Welcome to Our Parkinson's Place
I copy news articles pertaining to research, news and information for Parkinson's disease, Dementia, the Brain, Depression and Parkinson's with Dystonia. I also post about Fundraising for Parkinson's disease and events. I try to be up-to-date as possible. I have Parkinson's diseases as well and thought it would be nice to have a place where updated news is in one place. That is why I began this blog.
I am not responsible for it's contents, I am just a copier of information searched on the computer. Please understand the copies are just that, copies and at times, I am unable to enlarge the wording or keep it uniformed as I wish. This is for you to read and to always keep an open mind.
Please discuss this with your doctor, should you have any questions, or concerns. Never do anything without talking to your doctor. I do not make any money from this website. I volunteer my time to help all of us to be informed. Please No advertisers, and No Information about Herbal treatments. This is a free site for all.
Saturday, March 26, 2016
Friday, March 25, 2016
March 25, 2016 at 5:15 PM
By Eleanor McDermid
By Eleanor McDermid
Rare deletions at chromosome 22q11.2 are present at an increased rate in patients with Parkinson's disease (PD), researchers report in The Lancet Neurology.
PD has been reported in patients with 22q11.2 deletion syndrome, which is a heterogeneous, multisystem disorder, with features including cleft palate, cardiac and skeletal abnormalities and learning difficulties. This latest study shows the converse to be true, with 22q11.2 deletions present in eight of 9387 PD patients from four independent studies, but none of 13,863 controls.
The eight identified patients all had the 3 Mb deletion, the most common form of 22q11.2 deletion. The deletion was associated with an early age at PD onset, at an average of 42.1 years compared with 60.3 years among patients without the deletion.
Even among patients with early-onset (<45 years) PD, the rate of 22q11.2 deletions was just 0.49% (0.04% for later onset). But researcher Nicholas Wood (UCL Institute of Neurology, London, UK) and colleagues stress that "the presence of a 22q11.2 deletion has direct implications for management, especially the identification and medical management of comorbidities."
None of the patients had a diagnosis of 22q11.2 deletion syndrome, but the team says: "With hindsight, some cases had other features suggestive of 22q11.2 deletion syndrome, such as hypocalcaemia, depression, fatigue, mental retardation, and cleft palate."
They did not, however, have any of the cardiac features that are frequently reported in 22q11.2 deletion syndrome patients.
In a linked commentary, Eng-King Tan (Singapore General Hospital) stresses that, although the findings may focus a search for a novel PD gene, they do not prove that the deletion causes PD. For one thing, it is not clear why only 3% of patients with such deletions develop PD and what might trigger the condition in those who do develop it, he says.
"Despite many missing connections in the pathophysiological link between 22q11.2 deletion syndrome and Parkinson's disease, the present study will certainly raise clinicians' awareness and heighten their vigilance in looking for features of 22q11.2 deletion syndrome in patients with early-onset Parkinson's disease, and carefully considering Parkinson's disease as a differential diagnosis in patients with 22q11.2 deletion syndrome even if these patients are on antipsychotic drugs", he concludes.
March 25, 2016
Minister made comments the day before replacing Iain Duncan Smith - and later admitted they were 'inaccurate
Stephen Crabb has been appointed as the new Work
and Pensions Secretary AFP/Getty
People with brain tumours, motor neurone disease, Parkinson’s disease and a number of other conditions are “able to work”, new work and pensions secretary Stephen Crabb has said.
Mr Crabb made the comments the day before he replaced Iain Duncan Smith, who resigned from his position because he found the planned cuts to disability benefits announced in the latest Budget "not defensible".
The MP for Preseli Pembrokeshire wrote on his Facebook page last Thursday: “A decision was taken by MPs to change the benefit awarded to a specific group of people who receive Employment Support Allowance.”
The 43-year-old - who later backtracked on the statement - added: “These people are in the Work Related Activity Group (WRAG) and they do have a disability or illness but are able to work.”
In response to a freedom of information request, the Department for Work and Pensions confirmed disabilities and illness under the employment and support allowance work-related activity group include: strokes, brain haemorrhages, multiple sclerosis, brain tumours, motor neurone disease, Parkinson’s disease, quadraplegia, polio and cerebral palsy.
Mr Crabbs’ words were not well-received online.
Brian Davies, a member of the public, wrote on the Facebook post: “Could you explain how people who are admitted are unwell and really shouldn't be put under this kind of pressure, how does lowering money help them?”
Natalie Windsor added: “This would be great if it were true. The government, however, has not adequately responded to either help, correct error, or even apologise for the thousands of people who have wrongly been diagnosed as able to work.”
The controversy follows on from the Government’s u-turn on the Budget, which had previously suggested a saving of £4.4bn by 2020-21 through cuts to the disability budget.
Mr Crabbs has since updated his Facebook post, admitting “it previously contained a factual inaccuracy.”
He added: “Of course we absolutely continue to protect those who are ‘too ill to work’. There is no question about that. Those with the most severe health conditions and disabilities will quite rightly continue to get a higher rate of benefit and support.”
A few days ago:
A few days ago my constituency office was vandalised in response to my recent vote to approve changes to the Employment Support Allowance (ESA). This was not an isolated attack as other MPs offices were targeted by individuals involved in a social media campaign.
I’m disappointed that some individuals choose to do this instead of making an appointment to see me to discuss their concerns. Sadly all these individuals achieved on Saturday was to create an inconvenience to my office staff, local residents, and the Police. There are lots of ways to communicate to convey concerns but criminal damage just isn’t an option.
There has been a lot of miscommunication about this vote which I want to put right. A decision was taken by MPs to change the benefit awarded to a specific group of people who receive Employment Support Allowance. These people are in the Work Related Activity Group (WRAG) and they do have a disability or illness but are considered able to work with support in the future.
The overwhelming majority of people in this group say they want to work, and so I think it is right that we do all we can to help them get back into work. The changes mean that this group will now access the same level of benefit as those on Job Seekers Allowance, but will be given better tailored support to help them into employment. It doesn’t affect anyone who is already claiming ESA, they will receive the exactly the same amount of benefit as they do now.
The truth is that not all disabilities prevent people from working. A great many disabled people get enormous fulfilment from being in work. They would be extremely offended not to be considered equal in the job market, and this benefit change means that more people will be able to take these important steps from being benefit-dependent to the workplace.
Of course we absolutely continue to protect those who are ‘too ill to work’. There is no question about that. Those with the most severe health conditions and disabilities will quite rightly continue to get a higher rate of benefit and support. And despite the political banter from Labour, the disability budget is actually going to be rising by more than £1 billion over the next 5 years which means that more money is being spent in real terms on support for disabled people than at any point under the previous Labour government.
I can see that there have been a few comments on this page and I encourage people to email me directly if you would like a personal response from me. I don’t always have time to reply to every comment on Facebook as I am busy working on constituent casework via the telephone, email, letter and face to face appointments. If you email me, I will always provide a response to people who are living in Preseli Pembrokeshire. I cannot respond to people outside of the area and suggest they contact their own MP directly.
Note: This post has been updated, as it previously contained a factual inaccuracy.
March 25, 2016
When: Tuesday, April 5, 2016, 1:00 PM - 2:00
To sign up go to:
When: Tuesday, April 5, 2016, 1:00 PM - 2:00
To sign up go to:
Are there new therapies on the horizon to help treat PD? In the search for more effective treatments, two promising areas of research are gene therapies and cell therapies. Learn more about the potential of these two types of experimental treatments by joining a one-hour online seminar led by PDF and Roger Barker, M.B.B.S, M.R.C.P, Ph.D., Professor of Clinical Neuroscience and Honorary Consultant, Neurology, University of Cambridge and Addenbrooke's Hospital.
- Learn how cell-based therapies for Parkinson’s are designed to replace dopamine cells lost to the disease.
- Understand how gene therapies are designed to either rescue dopamine cells or produce dopamine more efficiently in the brain.
- Understand why neither approach is a cure, but how each might one day offer exciting ways to help people with Parkinson’s live better and reduce their other medications.
Roger Barker, M.B.B.S, M.R.C.P, Ph.D., is Professor of Clinical Neuroscience and Honorary Consultant, Neurology, University of Cambridge and Addenbrooke's Hospital in the United Kingdom.
Since setting up his own research group in 1997, Dr. Barker has run a laboratory investigating basic and clinical aspects of Parkinson’s disease. He has been involved in several clinical trials studying gene and cell-based therapies for people living with PD. Dr. Baker also currently coordinates a European Union funded transplant program for PD. In addition to publishing over 300 papers, he is Co-Editor in Chief of the Journal of Neurology.
Dr. Barker completed his neurology training and obtained his doctorate in neural grafting at the University of Cambridge. He received additional training at Oxford University and St. Thomas Hospital.
March 24, 2016 11:58 AM
The Foundation for Mitochondrial Medicine (FMM) hosts its next Hope Flies Health Series Webinar:
Research Connecting Parkinson’s Disease and Mitochondrial Disease on Wednesday, April 6, 2016 at 1:00 pm EDT.
The Foundation developed the webinar with partners including the
Michael J. Fox Foundation (MJFF), Wilkins Parkinson’s Foundation and Sharecare to particularly bring greater awareness to mitochondrial disease and its connection to Parkinson’s disease.
The webinar is free; however registration is requested in advance at
Free webinar on Parkinson's and mitochondrial disease
on April 6: www.mitochondrialdiseases.org/hfhswebinars.
During the webinar, participants can learn more about the scientific connection and interest Parkinson’s researchers have inmitochondria and mitochondrial function. Experts on the call willshare the latest developments from a specific research projectthe FMM and MJFF co-funded exploring this link to activate and
stabilize the Parkin protein, which may allow it to break down damaged mitochondria and thereby prevent cell death in some Parkinson’s patients. Stabilizing Parkin will be a positive strike for Parkinson’s disease and for mitochondrial disease.
Panelists for the webinar include Wolfdieter Springer, PhD, Assistant
Professor of Neuroscience, Mayo Clinic; Laura Stanley, Executive
Director, FMM; Bill Wilkins, Founder of the Wilkins Parkinson’s
Foundation, and the moderator will be Darria Gillespie, MD MBA,
FACEP, SVP Clinical Strategy of Shareware.
Dr. Springer will provide an update on his primary research focus: the molecular and cellular mechanisms underlying the pathogenesis of Parkinson's disease and other related neurodegenerative disorders.
Additional topics include an overview of Parkinson’s and the challenges and progress today surrounding research of Parkinson’s and mitochondrial function; an overview of mitochondrial disease today and progress being made; and how patients and caregivers can manage both diseases.
About the Foundation for Mitochondrial Medicine
The Foundation for Mitochondrial Medicine is a 501(c) (3) non-profit organization dedicated to supporting the development of the most promising research and treatments of the many forms of mitochondrial disease. Visit www.mitochondrialdiseases.org for more information.
Contacts For The Foundation for Mitochondrial Medicine
Jennifer Grizzle, 770-409-1152