Update from 5th Congress on MSA – April 27th 2016

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An update from the 5th Congress on MSA

globe-brain
At the 2016 International Congress on MSA, over 130 experts in the field came together for a 2-day intensive meeting in Salerno, Southern Italy. The congress faculty covered MSA from all angles with each speaker describing how advances in MSA research are shaping the way we now approach this degenerative brain disease. The scientific program took us from the bench to the bedside. It provided an update into why the brain cells die and how we might protect them to stop the progressive movement and balance impairment, together with loss of bladder and blood pressure control.

Pathogenesis

Culture_of_rat_brain_cells_stained_with_antibody_to_MAP2_green_Neurofilament_red_and_DNA_blue.jpgThe recent discovery that MSA maybe a prion disease, caused by the spread of the mis-folded rogue protein alpha-synuclein (read more here) has sparked a flurry of interest in the underlying cause of the disease. The Congress opened with a session dedicated to the pathogenesis of MSA. Dr. Janice Holton discussed the insights that can be gained from examining at the brains of patients with MSA. She highlighted how the mis-folded protein alpha-synuclein accumulates and ultimately kills cells in the brain. Dr. Sonja Scholz took to the stage to review work being done to find hereditary factors that influence susceptibility to MSA. She emphasized the need for specialist MSA Centers to come together so that we can assemble enough patient samples to fully unravel the genetics of MSA. Dr. Glenda Halliday discussed the prion hypothesis of MSA and the idea that alpha-synuclein is an infectious protein spreading throughout the nervous system. The session ended with Dr. Nadia Stefanova, who described the evidence linking inflammation in the death of cells in patients with MSA.

Dr. Pierre-Olivier Femagut gave the keynote lecture that described the progress and pitfalls of using mouse models of MSA to understand the disease process at a molecular level. He described the different compounds that have been shown to work in experimental animal models of MSA, but how the search for an effective treatment that cures the disease in patients remains on going.

Registries and Networks

Because MSA is a sporadic disease, cases are geographically spread throughout the world. No one single center and probably no one individual country has a sufficient number of patients to adequately power clinical research studies. Over the last few years, several specialist MSA Centers have come together with the concept that a strength in numbers approach is needed to tackle this rare disease. Dr. Anne Pavy Le Traon began the Registries and Networks session describing the French MSA network and the national collaboration between Centers in Toulouse and Bordeaux. Following the recent discovery that mutations in the COQ2 gene were found in Japanese patients with MSA, Dr. Shoji Tsuji described the work of the Japanese MSA Registry. He ended his talk echoing the message that we should work together to share information in a collective effort.

The best chance for success will come from uniting the MSA clinical research community in a global collective effort. Fortunately the framework for an international collaborative effort now exists.
Dr. Lucy Norcliffe-Kaufmann (from NYU’s Dysautonomia Center) described the Global MSA Registry (join here) and Natural History Study (learn more here). The study, an initiative of the NIH’s Rare Disease Clinical Research Network and in partnership with the MSA Coalition, brings together an international faculty of MSA experts to understand the clinical evolution of MSA from the pre-motor stage to advanced disease. Dr. Norcliffe-Kaufmann showed how the study is helping identify patients with MSA in the pre-motor stage. The ability to diagnose MSA this early on will provide a unique opportunity for us to intervene with strategies to halt the disease process, before the brain centers that control movement are irreversibly damaged. Dr. Gregor Wenning drew the session to a close by describing the activities of the MSA Study Group within the Movement Disorders Society. He described how leaders in MSA from Europe, America and Oceania are spearheading task forces to address key areas for future MSA research and treatment.

Jill Lyons, a Nurse Specialist working with the UK-based MSA Trust, described the advantages for MSA patients in having access to a skilled nurse. Nurses with the abilities to care for the wide variety of complications that patients with MSA face along the disease course, provide vital access to knowledge that can improve quality of life, lessen suffering and support families battling this brutal illness.

Imaging and Biomarkers

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A brain MRI scan from a patient with MSA. Note the “hot crossbun” sign at the center of the image.
Distinguishing MSA from other neurodegenerative brain diseases – particularly in the early stages – can often be difficult. Dr. Florian Krismer (from the University of Innsbruck, Austria) began the session describing the work being done to discover signals within the brain MRI to map the disease course overtime. Dr. Krismer highlighted how non-invasive imaging techniques are advancing to show the brain regions affected in MSA with increasing detail. Such progress is helping develop ways to monitor responses to treatment in clinical trials. Dr. Wassilios Meissner provided an in depth description on the work being done to identify biological markers in the cerebral spinal fluid of patients with MSA that provide clues as to the burden of alpha synuclein accumulation in the nervous system. Dr. Alessandra Fanciulli reviewed how clinical measurements of autonomic function can be used to map the progression of MSA. Dr. Pietro Cortelli addressed the issue of sleep in MSA and how abnormalities in the control of breathing and movement are common in MSA. Dr. Angelo Antonini spoke about cognitive function in patients with MSA. While it was once thought that difficulties with cognitive function were not part of the disease, clinical researchers are now showing that they can occur.

Therapy

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The final session of the Congress was dedicated to the treatment of MSA. It opened with Dr. Horacio Kaufmann providing an update on autonomic failure. Dr. Kaufmann described how orthostatic hypotension is a common, but manageable feature of MSA. He described how treatment should begin with simple (non-pharmacological) measures like sleeping with the head of the bed raised. He went on to describe the different drugs that can be used to increase blood pressure for short periods during the day, and new compounds that are now being tested in clinical trials. Dr. Eduardo Tolosa addressed the critical issue of how to treat sleep problems in MSA. He lead a discussion on how to manage patients that violently act out dreams; and shared practical advice on adapting the bed to prevent patients from injuring themselves at night. Dr. Tolosa spoke about the complicated issue of how to manage stridor. Dr. Joaquim Ferreria gave a review of the variety of research methods that have been used to measure responses to treatment in clinical trials involving patients with MSA. Dr. Florian Krismer highlighted important lessons that we should learn from these trials, and how we can use this information to plan successful trials for the future. Dr. Phillip Low closed the scientific sessions looking ahead by describing new therapies that are in the pipeline for treating MSA, including stem cell therapy currently being conducted at the Mayo Clinic, which showing promising preliminary results.

Many of the speakers had received research support from the MSA Coalition through their research grants program, which allowed them to do much needed studies.
The congress ended with the announcement of the top 3 abstracts selected from poster presentations. The abstract awards were sponsored by Fight MSA and given in honor of chef Kerry Simon, who recently lost his battle with the disease.

Plans for the future

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Meeting Chairs for the 5th International MSA Congress (left to right): Dr. Gregor Wenning (Austria), Paolo Barone (Italy) & Horacio Kaufmann (USA) with Local Organising Committee Chair Dr. Maria Teresa Pellecchia (Italy)
The 5th International Congress on MSA took place in spectacular setting of the San Nicola della Palma monastery, which was built in 1060, and known for it’s healing waters. The scientific program was organized by Dr. Paolo Barone, Dr. Gregor Wenning, Dr. Horacio Kaufmann, together with Dr. Maria Teresa Pellecchia.

The meeting brought together a diverse international community of over 130 experts, which is remarkable for a rare disease. The MSA clinical research shared ideas, discussed how to overcome the challenges of conducting research in this orphan disease, and planned studies for the future.

The progress made in MSA in recent years is no small part due to the organization and partnership of the MSA Coalition. Many of the speakers had received research support from the Coalition’s research grants program to do much needed studies. While nobody said that the road ahead would be easy, the message echoed by many was that the best chance for success will come from uniting the MSA clinical research community in a global collective effort. Fortunately the framework for an international collaborative effort now exists. Combining forces and working together will move us closer towards the ultimate conquest to find a cure for MSA

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Week 436 “March is MSA awareness month”

Support March as MSA Awareness Month

Supported by: MSA Awareness

Please join me in supporting  March as Multiple System Atrophy (MSA) Awareness Month by signing onto the MSA Awareness Month resolution.

MSA is a rare neurodegenerative disorder that has no cure. It causes the progressive loss of motor skills, unlabored breathing, speech, and other basic functions, ultimately leading to death. People with MSA typically live only six to ten years after the first signs of symptoms. It affects approximately 4.6 individuals per 100,000 world wide.

Though little is known about the disease, it is not a black box. According to the National Institute of Neurological Disorders and Stroke at the National Institutes of Health, MSA symptoms are caused by the slow death of nerve cells that control many of the functions that were previously done automatically or with little effort, like breathing or walking. It is possible that the nerve cells die because of an accumulation of a protein in the brain and spinal cord called alpha-synuclein. Alpha-synuclein accumulation is also thought to play a role in other neurological diseases like Parkinson’s disease. This important but basic knowledge is not enough.

The first step in accelerating research into MSA’s causes, potential treatments, and a cure is to raise public awareness.

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Expressing support for designation of March 2016 as “Multiple System Atrophy Awareness Month” to increase public awareness of this progressive neurodegenerative disorder that affects the autonomic functions of the body.

Multiple System Atrophy is a fatal neurological disease diagnosed in approximately 1000 patients in Australia;

 As many as 3,000 more patients in Australia with Multiple System Atrophy are misdiagnosed with other more recognizable neurodegenerative disorders;

 Patients with Multiple System Atrophy lose the ability to walk, talk, chew, swallow, and even breathe over the course of a few years;

The incidence of Multiple System Atrophy in Australia has increased in recent years;

No specific risk factors or causes of Multiple System Atrophy have been identified;

 There is currently no cure for Multiple System Atrophy;

The lack of awareness about Multiple System Atrophy has hindered research and the ability of researchers to obtain funding for their work;

 Public support and greater awareness of the need for research funding can aid in the discovery of the cause of and a cure for Multiple System Atrophy.

MARCH IS MSA AWARENESS MONTH

Multiple Systems Atrophy Awareness Logo

MSA – Awareness Logo

New Wheel cover has arrived

Wheel cover on back my Jeep

 

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Week 419 – 425 ” Time Passes quickly”

I have sat at my computer on many occasions and thought I must write another entry but I am easily sidetracked.

Over the past couple of months I have traveled north to Hervey Bay with my family and enjoyed the time with my grandsons. We got to swim , play in the sand , fish and just have a great time. I left home carrying a heavy cold and hoping the warn Queensland climate would help me get rid of it but it turned into asthma and I am still having the after affects.

Our trip included several stops in free camps – Mirrool NSW , Forbes NSW, Mendooran  NSW, Lake Broadwater Qld ($6 per person), They were all great stops and in a few cased a great meal at the local pub. I  am certain that these free stops will increase the number of travellers on the road . It amazes me how many caravans pull into these sites about 3 pm. In my conversations with the fellow travellers it is obvious that many of them could not afford to stay at caravan parks . My van  is almost self sufficient  – 250 watt solar panels – full 12 volt system , gas heating and hot water, Fridge /freezer which is three way 12v , 240v and gas ,2 x 9 kg gas bottles, 2 x 80 litre water tanks and toilet /shower. I have not pushed to the limit but guess I could last about 5-7 days. Water would be the main concern.

When I am in a town overnight I always walk around and have a look, buy a coffee, groceries , a meal and usually strike up a conversation with a local and am amazed at the history about a region that you can learn. We also visited the Radio Telescope Dish at Parkes – Riley was interested in the huge dish and all the experiments that he could try. On the return trip I went to the open range zoo at Dubbo – we will need to take Riley and Lucas next year.

While in Hervey Bay I was able to visit some friends who suffer from MSA and spend some time. I am always careful especially when I have a cold. I had intended to visit a couple on the Sunshine Coast and in Brisbane but my health made me head for home. I have since been able to talk to them and will make a real effort next year.

I am expecting some visitors for the weekend as there is a public holiday for the Melbourne Cup. I haven’t had a bet on the race since Jill passed away. She would make certain that I made a bet for her – usually the favourite and an outsider. We never won enough to cover our bets but Jill enjoyed the day. A glass of wine and  chicken salad and some excitement. It’s next Tuesday and I have no idea who is running.

As I have said time flies – no visitors – I have

The Dish at Parkes NSW

The Dish at Parkes NSW

Lake Broadwater Qld

Lake Broadwater Qld

Building sand castles at Hervey Bay

Building sand castles at Hervey Bay

Riley & Lucas on the bike at Fraser Lodge C/P

Riley & Lucas on the bike at Fraser Lodge C/P

Lucas in the water

Lucas in the water

The fisherkids

The fisherkids

had a great day watching the Melbourne Cup with my best friends & neighbours. I even picked the winner (100 to 1) based on Jill’s method – but as usual I didn’t put any money on for her.

I have had another visit to my boys got to watch them learning to swim and allowed Chris & Nicole another night out. I enjoy my time with the boys and I can brain wash them about their Grandma.

I have had another visit to Gentle Annie Caravan Park with my friends – 4 days enjoying their company and the peace and serenity of the King river. The park was very quiet only a few vans in – but that will change when the holidays come around.

Keiran , Louise & I went out to Keith’s clearing sale and hope that the farm is sold.

Back home to a green pool and a couple of trees down in the back yard looks like I will need to do some house keeping.

See you soon on the net

 

 

 

 

 

 

 

 

Keith's Clearing Sale - Oxley Flats

Keith’s Clearing Sale – Oxley Flats

King River at Gentle Annie Caravan Park

King River at Gentle Annie Caravan Park

King River at Gentle Annie Caravan Park

King River at Gentle Annie Caravan Park

Jillsgym at Gentle Annie Caravan park

Jillsgym at Gentle Annie Caravan park

Michael & Amanda of to the Melbourne Cup

Michael & Amanda of to the Melbourne Cup

My boys learning to swim

My boys learning to swim

Another Coffee with Jill at Forbes NSW

Another Coffee with Jill at Forbes NSW

 

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Week 411 “Kerry Simon passed away 1955 – 2015″

‘Iron Chef’ star Kerry Simon loses battle with MSA, dies peacefully in Las Vegas

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Week 410 “New Type of Prion May Cause, Transmit Neurodegeneration “

New Type of Prion May Cause, Transmit Neurodegeneration

Multiple System Atrophy is Described as First New Human Prion Disease Identified in 50 Years

Multiple System Atrophy (MSA), a neurodegenerative disorder with similarities to Parkinson’s disease, is caused by a newly discovered type of prion, akin to the misfolded proteins involved in incurable progressive brain diseases such Creutzfeldt-Jakob Disease (CJD), according to two new research papers led by scientists at UC San Francisco.

The findings suggest new approaches to developing treatments for MSA, which currently has no cure, but also raise a potential concern for clinicians or scientists who come in contact with MSA tissue.

The new findings mark the first discovery of a human disease caused by a new prion in 50 years, since work at the National Institutes of Health in the 1960s showed that human brain tissue infected with CJD could transmit neurodegeneration to chimpanzees.

Building on Nobel Prize-Winning Research

Stanley Prusiner, MD

It wasn’t until 1982 that UCSF’s Stanley Prusiner, MD, isolated the causative agent for a related disease called scrapie, found in sheep, and characterized it as a prion, for “infectious protein.” He then determined that the same prion protein caused bovine spongiform encephalopathy (BSE), or “mad cow” disease, in cattle, and so-called “variant” CJD in humans who subsequently consumed BSE-contaminated beef or other tissues.

At first, the idea that a simple protein could replicate and spread disease was dismissed by the scientific community, as a tenet of modern biology held that only viruses and living microbes such as bacteria could transmit disease. But subsequent work by Prusiner and others led to an understanding of how prions function at a molecular level. Prusiner, a professor of neurology and director of the Institute for Neurodegenerative Diseases (IND) at UCSF, was awarded the Nobel Prize in Physiology or Medicine for this work in 1997. Prion researchers have since suggested that similar misfolded proteins may contribute to more common forms of neurodegeneration, such as Parkinson’s disease and Alzheimer’s disease.

“Now we’ve conclusively shown that a new type of prion causes MSA,” said UCSF’s Kurt Giles, DPhil, associate professor of neurology, IND researcher and senior author on the second of the two new studies. “This is our mark in the sand.”

Sometimes compared to Dr. Jekyll and Mr. Hyde, the original prion protein identified by Prusiner as being responsible for CJD, known as PrP, can exist in two forms: one harmless and the other fatal. PrP prions in the dangerous, misfolded form latch on to other nearby PrP molecules, causing them to lose their normal shape and initiating a chain reaction that results in sticky, insoluble plaques throughout the brain that kill off cells and result in the typical “spongy” appearance of CJD-affected brains.

In the new research papers, published the weeks of Aug. 17 and Aug. 31, in the Proceedings of the National Academy of Sciences, Prusiner, Giles, post-doctoral researcherAmanda Woerman, PhD, and an international team of colleagues report that a misfolded version of a protein called alpha-synuclein seems to act in a similar way to transmit MSA from diseased human brain tissue to mice and to human cell cultures.

Testing Tissue Samples from Three Continents

First described in 1960, MSA is a progressive neurodegenerative disorder that is rare but more common than CJD: it annually affects 3 out of 100,000 people over the age of 50. Its early symptoms can be mistaken for those of Parkinson’s disease, and include movement and balance problems, as well as loss of bladder control, blood-pressure regulation and other functions governed by the autonomic nervous system. Unlike Parkinson’s patients, who often live 10 to 20 years after their diagnosis, MSA patients typically die within five to 10 years and do not respond to the drugs or deep brain stimulation used for Parkinson’s symptoms.

Nobel Prize for Prion Research

In 1997, Stanley Prusiner was awarded the Nobel Prize in Physiology or Medicine for his discovery that self-replicating misfolded proteins, which he dubbed prions, caused Creutzfeld-Jakob Disease and other related forms of neurodegeneration.

Take a step back in time to our original 1997 press release announcing Prusiner’s Nobel and describing the history of his discovery.

As in Parkinson’s disease, neurodegeneration in MSA is accompanied by a buildup of clumps of alpha-synuclein protein within brain cells. Both MSA and PD can arise sporadically in families with no history of the disease, but some inherited forms are associated with mutations in the alpha-synuclein gene. While the mechanisms aren’t fully understood, researchers believe these mutations predispose the normal proteins to misfold into infectious prions. Other factors, such as cellular stress and the aging process also are thought to make misfoldings more likely.

The new work has its origins in experiments conducted in Prusiner’s lab in 2013, showing that samples of brain tissue from two human MSA patients were able to transmit the disease to a mouse model for Parkinson’s disease, expressing a mutant human alpha-synuclein gene. To confirm this finding, Prusiner and colleagues expanded this experiment to include tissue samples from a dozen more MSA victims from tissue banks on three continents: the Massachusetts Alzheimer’s Disease Research Center in Boston, the Parkinson’s UK Brain Bank at Imperial College London, and the Sydney Brain Bank in Australia.

The results were the same: When exposed to human MSA tissue, the mice developed neurodegeneration. In addition, the team found that the brains of infected mice contained abnormally high levels of insoluble human alpha-synuclein, and that infected mouse brain tissue could itself spread the disease to other mice.

Raising Public Health Concerns

The discovery that alpha-synuclein prions can transmit MSA raises a public health concern about treatments and research that involve contact with brain tissue from neurodegeneration patients, because standard disinfection techniques that kill microbes do not eliminate the PrP prions that cause CJD. Whether the same challenges hold for alpha-synuclein prions in MSA remains to be determined.

The authors write that clinicians and researchers should adopt much more stringent safety protocols when dealing with tissue from patients with MSA and other neurodegenerative diseases, many of which they believe may also be caused by prions. For instance, MSA is frequently initially diagnosed as Parkinson’s disease, which is often treated with deep-brain stimulation. The disease could potentially be transmitted to other patients if deep-brain stimulation equipment is reused.

Alpha-synuclein immunohistochemistry showing many glial inclusions seen in Multiple System Atrophy (MSA), a neurodegenerative disorder.

“You can’t kill a protein,” Giles said. “And it can stick tightly to stainless steel, even when the surgical instrument is cleaned.” As a result, he said, “We’re advocating a precautionary approach. People are living longer and likely getting more brain surgeries. There could be undiagnosed neurodegenerative diseases that – if they’re caused by prions – mean infection could be a real worry.”

Unlike the danger of BSE from contaminated beef, the researchers stress that there is no apparent risk of infection by MSA prions outside of specialized medical or research settings.

Rapid New Method to Test Prion Transmission

In the earlier of the group’s two PNAS papers published this month, Woerman led a research team in the development of a rapid new method to test prion transmission using human cell cultures. The team demonstrated that it only takes four days for human MSA tissue to infect cultured cells with alpha-synuclein mutations, in contrast to the 120 days it takes for the disease to spread to mouse models.

“The challenge of studying neurodegeneration is that it’s a disease of aging,” Woerman said. “You have to let the mouse models develop for such a long time that research on cures is really slow to progress. Now, with these cell models, we can test how to inactivate alpha-synuclein aggregates at a speed that just wouldn’t be feasible in animals.”

The UCSF researchers are working with Japanese pharmaceutical company Daiichi Sankyo, as part of a collaboration established in 2014 to develop potential treatments for prion diseases.

Additional investigators of the study include researchers from UCSF; Daiichi Sankyo Co., Ltd.; the University of Texas Southwestern Medical Center; Imperial College London; Massachusetts General Hospital; Stanford University; UC Los Angeles, and the University of New South Wales. A complete list of authors appears in each paper.

Major funding for the research was provided by grants from the National Institutes of Health and gifts from the Sherman Fairchild Foundation and Mary Jane Brinton. The authors declare no financial interest or conflicts of interest in relation to this work.

UC San Francisco (UCSF) is a leading university dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care. It includes top-ranked graduate schools of dentistry, medicine, nursing and pharmacy, a graduate division with nationally renowned programs in basic, biomedical, translational and population sciences, as well as a preeminent biomedical research enterprise and two top-ranked hospitals, UCSF Medical Center and UCSF Benioff Children’s Hospital San Francisco.

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Week 407 “August 2015 – JILLSGYM”

A conflict of ideas on FB in the past few days has shocked me back into some activity.

I must admit that all my time in the past few months has been family orientated and a lack of enthusiasm  to any thing else. I have had the opportunity to be a full time grand father – something that Jill would have done anything for, to spend time with her grand children and see them grow as I have done. Riley my eldest (5) mentions his Grandma and we have little talks about what she would think about his swimming , playing hockey and reading. He remembers little things – riding on the foot pads of her wheel chair . Lucas (3) was just born and Jill got to hold him . I still show him Jill’s photo and I say this is Grandma – he now says the image on my iPad is Grandma. She would love to be here and see them in their Football gear – she would have said they should be Melbourne ( AFL) not Essendon.

Bombers Fans

Riley & Lucas in their Essendon gear

 

Seeing a song by Josh Groban “To where you are”on U Tube made me think more about what I have lost  It had been posted on MSA Australia & NewZealand FB page by a friend from UK who lost her husband 12 months ago

I also found Jill’s jewellery which I had hidden 3 years ago – well hidden I don’t even remember putting them where I found them. I wanted to get the family to share them rather than sit in a hidden location – Jill always wanted them to be used . I have been very upset at not remembering where they were – even contemplating going to the police to report there disappearance. That would have been embarrassing when they actually turned up. My neighbour and family keep saying they will turn up – stop worrying.

When Jill died I thought there was couple of things I would like to do to keep her memory alive for me and the family – to help others suffering from the is horrible disease.             We had set up a gym ( Jillsgym) in our garage and my thought was to donate the equipment to other MSA patients – the problem was to relocate the equipment into a space big enough to handle it. I had built a large carport to handle the car and caravan – leaving the garage free. It is still used ,my neighbour uses it regularly and her husband is about to have a knee replacement so it will be quite busy . Jill would have been annoyed that I was not using it more .

Jillsgym-1

 

 

I would like to write a book on Jills journey through MSA – fortunately I wrote in this blog regularly so I have the information but probably lack the expertise. I know there were some things that I was not allowed to write about as Jill thought they were to personnel or embarrassing. Jill always ( as a teacher) checked what I had written for spelling and grammar.

I am now at the point I would like to establish “JILLSGYM” as a MSA awareness and Fundraising entity. I am not sure how this can be done. I feel it is important that Australia be given the opportunity to donate to an actual MSA fund not some thing where we are under the umbrella of another organisation – there fore not knowing where your donation will end up.

I am heading north to Hervey Bay Queensland for some warmth with my family and while away will visit a few MSA patients I haven’t seen for a couple of years.

See you soon on the net

 

 

 

 

 

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