to Aerobic Exercise after Stroke

Sunday, October 15, 2017

Experimental device stimulates the tongue to improve stroke survivors’ balance

Pretty cool, where can I buy it?

AN experimental device that stimulates the brain with electrical currents via nerves in the tongue has been used to improve balance in stroke survivors for the first time.
Patients in the small Royal Melbourne Hospital pilot study used the device, which feels like having a fizzy drink in the mouth, while undertaking intensive rehabilitation ­exercises.
The hospital’s director of rehabilitation, Professor Fary Khan, said stroke was a leading cause of disability in Australian adults.
Rehabilitation helps them relearn lost abilities by taking advantage of the brain’s neuroplasticity — its ability to reorganise itself and form new pathways.
“There has been a lot of focus on trying to enhance the neuroplasticity of the brain by stimulating it,” said academic director of the Australian Rehabilitation Research Centre at the hospital, Professor Mary Galea.

Unlike other techniques that use magnetic and electrical stimulation via the head, this device from the US targets two cranial nerves running from the tongue to the brain.
The trigeminal and facial nerves are involved with chewing and facial expression, but they are close to nerve cells in the brain crucial to walking and balance.
“The device modulates the excitability of the circulation of the brain, enhancing or dampening it,” Prof Galea said.
It is believed that this technique improves the learning process when combined with repetitive targeted exercise.
In the pilot study, the 10 stroke victims had intensive rehabilitation, but half of the group also used the device.
“Adding this stimulation did improve people’s balance more than just physiotherapy by itself,” Prof Galea said.

There were no adverse events and the device was able to be integrated into the rehabilitation program.
Limitations of the study include that the patients were only followed for two weeks and that the sample size was small.
Professors Khan and Galea — both also of the University of Melbourne — said the findings of the trial, which was funded by a philanthropic ­don­ation, should prompt a larger randomised control study.
“Our results are very interesting and point to its potential in stroke patients, but we need larger and longer trials,” Prof Galea said.
Currently, the device is not approved or available for use in patients anywhere in the world.
The findings were published in the journal, Brain Stimulation.

VR could trick stroke victims' brains toward recovery

With 83 posts on virtual reality back to September, 2011 why the fucking hell is more research needed? You don't follow research in your field? Your mentor/senior researcher incompetently doesn't know about previous research?

Virtual reality proof of efficacy has been out there for years now. Somebody write up a fucking protocol, that might be the only way stroke departments will ever get it. Why is everyone WAITING FOR SOMEONE ELSE TO SOLVE THE PROBLEM? 

Dammed lazy assholes.
Researchers at the University of Southern California are examining how virtual reality could promote brain plasticity and recovery.
Could virtual reality help stroke survivors regain motor function?
That's a question Sook-Lei Liew is looking to answer.
Liew, an assistant professor at the University of Southern California and an affiliate of the Stevens Neuroimaging and Informatics Institute at the Keck School of Medicine, was inspired by research from Mel Slater and Jeremy Bailenson on embodiment in VR. If someone's given a child's body in VR, for example, they might start exhibiting more childlike behavior.
She wondered if giving stroke survivors with motor impairments a virtual avatar that moves properly could help promote brain plasticity (or the ability to change) and recovery. Maybe it would eventually lead to them to moving an impaired limb again.


"So, kind of like tricking the brain through visual input," said Liew, who is also director of the Neural Plasticity and Neurorehabilitation Laboratory. "There's a lot of emerging evidence from neuroscience and psychology that was showing that you can really identify [with the avatar], and it changes your behavior based on the avatar you're given in VR."
Virtual reality is a computer-generated simulation of a 3D environment. Using a VR headset with lenses that feed images to the eyes, a person can be virtually transported to another location, or interact with a setting in a seemingly realistic way. It's commonly been used in gaming, but it's being tested in other environments, too -- like rehab.
Implementing VR in health care and patient treatment isn't new. It's been used to help people overcome phobias and anxiety disorders. But the application is starting to take off now that the technology is more developed and commercially available. Some medical schools are looking to train students with virtual simulations, and it's even helping midwives learn how to deliver babies.
Liew's research team has been working on a study for about two years called REINVENT, an acronym for Rehabilitation Environment using the Integration of Neuromuscular-based Virtual Enhancements for Neural Training. The researchers also collaborated with the USC Institute for Creative Technologies to develop the prototype.
The process works by using a brain-computer interface, which takes a signal from the brain and uses it to control another device: a computer, a robot or, in REINVENT's case, an avatar in VR.
Next, researchers read electrical signatures of brain activity from the surface of the scalp using electroencephalography, or EEG, for short. The team also uses electromyography, which studies the electrical activity of the muscles. That can tell them whether somebody's moving or if they're trying to move.
Those signals are then fed into a program on a laptop. The program has thresholds so that when specific signals in the brain or muscle activity that correspond to an attempt to move are detected, they drive the movement of a virtual arm. The resulting visual feedback through a VR headset could help strengthen neural pathways from the damaged motor cortex to the impaired arm or limb.
While the researchers could theoretically extend this process to a patient's lower limbs, Liew said it can be dangerous for someone with a motor impairment in the lower extremities to try to move with VR, so seated studies are much safer.
The research group recently finished testing the prototype using an Oculus DK2 with 22 healthy older adults, who provided a sample of what the brain and muscle signals look like when they move. They're now starting to test with stroke patients in a controlled lab setting, aiming to work with 10 in the short term and hundreds in the long term, in both clinical and home environments.
The team also found that giving people neurofeedback of the virtual arm moving in a VR headset was more effective than simply showing it on a screen.
"Their brain activity in the motor regions that we're trying to target is higher, and they're able to control the brain-computer interface a little bit better and faster," Liew said. "It makes the case that there is an added benefit from doing this in virtual reality, which is one of the first things we wanted to know."

An unclear future

Because VR is still a relatively new technology, there are many unanswered questions on the best ways to use it in the medical profession.
"For the most part, nobody knows how to make great VR experiences, for business or consumer," Gartner analyst Brian Blau said. "Over time, those issues will get resolved. But for the medical industry, they have the extra added bonus of having even more types of physical behaviors that they have to either mimic or want to measure."
And while the possibilities for VR in health care are exciting, Liew is careful not to get ahead of herself.
"We think that VR is a promising medium, but we're moving ahead cautiously," she said. "A lot of the work that we're trying to do is to test assumptions, because there's a lot of excitement about VR, but there's not that much that's scientifically known."
Only time -- and plenty of research -- will tell.

Blinded by proximity - Stroke leaders are prime examples

Everyone around stroke thinks the same, tPA is the solution to all and everything else is just prevention press releases. I know of no stroke bloggers that are contacted by any stroke leaders to see what survivors think. 

This is proven by this fuckingly stupid meme from World Stroke Day 2016.

Seth Godin - Look Around

Proximity matters a great deal.
Detroit car executives in the 1970s and 1980s consistently failed to respond to the threat from Japanese imports. They weren't merely arrogant—they were blinded by proximity. Everyone in their neighborhood, everyone on their commute, everyone in their parking lot was driving an American car. How could there be a problem?
We define the universe around us as normal. It's one of the only ways to stay sane—we assume that the noise in our head is in the head of other people, that what we yearn for or buy is what others do as well. And we look to the world around us for confirmation.
This truth can take us to two insights:
  1. if you want to understand what part of the world is really like, you should make special efforts to surround yourself with that world. If you market to bodegas, consider taking an apartment upstairs from a bodega.
  2. there's a huge bonus to being famous to the family. If you can be locally dominant, the locals will instinctively decide that you are globally dominant. Have 100 customers in one neighborhood (virtual or real) is worth much much more than having one customer in each of 100 neighborhoods.


A dietary supplement dampens the brain hyperexcitability seen in seizures or epilepsy

You'll have to bring this to your doctors attention if you are in this cohort; seizures occur in about 10% of stroke patients. 
Or maybe you want this:

Cannabidiol May Reduce Seizures by Half in Hard-to-treat Epilepsy

Or maybe the nasal spray referred to in here:

Preventing Seizure-Caused Damage to the Brain

The answers are out there, does your doctor know about them?


A dietary supplement dampens the brain hyperexcitability seen in seizures or epilepsy 

Seizure disorders—including epilepsy—are associated with pathological hyperexcitability in brain neurons. Unfortunately, there are limited available treatments that can prevent this hyperexcitability. However, University of Alabama at Birmingham researchers have found that inducing a biochemical alteration in brain proteins via the dietary supplement glucosamine was able to rapidly dampen that pathological hyperexcitability in rat and mouse models.
These results represent a potentially novel therapeutic target for the treatment of seizure disorders, and they show the need to better understand the physiology underlying these neural and brain circuit changes.
Proteins are the workhorses of living cells, and their activities are tightly and rapidly regulated in responses to changing conditions. Adding or removing a phosphoryl group to proteins is a well-known regulator for many proteins, and it is estimated that human proteins may have as many as 230,000 sites for phosphorylation.
A lesser-known regulation comes from the addition or removal of N-acetylglucosamine to proteins, which is usually controlled by glucose, the primary fuel for neurons. Several years ago, neuroscientist Lori McMahon, Ph.D., professor of cell, developmental and integrative biology at UAB, found out from her colleague John Chatham, D.Phil., a UAB professor of pathology and a cardiac physiologist, that brain cells had the second-highest amounts of proteins with N-acetylglucosamine, or O-GlcNAcylation, in the body.
At the time, very little was known about how O-GlcNAcylation might affect brain function, so McMahon and Chatham started working together. In 2014, McMahon and Chatham, in a study led by graduate student Erica Taylor and colleagues, reported that acute increases in O-GlcNAcylation caused long-term synaptic depression, a reduction in neuronal synaptic strength, in the hippocampus of the brain. This was the first time acute changes in O-GlcNAcylation of neuronal proteins were shown to directly change synaptic function.
Since neural excitability in the hippocampus is a key feature of seizures and epilepsy, they hypothesized that acutely increasing protein O-GlcNAcylation might dampen the pathological hyperexcitability associated with these brain disorders.
That turned out to be the case, as reported in the Journal of Neuroscience study, "Acute increases in protein O-GlcNAcylation dampen epileptiform activity in hippocampus." The study was led by corresponding author McMahon and first author Luke Stewart, a doctoral student in the Neuroscience Theme of the Graduate Biomedical Sciences Program. Stewart is co-mentored by McMahon and Chatham.
"Our findings support the conclusion that protein O-GlcNAcylation is a regulator of neuronal excitability, and it represents a promising target for further research on seizure disorder therapeutics," they wrote in their research significance statement. The researchers caution that the mechanism underlying the dampening is likely to be complex.
Research details
Glucose, the major fuel for neurons, also controls the levels of protein O-GlcNAcylation on proteins. However, high levels of the dietary supplement glucosamine, or an inhibitor of the enzyme that removes O-GlcNAcylation, leads to rapid increases in O-GlcNAc levels.
In experiments with hippocampal brain slices treated to induce a stable and ongoing hyperexcitability, UAB researchers found that an acute increase in protein O-GlcNAcylation significantly decreased the sudden bursts of electrical activity known as epileptiform activity in area CA1 of the hippocampus. An increased protein O-GlcNAcylation in normal cells also protected against a later induction of drug-induced hyperexcitability.
The effects were seen in slices treated with both glucosamine and an inhibitor of the enzyme that removes O-GlcNAc groups. They also found that treatment with glucosamine alone for as short a time as 10 minutes was able to dampen ongoing drug-induced hyperexcitability.
In common with the long-term synaptic depression provoked by increased O-GlcNAcylation, the dampening of hyperexcitability required the GluA2 subunit of the AMPA receptor, which is a glutamate-gated ion channel responsible for fast synaptic transmission in the brain. This finding suggested a conserved mechanism for the two changes provoked by increased O-GlcNAcylation—synaptic depression and dampening of hyperexcitability.
The researchers also found that the spontaneous firing of in another region of hippocampus, area CA3, was reduced by increased O-GlcNAcylation in normal brain slices and in slices with drug-induced hyperexcitability. This reduction in spontaneous firing of CA3 pyramidal neurons likely contributes to decreased hyperexcitability in area CA1 since the CA3 neurons directly excite those in CA1.
Similar to the findings for brain slices, mice that were treated to increase O-GlcNAcylation before getting drug-induced hyperexcitability had fewer of the brain activity spikes associated with epilepsy that are called interictal spikes. Several drug-induced hyperexcitable mice had convulsive seizures during the experiments—this occurred in both the increased O-GlcNAcylation mice and the control mice. Brain activity during the seizures differed between these two groups: The peak power of the activity for the mice with increased O-GlcNAcylation occurred at a lower frequency, as compared with the control mice.
More information: Luke T. Stewart et al, Acute Increases in Protein O-GlcNAcylation Dampen Epileptiform Activity in Hippocampus, The Journal of Neuroscience (2017). DOI: 10.1523/JNEUROSCI.0173-16.2017

Journal reference: Journal of Neuroscience search and more info website
Provided by: University of Alabama at Birmingham search and more info website

A Little Wine Can Protect, But a Double Can Double Dementia

The four questions in CAGE are all NO for me. I actually consider alcohol to be the great social engagement lubricant, and stroke survivors needs lots of social interaction to prevent dementia.
It's well known that a little red wine each day lowers dementia risk. But just how bad is overdoing it? This study of 6,000 adults over 8 years may shock you.

A study published in the American Journal of Geriatric Psychiatry indicates that middle-aged adults with a history of problem drinking are more than twice as likely to suffer from severe memory impairment in later life.

The study highlights the hitherto largely unknown link between harmful patterns of alcohol consumption and problems with memory later in life -- problems which may place people at a high risk of developing dementia.

The study was carried out by researchers from the University of Exeter Medical School with support from the NIHR Collaboration for Leadership in Applied Health Research and Care South West Peninsula (NIHR PenCLAHRC).

AUD (Alcohol Use Disorder)

The research team studied the association between a history of alcohol use disorders (AUDs) and the onset of severe cognitive and memory impairment in 6542 middle-aged adults. These individuals participated in the Health and Retirement Study in the US over a span of 8 years.

A history of AUDs was identified using the CAGE* questionnaire (short for Cut down, Annoyed, Guilty, Eye-opener). Where participants registered a history of AUDs their chances of developing severe memory impairment more than doubled.

The study was led by Dr Iain Lang. He commented: "We already know there is an association between dementia risk and levels of current alcohol consumption -- that understanding is based on asking older people how much they drink and then observing whether they develop problems. But this is only one part of the puzzle and we know little about the consequences of alcohol consumption earlier in life. What we did here is investigate the relatively unknown association between having a drinking problem at any point in life and experiencing problems with memory later in life."

3 Points

He added: "This finding -- that middle-aged people with a history of problem drinking more than double their chances of memory impairment when they are older -- suggests three things: that this is a public health issue that needs to be addressed; that more research is required to investigate the potential harms associated with alcohol consumption throughout life; and that the CAGE questionnaire may offer doctors a practical way to identify those at risk of memory/cognitive impairment and who may benefit from help to tackle their relationship with alcohol."

Dr Doug Brown, Director of Research and Development at Alzheimer's Society said:

'When we talk about drinking too much, the media often focuses on young people ending up in A&E after a night out. However, there's also a hidden cost of alcohol abuse given the mounting evidence that alcohol abuse can also impact on cognition later in life. This small study shows that people who admitted to alcohol abuse at some point in their lives were twice as likely to have severe memory problems, and as the research relied on self-reporting that number may be even higher.

This isn't to say that people need to abstain from alcohol altogether. As well as eating a healthy diet, not smoking and maintaining a healthy weight, the odd glass of red wine could even help reduce your risk of developing dementia.'


* The CAGE asks four questions (and the acronym comes from words in each question: Cut down, Annoyed, Guilty, Eye-opener):
  1. Have you ever felt you should cut down on your drinking?
  2. Have people annoyed you by criticizing your drinking?
  3. Have you ever felt bad or guilty about your drinking?
  4. Have you ever had a drink first thing in the morning to steady your nerves or get rid of a hangover (eye-opener)?


University of Exeter

F18 Scans Diagnose Dementia Better

What is your doctor doing to rule out or confirm dementia? ANYTHING AT ALL?
You need to know. Lots of words used here so you can't even tell how accurate it is. 

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. 
At $3,000 per scan, are F18 Scans worth it? They let doctors see plaque in the brain, the main suspect behind Alzheimer's. They show doctors if, where and how much plaque there is. They can sharpen an Alzheimer's diagnosis or rule it out completely. Learn how F18 Scans improve care and diagnosis.

INDIANAPOLIS -- Eli Lilly released important data showing that F18 beta-amyloid imaging was associated with better diagnosis and management of patients with dementia.

There are over 100 tpyes of dementia. Some are curable, some demand different treatments than others. The differences in treatment can be critical.

The most common type of dementia is Alzheimer's disease. It is so common that it is common for doctors to diagnose a patient with Alzheimer's when they really have a different type of dementia. This can lead to ineffective or even dangerous treatments. Furthermore, even when a person has Alzheimer's, it is challenging to treat it. Doctors usually base the medications they prescribe, as well as recommended treatments, on a somewhat subjective judgement call referred to as a "clinical diagnosis".

With new F18 scanning technologies, doctors can actually "see" how much Alzheimer's plaque is in a person's brain, if any. They now have an objective tool to help them dramatically sharpen their diagnosis.

To see an invterview of a patient who benefitted from an F18 Scan after he was diagnosed with dementia, watch the video,
"F18 Alzheimer's Scan Delivers Better Prescriptions & Fewer Tests".

In this latest study from Ely Lilly, change in management  was observed in both patients who met and did not meet the Appropriate Use Criteria (AUC), which were developed by the Society of Nuclear Medicine and Molecular Imaging and the Alzheimer's Association to provide guidance on which patients are most appropriate for imaging and how best to use the results. These data were presented at the Alzheimer's Association International Conference (AAIC) by Andrew Siderowf, M.D., MSCE, medical director, Avid Radiopharmaceuticals, a subsidiary of Lilly.

"This study included patients in which there was diagnostic uncertainty by the treating physician and found that changes in diagnosis and management of Alzheimer's disease did not vary between patients depending on whether they met the Appropriate Use Criteria or not. In addition, analysis of beta-amyloid scans conducted post-diagnosis indicated that many patients being treated with medications may have potentially been misdiagnosed and inappropriately treated," said Dr. Siderowf. "While we support the development of the Appropriate Use Criteria, one of the clearest insights resulting from these data is that we need to continue to fine tune our understanding of the appropriate use of these tools and their utility for patients facing a diagnosis of Alzheimer's disease."

The objective of the study was to evaluate which patients are most likely to receive different care if they had an amyloid PET scan as part of their diagnostic work-up. In particular, the study evaluated if patients who met the working definition of the AUC would be more affected than those who did not. The AUC guidelines propose that patients who are being evaluated for dementia with atypical presentations, younger patients, and patients with unexplained mild cognitive impairment, are most appropriate for amyloid PET imaging. For the patient to be included in the study, Alzheimer's disease had to be under consideration and the treating physician had to have uncertainty regarding the diagnosis.
Results showed that 59 percent of subjects met the working definition of AUC. Forty-seven percent of the AUC-like cases were amyloid positive compared to 62 percent of non-AUC cases. Diagnosis changed after PET scan for 58 percent of AUC cases versus 45 percent of non-AUC cases (p=0.10). The proportion of patients with change in management plan was high for both AUC (88 percent) and non-AUC (77 percent) cases. In particular, the use of Alzheimer's disease medications including cholinesterase inhibitors, or memantine, declined after a negative florbetapir F 18 scan by 20 percent (from 26/54 to 15/54 cases; p=0.002) in AUC cases and by 33 percent (from 17/27 to 8/27 cases; p=0.004) in non-AUC cases. Diagnoses for non-AUC cases in which Alzheimer's disease medications were withdrawn after a negative scan included prodromal Alzheimer's disease/mild cognitive impairment due to Alzheimer's disease (n=8), or mild cognitive impairment of uncertain etiology (n=1). This study found that patients with an uncertain diagnosis, but who are not otherwise explicitly captured by AUC, may be reasonable candidates for amyloid imaging.

"Alzheimer's disease is one of many possible causes of cognitive impairment, which can make diagnosis challenging. In fact, it is estimated that up to one in five patients clinically diagnosed with probable Alzheimer's disease during life do not exhibit Alzheimer's disease pathology upon autopsy[1],[2]," said Dr. Siderowf. "These results reinforce how knowledge of the presence or absence of amyloid pathology can substantially affect both diagnosis and management in these patients being evaluated for Alzheimer's disease or other possible causes of cognitive decline."


Study Methods
The impact of amyloid PET on actual patient care was examined in a previous study.[3]

In the prior study, performed at 19 clinical sites, treating physicians provided a provisional diagnosis and management plan prior to receiving results of amyloid PET imaging with florbetapir F 18. Participants' medical records for the three months immediately after imaging were abstracted to capture their actual diagnosis and management. For the current study, participants were classified as meeting an operational definition of AUC-like or not, based on pre-scan diagnosis and demographic features.

About Florbetapir F 18 Injection[6]
Florbetapir F 18 is indicated for Positron Emission Tomography (PET) imaging of the brain to estimate beta-amyloid neuritic plaque density in adult patients with cognitive impairment who are being evaluated for Alzheimer's Disease (AD) and other causes of cognitive decline. A negative florbetapir F 18 scan indicates sparse to no neuritic plaques and is inconsistent with a neuropathological diagnosis of AD at the time of image acquisition; a negative scan result reduces the likelihood that a patient's cognitive impairment is due to AD. A positive florbetapir F 18 scan indicates moderate to frequent amyloid neuritic plaques; neuropathological examination has shown this amount of amyloid neuritic plaque is present in patients with AD, but may also be present in patients with other types of neurologic conditions as well as older people with normal cognition. Florbetapir F 18 is an adjunct to other diagnostic evaluations.

Limitations of Use:
  • A positive florbetapir F 18 scan does not establish a diagnosis of AD or other cognitive disorder
  • Safety and effectiveness of florbetapir F 18 have not been established for:
    • Predicting development of dementia or other neurologic condition
    • Monitoring responses to therapies

Risk for Image Misinterpretation and Other Errors
  • Errors may occur in the florbetapir F 18 estimation of brain neuritic plaque density during image interpretation
  • Image interpretation should be performed independently of the patient's clinical information. The use of clinical information in the interpretation of florbetapir F 18 images has not been evaluated and may lead to errors. Other errors may be due to extensive brain atrophy that limits the ability to distinguish gray and white matter on the florbetapir F 18 scan as well as motion artifacts that distort the image
  • Florbetapir F 18 scan results are indicative of the brain neuritic amyloid plaque content only at the time of image acquisition and a negative scan result does not preclude the development of brain amyloid in the future
Radiation Risk
  • Florbetapir F 18, similar to other radiopharmaceuticals, contributes to a patient's overall long‐term cumulative radiation exposure. Long-term cumulative radiation exposure is associated with an increased risk of cancer. Ensure safe handling to protect patients and health care workers from unintentional radiation exposure
  • The most common adverse reactions reported in clinical trials were headache (1.8%), musculoskeletal pain (0.7%), blood pressure increased (0.7%), nausea (0.7%), fatigue (0.5%), and injection site reaction (0.5%)
For more information about florbetapir F 18, please see the Prescribing Information at

About Eli Lilly and Company
Lilly is a global healthcare leader that unites caring with discovery to make life better for people around the world. We were founded more than a century ago by a man committed to creating high-quality medicines that meet real needs, and today we remain true to that mission in all our work. Across the globe, Lilly employees work to discover and bring life-changing medicines to those who need them, improve the understanding and management of disease, and give back to communities through philanthropy and volunteerism. To learn more about Lilly, please visit us at and

Amyvid™ is a trademark of Eli Lilly and Company.

[1] Petrovitch H, White LR, Ross GW, et al. Accuracy of clinical criteria for AD in the Honolulu-Asia Aging Study, a population-based study. Neurology. 2001;57(2):226–234.
[2] Lim A, Tsuang D, Kukull W, et al. Clinico-neuropathological correlation of Alzheimer's disease in a community-based case series. J Am Geriatr Soc. 1999;47(5):564–569.
[3] Grundman M, Pontecorvo MJ, Salloway SP, et al. Potential impact of amyloid imaging on diagnosis and intended management in patients with progressive cognitive decline. Alzheimer Dis Assoc Disord. 2013 Jan;27(1):4-15.
[4] Alzheimer's Association. 2014 Alzheimer's Disease Facts and Figures. Accessed on June 4, 2014.
[5] Alzheimer's Disease International. Policy Brief for Heads of Government: The Global Impact of Dementia 2013 - 2050. Published December 2013. Accessed onJune 4, 2014.
[6] Amyvid [package insert]. Indianapolis, IN: Lilly USA, LLC; 2012.

Saturday, October 14, 2017

Nanotherapeutics for Gene Modulation that Prevents Apoptosis in the Brain and Fatal Neuroinflammation

Stopping apoptosis and neuroinflammation sounds wonderful for stroke survivors. Now if we only had a stroke leader we could ask to follow this up with translational protocols.


The failure of therapeutic agents to cross the blood-brain barrier (BBB) has been a major impediment in the treatment of neurological disorders and brain tumors. We have addressed this issue using an immunoliposome nanocomplex (designated scL) that delivers therapeutic nucleic acids across the BBB into the deep brain via transcytosis mediated by transferrin receptors. We validated brain delivery of payloads after systemic administration by monitoring uptake of fluorescently labeled payloads and by confirming up- or down-modulation of specific target gene expression in the brain, mainly in neuronal cells. As proof of concept for the therapeutic potential of our delivery system, we employed scL delivering an siRNA targeting tumor necrosis factor alpha to suppress neuroinflammation and neuronal apoptosis and to protect mice in lethal endotoxemia triggered by bacterial lipopolysaccharide. Brain delivery of therapeutic payloads via scL has major implications for the development of treatments for neurological disorders and brain tumors.
Choose an option to locate/access this article:
Check if you have access through your login credentials or your institution
Check Access

Corresponding author Esther H Chang, Department of Oncology, Georgetown University Medical Center, Lombardi Comprehensive Cancer Center, 3970 Reservoir Rd NW, TRB/E420, Washington, DC 20057-1468, USA. Phone: 202-687-8418, Fax: 202-687-8434.

The status quo is not kind. It works overtime to stay the status quo, and that means that new ideas, urgent pleas and cries for justice are rarely easily voiced.

Our stroke medical world is so enamored of the status quo because they don't have to do one damn thing. It is nice safe and quiet when your head is stuck up your ass. SO SPEAK UP AND TELL YOUR DOCTOR AND STROKE HOSPITAL THEY ARE COMPLETELY FAILING SURVIVORS!
From Seth Godin.

On speaking up

The status quo is not kind. It works overtime to stay the status quo, and that means that new ideas, urgent pleas and cries for justice are rarely easily voiced.
We're pleased that Annie Kenney stood up for a woman's right to vote all those years ago, even if she got arrested for doing so. And we're proud of Elijah Harper, who brought a debate to a standstill when he stood up for the rights of indigenous people. We're glad that Lois Gibbs stood up to fight for the families near Love Canal, and that Rachel Carson was able to save countless lives by blowing the whistle on how we were poisoning ourselves.
The historical examples are pretty much beyond dispute. When we think about the past, our heroes are those that were willing to persist even when their critics tried to silence them.
Where it becomes challenging is when someone around us chooses to speak up. Today. Now.
It might be someone in HR who risks his job to report the boss to the board. Or it might be an unlikely activist, standing up for a cause that wasn't on our radar. It might be someone in accounting who has found a better way to do things, or an unknown with no power or authority who stands up and says, "follow me."
We can't judge those that challenge the status quo merely on their rule breaking. Because the rules only exist to maintain the status quo.
Instead, we have to work ever harder on seeing, listening and supporting the quiet voices who have something important to say. Perhaps, if we listen a bit harder, we'll be able to do the right thing that much sooner.

Eating This One Food Every Day Could Prevent Heart Attacks and Strokes - bananas

Well fuck, this has been known for years. So for 5 years your doctor has been incompetent in not giving you a diet protocol with potassium in it.  And just why the fuck was this research needed? You are so fucking incompetent that you don't keep up with research in your field?

Why eat three bananas a day?    April 2012

Eating This One Food Every Day Could Prevent Heart Attacks and Strokes

You may know the silent signs of a heart attack or stroke, but preventing one is another beast altogether. Although exercise and sleep are great habits that reduce your risk, few people have the time to fit both into their crazy schedules. Thankfully, adding one simple thing to your plate could be just as effective—but way less time-consuming.
Researchers at the University of Alabama have found that eating bananas every day could help prevent heart attacks and strokes. Their study, which aimed to determine how the mineral potassium affects blood flow and artery health, examined mice who received a diet containing either low, normal, or high levels of potassium.
Overall, mice given a low-potassium diet had much harder arteries than their counterparts. Mice who received high levels of potassium, on the other hand, showed significantly less artery hardening and reduced stiffness in their aorta, as well.
Previous studies have found that potassium can lower blood pressure, but this is among the first to investigate the mineral’s impact on artery health. According to experts, potassium improves your heart’s function by regulating your heartbeat, digesting carbohydrates, and building muscle. The combination of these perks could do wonders for your arteries, preventing heart disease and strokes down the road.
Now, researchers hope to test the effects of a high-potassium diet on humans, as well. 'With more research, we might be able to see if the disease forms in humans in a similar way and develop treatments,' Dr. Mike Knapton, associate medical director for the British Heart Foundation, told The Sun.
You’ll have to work hard to get your daily recommended intake of potassium, though. The National Institute of Health recommends that adults consume about 3,500 mg of potassium per day. While bananas will certainly do the trick, shake up your diet every once in a while with any of these 10 foods with more potassium than a banana.
[Source: The Independent]