I Ask This Of You!

I have Parkinson's diseases and thought it would be nice to have a place where the contents of updated news is found in one place. That is why I began this blog.

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 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. I will not accept any information about Herbal treatments curing Parkinson's, dementia and etc. It will go into Spam.

This is a free site for all with no advertisements.

Thank you for visiting!

Saturday, October 11, 2014

Needs to be said by Lisa Rainey

Please watch and share. We are trying to raise awareness about this issue.

The legendary heavyweight was once known as 'The Louisville Lip' because of his fast tongue but is now a virtual mute as his condition deteriorate

Muhammad Ali – once famed for his lightning speed and even faster tongue – is now so ill he can hardly speak, his brother has revealed.
The boxing legend, 72, who has been battling debilitating Parkinson’s disease for years, has become increasingly frail and is now largely housebound.
And fresh health fears were sparked after he was too ill to attend the premiere of a new movie about his life last week and could not take part in any of the filming.
Speaking at the screening of I Am Ali in Hollywood, his brother Rahman, 71, told the Sunday People: “I have not been able to talk to my brother about this because he is sick.
“He doesn’t speak too well. But he is proud that we are here for him. He has given this film his blessing.”
The film focuses on the family life of the charismatic three-time world heavyweight champ nicknamed the Louisville Lip for his infamous wit.

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Using Ali’s “audio journals” it presents an intimate portrait of the sporting icon also using interviews with his family and anecdotes from boxers such as Mike Tyson and George Foreman.
His daughter Maryum, 46, was also at the screening. She said of her famous dad: “He has not seen the film yet, but I am very excited for him to see it.
"He is going to love it. I know he is. He is going to cry, he is going to laugh. He will be very proud.”
Director Clare Lewins says Ali’s daughter Hana, 38, plans to show the movie to her father – also known for his pre-fight poems including “float like a butterfly, sting like a bee” – later this month at his Arizona home.
In January, Muhammad’s son Ali Jnr said he believed there was “no chance” of his dad surviving another year.
He said: “I just want, hope and pray to God that this awful disease takes my dad sooner rather than later.
"Take him away from all the suffering he’s in.”
I Am Ali hits UK cinemas on November 28.   
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Friday, October 10, 2014


Having Parkinson's Disease for more than twenty years has been found to be associated with major milestones of disease disability, fractures, or being confined to a wheelchair or bed.
There are a very limited number of studies on the clinical features of Parkinson's Disease twenty years after onset. So an assessment was carried out for several years on people who had Parkinson's Disease for more than twenty years

Those people considered were those who had Parkinson's
Disease for 20 to 22 years. They were assessed for an average
of nearly four years. Older age at onset and longer duration of
Parkinson's Disease were each associated with a higher
prevalence of major motor and non-motor milestones of
disease disability. Confinement to a wheelchair or bed had by
then occurred in just over 1 in 5 people (21%). Those factors
making confinement to a wheelchair or bed were older age,
postural instability and institutionalisation. Fractures occurred
in 16% of people. Fractures were associated with postural

The most frequent outcome was death (28%). However, given the age of diagnosis and the duration of Parkinson's Disease this might have been no more than normal. Mortality was associated with male gender, older age, dysphagia (difficulty in swallowing), orthostatic hypotension, postural instability, fractures and institutionalization.

Reference : Journal of Neurology, Neurosurgery and Psychiatry [2014] Oct 3 [Epub ahead of
print] (R.Cilia, E.Cereda, C.Klersy, M.Canesi, A.L.Zecchinelli, C.B.Mariani, S.Tesei,
G.Sacilotto, N.Meucci, M.Zini, C.Ruffmann, I.U.Isaias, S.Goldwurm, G.Pezzoli)

Complete abstract :
©2014 Viartis

Nobel Prize in chemistry awarded for microscope breakthrough

Sven Lidin, left , Staffan Nordmark, centre, and Mans Ehrenberg at the Royal Academy of Sciences announce the Nobel Chemistry laureates on Oct. 8, 2014. Americans Eric Betzig and William Moerner and German scientist Stefan Hell won the Nobel Prize in Chemistry for "the development of super-resolved fluorescence microscopy. AP PHOTO/BERTIL ERICSON
STOCKHOLM -- Americans Eric Betzig and William Moerner and German scientist Stefan Hell won the Nobel Prize in chemistry on Wednesday for developing new methods that let microscopes see finer details than they could before.
Their breakthroughs, starting in the 1990s, shattered previous limits on the resolution of optical microscopes, giving scientists improved tools to study diseases such as Parkinson's, Alzheimer's and Huntington's at a molecular level.
The three scientists will split the 8 million-kronor ($1.1 million) award for "the development of super-resolved fluorescence microscopy," which the Royal Swedish Academy of Sciences said has "brought optical microscopy into the nanodimension."
Betzig, 54, works at the Howard Hughes Medical Institute in Ashburn, Virginia. Hell, 51, is director at the Max Planck Institute for Biophysical Chemistry in Goettingen, Germany. Moerner, 61, is a professor at Stanford University in California.
"I was totally surprised, I couldn't believe it," Hell said. "Fortunately I remembered the voice of Nordmark and I realized it was real," he added, referring to Staffan Nordmark of the Royal Swedish Academy of Sciences.
The Nobel judges didn't immediately reach Moerner, who was at a conference in Brazil. He found out about the prize from his wife after she was told by The Associated Press.
"I'm incredibly excited and happy to be included with Eric Betzig and Stefan Hell," Moerner told AP.
For a long time optical microscopes were limited by among other things the wavelength of light. So scientists believed they could never yield a resolution better than 0.2 micrometers.
But helped by fluorescent molecules, the three scientists, working independently, were able to break that limit, taking optical microscopy into a new dimension that made it possible to study the interplay between molecules inside cells, including the aggregation of disease-related proteins, the academy said.
Each of the laureates has used these methods to study tiny components of life. Hell has studied nerve cells to get a better understanding of brain synapses; Moerner has studied proteins related to Huntington's disease; and Betzig has tracked cell division inside embryos, the academy said.
"We can tell whether (individual molecules are) different or whether they're the same. It's very much like asking whether they all march to the same drummer or not," Moerner told the AP. "When you can watch one by one, then we are able to observe exactly when it changes from one state to another."
Tom Barton, president of the American Chemical Society, said the laureates' work allowed progress in many fields because it let scientists see molecules and other features with unprecedented resolution. And for biology, he noted, it allows researchers to study very fine details of living things. In contrast, while an electron microscope can see even finer details, it can't be used on living cells.
"Before maybe we could just see the contours of bacteria but now we can look inside the bacteria and we can see things as small as individual molecules," said Nobel committee member Claes Gustafsson.
"This technique means that suddenly we can start studying details that we could only dream of before. This is really a revolution because as recently as 15 years ago, it was believed to be theoretically impossible to break this barrier," he said.
Last year's chemistry prize went to three U.S.-based scientists who developed powerful computer models that researchers use to understand complex chemical interactions and create new drugs.
This year's Nobel announcements started Monday with U.S.-British scientist John O'Keefe splitting the medicine award with Norwegian couple May-Britt Moser and Edvard Moser for breakthroughs in brain cell research that could pave the way for a better understanding of diseases like Alzheimer's.
On Tuesday, Isamu Akasaki and Hiroshi Amano of Japan and U.S. scientist Shuji Nakamura won physics award for the invention of blue light-emitting diodes - a breakthrough that spurred the development of LED technology that can be used to light up homes and offices and the screens of mobile phones, computers and TVs.
The Nobel Prize in literature will be announced Thursday, followed by the Nobel Peace Prize on Friday and the economics prize on Monday.
The prizes are always handed out in ceremonies on Dec. 10, the date that prize founder Alfred Nobel died in 1896.

Wearable Technology That Feels Like Skin

MC10 is working on attachable computers that look like small rectangular stickers and that can be placed on various parts of the body.

John A. Rogers/The University of Illinois at Urbana-Champaign

When it comes to the future of computing, there is one major known and a principal unknown.
The known, with almost guaranteed certainty, is that the next era of computing will be wearables. The unknown, with commensurate guaranteed uncertainty, is what these wearables will be and where on your body they will live.
Apple and Samsung, for example, are betting on the wrist; Google, the face. A slew of tech companies believe clothing will simply become electronic. Yet there’s a whole new segment of start-ups that believe all of the above are destined for failure and that we humans will become the actual computers, or at least the place where the technology will reside.
Their enthusiasm is on an emerging class of wearable computers that adhere to the skin like temporary tattoos, or attach to the body like an old-fashioned Band-Aid.
Many of these technologies don’t look anything like today’s gadgets. Instead, they are stretchable, bendable and incredibly thin. They can also be given unique designs, to stand out like a bold tattoo, or to blend in to the color of your skin.
MC10 attachable computers.
John A. Rogers/The University of Illinois at Urbana-Champaign

While these wearables raise novel privacy concerns, their advocates say there are numerous benefits. Attachable computers will be less expensive to make, provide greater accuracy because sensors will be closer to a person’s body (or even inside us) and offer the most utility, as something people won’t forget to wear.
MC10, a company based in Cambridge, Mass., is testing attachable computers that look like small rectangular stickers, about the size of a piece of gum, and can include wireless antennas, temperature and heart-rate sensors and a tiny battery.
“Our devices are not like wearables that are used today, where people wear them for a little bit and then throw them into a drawer,” said Scott Pomerantz, the chief executive of MC10. “Ours are always on you. We have the smallest, most flexible, stretchable, wearable computer, and you can collect all sorts of biometric data tied to your motion.”
MC10 recently teamed up with John A. Rogers, a professor of materials science and engineering at the University of Illinois at Urbana-Champaign, who has been working for nearly a decade to perfect flexible devices that can be worn on the skin or implanted internally.
How would these gadgets work? Imagine being able to slap a few Band-Aid-size sensors to your body when you go for a run, then seeing a micro-level reading of your exercise on your phone.
Maybe you want to figure out which deodorant would be best for you. This would be done with a sticker that tracks your sweat level, then emails you a few brand recommendations. Or if you want to monitor your baby’s breathing, you would stick a little sensor on the baby’s chest that will alert you to any problems.
MC10 attachable computers.

“We’ll eventually see a more intimate integration of electronics and biological systems,” Mr. Rogers said in a phone interview. “Without that kind of intimate physical contact, it’s going to be difficult, or maybe even impossible, to extract meaningful data.”

The health applications are enormous. Over the past year, Mr. Rogers and his team of scientists have been working with patients with Parkinson’s disease to monitor their motions, dermatologists to treat skin diseases, and beauty companies like L’Oréal to develop digital stickers that track skin hydration.
Wearable-computer advocates are also giddy about the infinite style possibilities. “It turns out that the mechanics of these devices are 100 percent compatible with kids’ standard temporary tattoos,” Mr. Rogers said. Meaning, they can be made to look like tattoos, with each segment containing different sensors.
Anke Loh, the chairwoman of the fashion department at the School of the Art Institute of Chicago, has been experimenting with making the attachable computers look like body art. “You see these patches and you really want to put them on your skin, even without knowing what the function is,” Ms. Loh said, noting that most wearable computers today are clunky and ugly. “There’s a lot of potential to combine fashion and technology.”
On a more futuristic front, scientists at the University of Tokyo have been working on an “e-skin,” which, as you may have guessed, is an electronic skin that sits on top of real skin. It looks like a flexible and stretchable sheet of plastic wrap, yet contains lots of health-related sensors.
In another iteration of e-skin, scientists are working to add a layer of LEDs, turning it into a functional screen that sits on the body.
Digital skins offer numerous applications, not only in monitoring a user’s health, but also as a visual user interface. They can be used on lifelike prosthetics and even replace smartphones one day. (Imagine your forearm as a touch-screen display.)

But don’t throw aside your smartwatch or say goodbye to Google Glass just yet. It will be a while before our wearable future becomes known.

Thursday, October 9, 2014

Drug used for another disease slows progression of Parkinson's

October 8, 2014

University of California, Los Angeles (UCLA), Health Sciences

A drug being evaluated to treat an entirely different disorder helped slow the progression of Parkinson’s disease in mice, a team of researchers has reported. Their study found that the drug, AT2101, which has also been studied for Gaucher disease, improved motor function, stopped inflammation in the brain and reduced levels of alpha-synuclein, a protein critically involved in Parkinson's.
A new study from UCLA found that a drug being evaluated to treat an entirely different disorder helped slow the progression of Parkinson's disease in mice.
The study, published in the October edition of the journal Neurotherapeutics, found that the drug, AT2101, which has also been studied for Gaucher disease, improved motor function, stopped inflammation in the brain and reduced levels of alpha-synuclein, a protein critically involved in Parkinson's.
though the exact cause of Parkinson's is unknown, evidence points to an accumulation of alpha-synuclein, which has been found to be common to all people with the disorder. The protein is thought to destroy the neurons in the brain that make dopamine, a neurotransmitter that helps regulate a number of functions, including movement and coordination. Dopamine deficiency is associated with Parkinson's disease.
Gaucher disease is a rare genetic disorder in which the body cannot produce enough of an enzyme called β-glucocerebrosidase, or GCase. Researchers seeking genetic factors that increase people's risk for developing Parkinson's have determined that there may be a close relationship between Gaucher and Parkinson's due to a GCase gene. Mutation of this gene, which leads to decreased GCase activity in the brain, has been found to be a genetic risk factor for Parkinson's, although the majority of patients with Parkinson's do not carry mutations in the Gaucher gene.
"This is the first time a compound targeting Gaucher disease has been tested in a mouse model of Parkinson's disease and was shown to be effective," said the study's senior author, Marie-Francoise Chesselet, the Charles H. Markham Professor of Neurology at UCLA and director of the UCLA Center for the Study of Parkinson's Disease. "The promising findings in this study suggest that further investigation of this compound in Parkinson's disease is warranted."
In the study, the researchers used mice that were genetically engineered to make too much alpha-synuclein which, over time, led the animals to develop deficits similar to those observed in humans with Parkinson's. The researchers found that the mice's symptoms improved after they received AT2101 for four months.
The researchers also observed that AT2101 was effective in treating Parkinson's in mice even though they did not carry a mutant version of the Gaucher gene, suggesting that the compound may have a clinical effect in the broader Parkinson's population.
AT2101 is a first-generation "pharmacological chaperone" -- a drug that can bind malfunctioning, mutated enzymes and lead them through the cell to their normal location, which allows the enzymes to carry on with their normal work. This was the first time that a pharmacological chaperone showed promise in a model of Parkinson's, according to Chesselet.
Parkinson's disease affects as many as 1 million Americans, and 60,000 new cases are diagnosed each year. The disorder continues to puzzle scientists. There is no cure and researchers have been unable to pin down its cause and no drug has been proven to stop the progression of the disease, which causes tremors, stiffness and other debilitating symptoms. Current Parkinson's treatments only address its symptoms.

Story Source:
The above story is based on materials provided by University of California, Los Angeles (UCLA), Health Sciences. Note: Materials may be edited for content and length.
end story_source

Journal Reference:
1  Franziska Richter, Sheila M. Fleming, Melanie Watson, Vincent Lemesre, Lee Pellegrino, Brian Ranes, Chunni Zhu, Farzad Mortazavi, Caitlin K. Mulligan, Pedrom C. Sioshansi, Sindalana Hean, Krystal De La Rosa, Richie Khanna, John Flanagan, David J. Lockhart, Brandon A. Wustman, Sean W. Clark, Marie-Françoise Chesselet. A GCase Chaperone Improves Motor Function in a Mouse Model of Synucleinopathy. Neurotherapeutics, 2014; DOI: 10.1007/s13311-014-0294-x

end journal_references
Cite This Page:
University of California, Los Angeles (UCLA), Health Sciences. "Drug used for another disease slows progression of Parkinson's." ScienceDaily. ScienceDaily, 8 October 2014. <

Wednesday, October 8, 2014

What is LSVT LOUD? and What is LSVT BIG?


LSVT LOUD® is an effective speech treatment for individuals with Parkinson disease (PD) and other neurological conditions.  LSVT LOUD, named for Mrs. Lee Silverman (Lee Silverman Voice Treatment – LSVT) was developed in 1987 and has been scientifically studied for nearly 20 years with funding support from the National Institute for Deafness and other Communication Disorders (NIDCD) of the National Institutes of Health. Published research data support improvements in vocal loudness, intonation, and voice quality for individuals with PD who received LSVT LOUD, with improvements maintained up to two years after treatment. Recent research studies have also documented the effectiveness of this therapy in improving the common problems of disordered articulation, diminished facial expression and impaired swallowing. Additionally, two brain imaging studies have documented evidence of positive changes in the brain following administration of the therapy.
LSVT LOUD improves vocal loudness by stimulating the muscles of the voice box (larynx) and speech mechanism through a systematic hierarchy of exercises. Focused on a single goal “speak LOUD!” – the treatment improves respiratory, laryngeal and articulatory function to  maximize speech intelligibility. The treatment does not train people for shouting or yelling; rather, LSVT LOUD uses loudness training to bring the voice to an improved, healthy vocal loudness with no strain.
Treatment is administered in 16 sessions over a single month (four individual 60 minute sessions per week). This intensive mode of administration is consistent with theories of motor leaning and skill acquisition, as well as with principles of neural plasticity (the capacity of the nervous system to change in response to signals), and is critical to attaining optimal results. The treatment not only simulates the motor system but also incorporates sensory awareness training to help individuals with PD recognize that their voice is too soft, convincing them that the louder voice is within normal limits, and making them comfortable with their new louder voice.
Patients are trained to self-generate the adequate amount of loudness to make their speech understood. While LSVT LOUD has been successfully administered to individuals in all stages of PD, the treatment has been most effective among those who are in early or middle stages of the condition. LSVT LOUD has also been applied to individuals with sub-types of PD (Shy-Drager syndrome, multi-system atrophy and progressive supranuclear palsy), however the largest dataset is for individuals with Idiopathic Parkinson disease (IPD). Recently, LSVT LOUD has been applied to select individuals with stroke, multiple sclerosis, Down syndrome, and cerebral palsy with positive outcomes.


Recently principles of LSVT LOUD® were applied to limb movement in people with Parkinson disease (LSVT BIG®) and have been documented to be effective in the short term. Specifically, training increased amplitude of limb and body movement (Bigness) in people with Parkinson disease has documented improvements in amplitude (trunk rotation/gait) that generalized to improved speed (upper/lower limbs), balance, and quality of life. In addition, people were able to maintain these improvements when challenged with a dual task.
LSVT BIG can be delivered by a physical or occupational therapist. Treatment is administered in 16 sessions over a single month (four individual 60 minute sessions per week). This protocol was developed specifically to address the unique movement impairments for people with Parkinson disease. The protocol is both intensive and complex, with many repetitions of core movements that are used in daily living. This type of practice is necessary to optimize learning and carryover of your better movement into everyday life!
Start exercising NOW – as soon as possible. Physicians rarely refer their patients to health and fitness programs at diagnosis because medications are very effective early on at alleviating most of the symptoms, and patients experience little change in function. Yet, according to a recent survey it is at the time of diagnosis that patients often begin to consider lifestyle changes and seek education about conventional and complementary/alternative treatment options. Thus referrals to exercise, wellness programs and physical/occupational therapy would be best initiated at diagnosis, when it may have the most impact on quality of life.

Locate an LSVT Certified Clinician go to: