Jun 17, 2016

Nine Years Later, Post Polio Aggravation

Barbara, a 54 year old woman, called in a crisis. She had unbearable stabbing and piecing pain in both hips and had exhausted all her options. During her follow-up consult, she talked about seeing a doctor, going back on codeine and into a wheelchair, as she had been nine years ago. “There is a black cloud hanging over us,” she sighed. She saw no alternative.
Nine years ago, I had been consulted by her for post polio syndrome. Over time, using multiple daily remedies and many clearing remedies, we had successfully gotten her out of the wheelchair, off pain medications and moving freely with virtually no pain or discomfort. She had been suffering for more than 30 years at the time she consulted with me.
After this follow-up consult I told her I had to study the matter. In the mean time, she was to take MSG30C (a homeopathic remedy made from potentized Monosodium Glutamate, a food additive that is a potent neurotoxin), followed an hour later by Bryonia alba 30C. That evening at 8PM, the phone rang. It was Donna, sounding all choked up. My voicemail recorded the following message:
“You did it again, Dr. Mueller. I took the MSG, and an hour later the Bryonia,” she said with a voice full of emotion. “I fell asleep, and woke up, and there was no piercing pain, no excruciating pain, nothing.” She choked up. “I am myself again. Thank you…” She could not go on, so strong was her emotion, and hung up.
If you are interested in the full video testimonial from Barbara of her cure from Post-Polio Syndrome, please click here.

Post Polio Litaff, Association A.C _APPLAC Mexico

All Wheels Up Wants You to be Able to Stay in Your Wheelchair While Flying

By | June 6th, 2016

All-Wheels-UpThe advocacy group All Wheels Up thinks you should be able to stay in your wheelchair while you are flying, if that’s your preference. To reach this goal, the nonprofit is pushing for federal legislation to allow it, and also will begin crash testing wheelchairs to ensure flying while seated in one is safe.

First, the Legislation

The Federal Aviation Administration Reauthorization Act is wending its way through Congress, and this time around it contains four amendments addressing the disability community. One of those would require the Architectural and Transportation Barriers Compliance Board, in consultation with the DOT, to study how wheelchair users, both manual and power, could be accommodated with in-cabin restraints.
“We need everyone who uses a wheelchair or cares about someone who does to know about this bill,” said All Wheels Up Founder Michele Erwin. “If they want to fly in the safety of their wheelchairs, or want wheelchair accessible golf carts for gate transfers (another one of our projects), they need to reach out to their congressperson, tell them about this bill.”

Crash Testing Wheelchairs 

All Wheels Up has a contract to conduct the first ever crash test of wheelchairs testing airplane restraint systems at an FAA-approved aerospace facility. Erwin is optimistic these tests will go well, based on the results of previous wheelchair crash testing done by the restraint company Q’Straint.
“A large majority of the work and reports have already been conducted, regarding crash testing wheelchairs,” says Erwin. “The FAA would only need to expand on the research already done from Q’straint, whose restraining systems have passed the 20 G crash test, while all air craft passenger seats have only passed a 16 G crash test. Due to this study alone, the FAA is excited to work on the crash testing wheelchairs for commercial flight.”
Erwin will be speaking in Washington, D.C. this July where she hopes to garner more support from Congress and key disability organizations. She encourages everyone interested in this cause to get involved. “We are asking our followers to reach out to their congress people to pass the bill and tell them why these two sections are important to them.”

Jun 15, 2016

Researchers Block Action of Alzheimer’s Tau Protein in Mice


Summary: Researchers report a drug called phenylbutyrate may protect against damage caused by the tau protein in Alzheimer’s disease.
Source: Alzheimer’s Research UK.
A research team at King’s College London has used a new approach to study a hallmark dementia protein called tau in mice, revealing that a drug called phenyl butyrate can protect against damage caused by the protein.

The findings are published in the journal Brain and funded by Alzheimer’s Research UK and the Wellcome Trust.
One of the key hallmark features of Alzheimer’s is an abnormal build-up of a protein called tau in the brain, but there are several different neurodegenerative diseases that are caused by abnormal tau. These so-called ‘tauopathies’ can have a range of symptoms from memory and thinking problems to severe movement disorders.

The team, led by Dr Diane Hanger at the Maurice Wohl Clinical Research Institute, King’s College London, studied donated brain tissue from the London Neurodegenerative Diseases Brain Bank at King’s College London. They had previously identified a fragment of tau protein that was found in the brains of people with a tauopathy called progressive supranuclear palsy and wasn’t present in healthy brains.
They bred mice to produce low levels of this form of the tau protein, which they called Tau35. Despite only producing a relatively low level of the protein, the mice developed memory, thinking and movement problems that became progressively worse with age. The findings indicate the importance of the tau protein in orchestrating damage in the brain in diseases like Alzheimer’s. The researchers then studied the function of nerve cells in the mice in more detail. The study revealed that the tau fragment caused defects in how the cells get rid of unwanted or damaged proteins – one mechanism through which tau could damage nerve cells in the brain.

When the mice were eight and a half months old they started experiencing significant memory and motor symptoms. At this stage, they were treated daily for six weeks either with an injection of phenylbutyrate or sterile water as a control. Phenylbutyrate is a drug already used to treat urea cycle disorders – inherited metabolic disorders that affect how ammonia is removed from the bloodstream. Previous research had suggested the drug could target some aspects of Alzheimer’s in mice and it has also been explored in clinical studies for cancer, cystic fibrosis and neurodegenerative diseases like motor neurone disease and Huntington’s disease. After treatment with phenyl butyrate, the mice showed improvements to their memory and motor symptoms suggesting phenylbutyrate could rescue damage caused by the tau protein.

Dr Diane Hanger, said: “Tau protein is becoming an increasingly attractive target for the development of new medicines for dementia, because it’s central to several different neurodegenerative diseases including Alzheimer’s. This new approach to studying the effect of low levels of tau protein in mice helps us to recreate aspects of these diseases in a way that more closely represents what’s seen in patients. By studying these mice, we’re starting to identify key mechanisms driving damage in the brain and we hope that teams across the world can use this method to study these complex diseases and search for new treatments.”
Phenylbutyrate is a drug already being investigated for benefits in a range of conditions and it was interesting to see it may also have the potential to protect against damage caused by tau protein in mice. The findings are an important basis for future drug development studies to understand the mechanism through which phenylbutyrate may protect against neurodegeneration and whether this could point us towards new treatments. In future we’re keen to continue building on our new approach to learn more about the mechanisms driving neurodegeneration in these mice, with the aim of identifying promising targets for the development of new treatments.”
Image shows the tau protein.
After treatment with phenylbutyrate, the mice showed improvements to their memory and motor symptoms suggesting phenylbutyrate could rescue damage caused by the tau protein. NeuroscienceNews.com image is in the public domain.Dr Simon Ridley, Director of Research at Alzheimer’s Research UK, said: “The human brain is a hard-to-reach organ, making it difficult to study the molecular changes in diseases like Alzheimer’s in a living system. This study has allowed the research team to better understand how tau can damage cells in diseases like Alzheimer’s, as well as a range of other neurodegenerative diseases associated with the protein. It’s important to expand the tools researchers have to study the diseases that cause dementia, as they provide a way both to understand these diseases and to screen new drugs.
“While clinical trials in people will always be the gold standard to prove the benefit of any new drug for diseases like Alzheimer’s, research in mice is an important part of the drug development process. We must continue to invest in research to understand the biology of the different forms of dementias as well as using this to narrow down the most promising new therapeutic approaches to drive towards clinical trials.”
Funding: The study was funded by Alzheimer’s Research UK and the Wellcome Trust.
Source: Alzheimer’s Research UK 
Image Source: This NeuroscienceNews.com image is in the public domain.
Original Research: Full open access research for “Tauopathy induced by low level expression of a human brain-derived tau fragment in mice is rescued by phenylbutyrate” by Marie K. Bondulich, Tong Guo, Christopher Meehan, John Manion, Teresa Rodriguez Martin, Jacqueline C. Mitchell, Tibor Hortobagyi, Natalia Yankova, Virginie Stygelbout, Jean-Pierre Brion, Wendy Noble, and Diane P. Hanger in Brain. Published online June 12 016 doi:10.1093/brain/aww137
Post Polio Litaff, Association A.C _APPLAC Mexico

Survey of young patients with polio and a foreign background at a Swedish post-polio outpatient clinic

Original Article
pp 1-5
First online: 

Survey of young patients with polio and a foreign background at a Swedish post-polio outpatient clinic

  • Lars Werhagen 
  • Kristian Borg
Nowadays, polio survivors aged under 60 years are non-native Swedes which pose new aspects and challenges to a post-polio outpatient clinic. To analyze the medical data, walking aids, occupational, and family situation in non-native polio survivors aged less than 60 years at a Swedish post-polio outpatient clinic. Retrospective data analysis. Data were retrieved from medical records at the post-polio outpatient clinic. Actual age, age at acute polio infection, walking capacity, pain, concomitant diseases, working and family situation, and ethnical origin were analyzed. Data are presented in numbers and percentage. 153 patients were included. Mean age was 45 (17–60) years, and mean age at acute polio infection was 2 (0–12) years. Paresis of the lower extremities was the most common disability. 10 % were wheelchair dependent. Pain occurred in 70 % with a mean intensity of 55 measured with the visual analog scale. Hypertension was the most common concomitant disease. Half of the polio survivors were working at least part time, and roughly half were singles. Data were comparable with data earlier published in Swedish native polio survivors. Non-native polio survivors aged under 60 years showed similarities in age at acute polio infection, paresis, prevalence, and intensity of pain when compared with native Swedish polio survivors. They were, however, younger, and were less often working and married/cohabitants than native Swedish polio survivors. The results of this study underline the importance of social and vocational rehabilitation tailoring rehabilitation suitable for polio survivors with a foreign background.


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