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. This is a free site for all.
Thank you.

Thursday, May 25, 2017

Giving Parkinson’s Disease the one-two punch — patients benefit from boxing, singing and yoga

According to the Davis Phinney Foundation for Parkinson’s, exercise has been found to improve mood and balance, while reducing stiffness and fatigue. Roberts said there is no medication to slow the disease besides exercise

AURORA | Activities like boxing, singing and yoga might be the best medicine for people with Parkinson’s disease.

At least that’s the opinion of physical therapist Meredith Roberts and musical therapist Rebekah Stewart, who together hosted Parkinson’s Warrior May 19 at the The Aurora Center for Active Adults. The biannual event — another is slated for the fall on a date to be determined — aims to help people with Parkinson’s learn how to battle the disease with exercise and other therapy. Roberts has developed and teaches a host of similar exercise classes in Aurora and around the Denver-metro area, all of them designed to help people cope with Parkinson’s in a healthy way.
“I found Parkinson’s to be the most challenging of the diagnoses,” she said. “When I went to school, there weren’t a lot of options. Give them a walker, give them a wheelchair, make them safe — and that was about it.”
According to the Davis Phinney Foundation for Parkinson’s, exercise has been found to improve mood and balance, while reducing stiffness and fatigue. Roberts said there is no medication to slow the disease besides exercise.
Anne Green, a cheerful 70-year-old who attended the May 19 workshop and is a regular at many of Roberts’ other classes, agreed.
“It’s the only solution to the problem,” she said. “There are lots of programs around, and each group becomes a support group itself.”
At the May 19 workshop, Roberts and Stewart gave examples of home exercises for people with Parkinson’s and explained how and why the exercises help.
“Music and movement is medicine,” Roberts explained.
She said proper exercise for Parkinson’s has to be complex and intense, but fun. Roberts said boxing is one of the best workouts because it includes cardio and requires more thought, like multi-tasking and using muscles asymmetrically.
Research can help determine what works best for each individual, but Roberts said those with Parkinson’s benefit most if they keep a steady routine. Exercising five or six days a week is best, because quitting or taking time off could actually make the pain and stiffness worse, she said.
Before getting into a routine, however, Roberts suggested getting the permission from a doctor. After that, she said keeping up with a therapist or coach is recommended for maximum benefits.
“If you don’t use it, you lose it. So, let’s use it, and improve it,” she said. “If we are going to use it like medicine, think of it like medicine.”
A key component to the “medicine” of exercise and physical therapy is music, according to Stewart, because it adds value to the exercise. Tunes substitute as a timekeeper when that part of the brain is unable to do it internally, something Stewart said is called rhythmic auditory stimulation. She said listening to the music while exercising or walking has been found to increase stride lengths and helps muscles work together.
One of the exercises demonstrated was simply walking heel to toe, around a chair, to Johnny Cash’s “Ring of Fire.” As the music went on, the steps to the beat became more synchronized and strides increased.
Another element of music with its own health benefits is singing, which Stewart said loosens the muscles used to swallow and talk. It also helps with that aforementioned multi-tasking or dual-tasking, referred to by Roberts.
To demonstrate, Roberts and Stewart played novelty song “Witch Doctor” and had everyone sing along, exaggerating their facial expressions and achieving exercise — along with some welcome comedic relief.
“‘Witch Doctor’ … always seems to be a crowd-pleaser,” Stewart said. “It is great for working on articulation.”
Nancy Williams Johnson, a sardonic 72-year-old at the workshop who attends many of Roberts’ other classes (including her Parkinson’s support group) said she enjoyed the support the therapists and others in the group offer.
“We learn from each other and support each other,” she said. “We have fun.”
Area Parkinson’s disease activities
Power Punch Boxing 
Led by Meredith Roberts and Alejandro Ayala every Tuesday from 3 p.m. to 4 p.m. at Title Boxing Club, 9650 E. Arapahoe Rd, Greenwood Village. Care partners welcome.
PWR! Class: Exercise for Brain Changes
Led by Meredith Roberts every Wednesday from 11 a.m. to 12 p.m. at Garden Plaza of Aurora Multi Media Room, 14221 E. Evans Ave., Aurora. Care-partners welcome.
Good Vibrations Music and Movement Class
Led by Rebekah Stewart of Rehabilitative Rhythms every Thursday at 1 p.m. at Rehabilitative Rhythms, 2222 S. Fraser St., Unit 2, Aurora.
Parkinson’s Support Group 
Led by Meredith Roberts the second Tuesday of every month from 1 p.m. to 3 p.m. at the Aspen Room, 2888 S. Heather Gardens Way, Aurora.

NeuroDerm to Present Updates on 2 Parkinson’s Therapies at Vancouver MDS Congress


Israel’s NeuroDerm will update its ND0612H and ND0701 therapies for Parkinson’s disease during the 21st International Congress of Parkinson’s Disease and Movement Disorders, scheduled for June 4-8 in Vancouver.
ND0612H is a liquid formulation of levodopa/carbidopa (LD/CD) given subcutaneously to patients with advanced Parkinson’s. Trial 006 (NCT02577523) enrolled 38 participants across the United States, Europe and Israel, who were assigned to receive 24 hours (R1 group) or 14 hours (R2 group) of the ND0612H infusion.
The R1 group received ND0612H 720 mg of levodopa and 90 mg of carbidopa at a high daytime rate for 18 hours and a low nighttime rate for six hours. The R2 group received 538 mg of levodopa and 68 mg carbidopa during 14 hours in the day, and an additional morning dose of 150 mg and 15 mg of the two drugs. All patients were treated for 28 days.
Preliminary results released in March 2017 showed that nearly two-thirds of patients who responded to the treatment had no OFF-time. The presentation, “Safety, efficacy and tolerability of continuous SC LD/CD (ND0612) infusion in PD patients with motor fluctuations,” by Dr. Sheila Oren, NeuroDerm’s chief medical officer, will update these results.
Another presentation, “Baseline characteristics of the population enrolled to a randomized clinical study of subcutaneous levodopa/carbidopa (ND0612) infusion in patients with advanced PD,” by NeuroDerm’s medical director, Dr. Tami Rachmilevitz, will reveal additional data from the trial.
In addition, NeuroDerm will present findings of Trial 005 comparing ND0612 and LD/CD gel suspension delivered to the intestine. Liat Adar, Neuroderm’s director of clinical pharmacology and personalized medicine, will present the paper, “Pharmacokinetic profile of continuous levodopa/carbidopa delivery when administered subcutaneously (ND0612) versus duodenal infusion.”
Finally, the company will reveal data on the pharmacokinetics of its other product, ND0701 — a new liquid formulation of apomorphine for patients with moderate to severe Parkinson’s disease who do not respond well to LD/CD. In 2015, the U.S. Food and Drug Administration lifted its clinical hold on U.S. clinical studies of ND0612H and ND0612L. ND0612L is similar to ND0612H but is being developed to treat patients with moderate Parkinson’s.

Brain-penetrating nanoparticles restore neuron function

May 25, 2017

FUS-mediated delivery of GDNF-BPN to the striatum of PD rats leads to a significant increase in GDNF protein levels in the striatum. Courtesy: Nano Letters

Researchers at the University of Virginia and Johns Hopkins University School of Medicine in Baltimore have developed a new, non-invasive and non-toxic genetic therapeutic technique to restore dopaminergic neuron function in rats suffering from Parkinson’s disease. The technique, which makes use of magnetic-resonance-image-guided ultrasound and brain-penetrating nanoparticles, reverses neurodegeneration thanks to expression of the neurotrophic growth factor GDNF in motor-neuron pathways. A singe injection of the nanoparticles continues to act for at least 10 weeks.

Parkinson’s disease is a largely idiopathic neurodegenerative disorder that affects roughly 2% of the over-65 population. It is thought to cost more than $14 billion a year in the US alone and looks set to double as early as 2040. One of the main hallmarks of the disease is degeneration of the neurons responsible for producing the neurotransmitter dopamine. This produces progressive and debilitating motor-control deficits, including bradykinesia, rigidity and uncontrolled trembling. 
Current treatments for Parkinson’s include administering pharmaceutical dopamine or surgical therapies like deep-brain stimulation. While these can improve symptoms in early stages of the disease, they do not protect neurons and the disease continues to progress. What's more, late-stage patients often develop other motor symptoms as a side effect of long-term dopamine replacement. All in all, therapies that can slow or stop the neurodegenerative process are still lacking.

Gene therapy

Gene therapy could be a solution here, with neurotrophic factors like the glial cell-line neurotrophic factor (GDNF) showing particular promise. These factors protect neurons from degenerating further and even regenerate neurons, enhancing the amount of dopamine generated. Many gene-therapy clinical trials have been completed in recent years using genes that encode for neurotrophic factors like GDNF or its close relative neurturin (NTRN). However, therapeutic outcomes have unfortunately proved rather disappointing. 
Direct injection strategies to deliver genes into the brain appear to be safe, but they are of course invasive, so they are often not considered for early-stage patients. To complicate matters further, the blood–brain barrier (BBB) prevents nearly all molecules larger than about 400 Da in size from entering the brain. Although this problem can be overcome to some extent using viral vectors and nanoparticles with BBB-targeting ligands in large systemic doses, these can lead to serious side effects.

MR image-guided focused ultrasound

MR image-guided focused ultrasound (FUS) is emerging as a way to non-invasively open the BBB for delivering nanoparticles as large as 100 nm into specific parts of the brain. This technique works thanks to activated microbubbles exerting mechanical forces on the brain vessel wall, temporarily disrupting tight vessel junctions, so allowing the particles to pass through. The good thing is that the brain’s barrier restores within four to six hours. The method has been FDA-approved for use in patients with essential tremor, and clinical trials for other central nervous disorders are now under way too. 
The story does not end there. Once across the BBB, vectors must pass through a dense, nanoporous and negatively charged extracellular matrix that blocks nanoparticles and viruses thanks to both adhesive interactions and so-called steric obstruction. Researchers recently found, however, that particles smaller than 114 nm and densely coated with hydrophilic and neutrally charged polyethylene glycol can overcome this barrier and rapidly diffuse across the brain-vessel walls. Importantly, these “brain-penetrating particles” (BPNs) can be complexed into nanosized and stable gene vectors by incorporating them into colloids. 

FUS opens blood–brain barrier in a targeted region

Researchers led by Richard Price of the University of Virginia recently showed that FUS can be used to deliver BPNs loaded with plasmid-DNA into the rat brain in a targeted region. They have now found that they can deliver BPNs loaded with a GDNF gene-bearing plasmid to the striatum of rats suffering from Parkinson’s whose BBBs had been transiently opened in a specific area using MR image-guided FUS. 
“The blood–brain barrier is only opened where we apply the focused ultrasound,” explains Price. “In essence, we ‘paint’ the brain volume we wish to transfect with the ultrasound probe so brain-penetrating nanoparticles are only delivered in that specific region.”

Reversing motor-behaviour deficits

The enhanced GDNF protein causes the neurons to either stop degenerating or to regenerate, he told This then allows the neurons to express dopamine, which reverses the motor-behaviour deficits associated with the disease.
The study could open the way to using minimally invasive MR image-guided focused ultrasound to treat the underlying causes of Parkinson’s through gene therapy, he adds. The same general concept could be applied to treating brain tumours, for example, as well as other pathologies of the central nervous system.
The researchers, reporting their work in Nano Letters, say that they will now begin a set of additional experiments that will help them understand how best to translate their approach to clinical trials. “The second step is to test alternative therapeutic genes in the context of more sophisticated Parkinson’s models to potentially identify other approaches that may also be efficient when used with our delivery methods.”

Study provides understanding of how nerve cells are damaged by accumulation of abnormal proteins

May 25, 2017  By 

Degeneration of dendrites in mouse hippocampal neurons is seen in the beaded appearance of dendritic segments in the images on the left. The degeneration was induced by antibodies that blocked the normal interaction between the two ends of the prion protein. (Image credit: Wu et al., eLife, 2017)

A new study has uncovered a molecular mechanism in the prion protein that may explain why nerve cells degenerate in prion diseases such as Creutzfeldt-Jakob disease (CJD).
The findings, which appear in the journal eLife, may one day lead to better therapies and treatments for these diseases.
Prion diseases, including CJD in humans and "mad cow disease" in cattle, are fatal neurodegenerative brain disorders caused by a misfolded form of the normal cellular prion protein. Other, more common neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and frontotemporal dementia have also been found to involve abnormal accumulation of misfolded protein aggregates in the brain.
According to the researchers, how nerve cells are damaged in prion diseases has remained a mystery until now. The new research combined cellular studies, led by Dr. David Harris at Boston University School of Medicine (BUSM), with structural analysis of prion proteins performed at UC Santa Cruz using nuclear magnetic resonance (NMR).
“Our work shows that the prion protein acts like a molecular on-off switch. In the 'on' positon, one end of the protein delivers a toxic signal to nerve cells, while in the 'off' position, the other end of the protein serves as a brake to reduce the toxic signal,” said Harris, corresponding author of the paper and professor and chair of biochemistry at BUSM. “This novel mechanism, in which the two parts of the prion protein have opposing functions, had not been fully appreciated before.”
The study also showed that copper, a normal constituent of brain chemistry, promotes interaction between the two ends, biasing the prion protein toward the “off” state. Disruption of this interaction led to degenerative changes in nerve cells.
“These data provide the best picture yet of the prion protein's 'off' state,” said coauthor Glenn Millhauser, professor of chemistry and biochemistry at UC Santa Cruz. “Recognizing the nature of this state provides a platform for developing drugs to treat neurodegenerative diseases. This is an exciting time in prion biology.”
Using a multi-disciplinary approach involving electrophysiological, cellular, and biophysical techniques, the researchers found that parts of the prion protein lacking the “brake” region produced abnormal electrical currents in cells. Antibodies that interfered with the functioning of the brake region did the same. Importantly, the antibody treatment also caused severe degeneration of nerve cell dendrites, the regions that are essential for normal communication between nerve cells. In collaboration with Millhauser and others at UC Santa Cruz, the researchers applied a sophisticated chemical technique to demonstrate that the two ends of the prion protein interact with each to alter the amount of toxic signal that is delivered.
As a result of their findings, the researchers caution against administering antibodies against the prion as a possible therapy for both prion and Alzheimer’s diseases. “Our study sounds a serious warning about the possible detrimental side effects of this strategy, since we have shown that such antibodies cause dramatic degeneration of nerve cells by interfering with the normal on-off function of the prion protein,” Harris said.
The researchers hope their study will lead to better therapies for neurodegenerative disorders, as well as help clinicians avoid the possible dangerous side-effects of using anti-prion protein antibodies for therapeutic purposes.
Funding for this study was provided by the National Institutes of Health, the National Science Foundation, and the German Research Foundation.

New research into delaying the onset of motor neurone disease shows positive results

May 25, 2017

  • Drug candidate was discovered by British artificial intelligence company BenevolentAI
  • Researchers from the Sheffield Institute of Translational Neuroscience found significant indications that the drug prevents the death of motor neurones in patient cell models - delaying the onset of the diease in models 

The drug candidate was discovered by the British artificial intelligence company BenevolentAI.
The study, which was led by Dr Richard Mead and Dr Laura Ferraiuolo from the University’s Sheffield Institute of Translational Neuroscience (SITraN), found significant and reproducible indications that the drug prevents the death of motor neurones in patient cell models and delayed the onset of the disease in the gold standard of models.
Motor neurone disease, also known as Amyotrophic Lateral Sclerosis (ALS) is a progressive neurodegenerative disease that causes muscle weakness, paralysis, and ultimately, respiratory failure. 
Life expectancy following diagnosis is approximately two to five years.

There are currently only two FDA approved drugs available to patients, Riluzole, approved in 1995, and Edaravone, approved only a few weeks ago.
SITraN are now moving to the next phase of their research, advancing the existing study and assessing the suitability and potential for clinical development. Researchers expect to publish an abstract at the motor neurone disease Association 28th International Symposium in Boston, USA in December.
Dr Richard Mead from SITraN said: “This is an exciting development in our research for a treatment for ALS. BenevolentAI came to us with some newly identified compounds discovered by their technology - two of which were new to us in the field and, following this research, are now looking very promising. Our plan now is to conduct further detailed testing and continue to quickly progress towards a potential treatment for ALS.”
SITraN is one of the world leading centres for research into motor neurone disease, Alzheimer’s and Parkinson’s disease. From basic neuroscience research to novel therapies and clinical trials – SITraN’s aim is to improve the lives of patients with neurodegenerative disorders and their families worldwide.
The purpose-built facility uniquely allows the multidisciplinary collaboration of clinicians, scientists and health professionals to develop new treatments for the benefit of patients.
Ken Mulvany, Founder and Chairman of BenevolentAI commented: “We understand from SITraN their research demonstrates that the hypothesis and drug candidate that our technology identified has delayed the onset of cell death in the gold standard model of ALS. We are incredibly encouraged by these findings. We very much look forward to the results of SITraN’s further studies and are hopeful for the positive impact that this drug could have for people living with ALS.”

Additional information

BenevolentAI is the global leader in the development and application of AI for scientific innovation. It is the largest private AI company in Europe and one of the world’s top five private AI companies. Since it was founded in 2013, BenevolentAI has been building and applying AI to the world’s new natural resource – data, to generate and probe science’s ‘hidden knowledge’. By doing so, the Company is turning highly fragmented unstructured information into new insight and usable knowledge. The technology is transforming the process of scientific discovery and enabling previously unimaginable scientific advances. BenevolentAI has proven its technology by applying it to human biology and has made significant progress in accelerating drug development.
For more information please visit: 

The University of Sheffield
With almost 27,000 of the brightest students from over 140 countries, learning alongside over 1,200 of the best academics from across the globe, the University of Sheffield is one of the world’s leading universities.
A member of the UK’s prestigious Russell Group of leading research-led institutions, Sheffield offers world-class teaching and research excellence across a wide range of disciplines.
Unified by the power of discovery and understanding, staff and students at the university are committed to finding new ways to transform the world we live in.
Sheffield is the only university to feature in The Sunday Times 100 Best Not-For-Profit Organisations to Work For 2017 and was voted number one university in the UK for Student Satisfaction by Times Higher Education in 2014. In the last decade it has won four Queen’s Anniversary Prizes in recognition of the outstanding contribution to the United Kingdom’s intellectual, economic, cultural and social life.
Sheffield has six Nobel Prize winners among former staff and students and its alumni go on to hold positions of great responsibility and influence all over the world, making significant contributions in their chosen fields.
Global research partners and clients include Boeing, Rolls-Royce, Unilever, AstraZeneca, Glaxo SmithKline, Siemens and Airbus, as well as many UK and overseas government agencies and charitable foundations.


For further information please contact:
Amy Pullan
Media Relations Officer
University of Sheffield
0114 2229859

Wednesday, May 24, 2017

APDA Partners with Smart Patients to Support Parkinson’s Online Community


The American Parkinson Disease Association (APDA) is collaborating with Smart Patients — an online community connecting Parkinson’s patients and their families — to extend APDA’s resources to help people living with the disease.
Smart Patients provides resources so people can have the latest information related to their condition, share their questions and concerns with other members, and use those resources to improve their daily lives.
The software company believes patients are the most underutilized resource in healthcare and says that thanks to its resources, patients become experts in their conditions and that this knowledge improves the care they receive.
APDA is the nation’s largest grassroots network dedicated to fighting Parkinson’s. Since its establishment in 1961, the New York-based organization has raised and invested more than $170 million to provide patient services and educational programs, increase public awareness about Parkinson’s and support research designed to better understand, and ultimately end, the disease.
“We are thrilled with our partnership with Smart Patients to launch this community. This network is designed for people with Parkinson’s, care partners and family members,” Robin Kornhaber, APDA’s vice president of programs and patient services, said in a news release. “This innovative opportunity will further a dialogue to nurture the Parkinson’s community, provide socialization, education, and critical access to information — and will allow us to expand our reach across the country.”
By collaborating with Smart Patients, APDA empowers patients and families living with Parkinson’s to improve care for themselves and others.
“We are proud to work with the APDA to connect people with Parkinson’s with one another,” said Dr. Roni Zeiger, CEO of Smart Patients. “Community can provide peace of mind through social and emotional support, not to mention those practical tips patients and families learn through direct experience.”
Patients can join the community by registering here:
Once a registration process is complete, participants will have access to information, resources, and can take part in community chats and topics about Parkinson’s.

Parkinson’s Foundation Welcomes New Patient Advisors

Five New Members Added to Advisory Council to Improve Lives of People Living With Parkinson's

NEW YORK and MIAMIMay 24, 2017 /PRNewswire-USNewswire/ -- The Parkinson's Foundation is pleased to welcome five new members to its People with Parkinson's Advisory Council.  The appointments reflect the foundation's ongoing commitment to engage with the community in its work to create a world without Parkinson's disease.
"The Parkinson's Foundation has a track record of listening and responding to the needs of the Parkinson's community," said John L. Lehr, chief executive officer, Parkinson's Foundation.  "We look forward to partnering with our advisors to improve our programs and to ensure that people with Parkinson's live their best lives today."
The People with Parkinson's Advisory Council, established in 2006, is the first patient advisory council in the Parkinson's space.  Its members have guided the foundation's work and driven improvements in research, care and patient support.  For example, members have shed light on unmet needs, including underrecognized symptoms such as fatigue and constipation, and have prompted new programs, such as the Women and PD Initiative and the Community Choice Research Awards.
"As people who live with Parkinson's, our members represent a community of 10 million people worldwide.  We commit ourselves to working on their behalf every single day," said Daniel Novak, Ph.D., of Fort Worth, TX, chair of the advisory council.  "We applaud the Parkinson's Foundation for continuing to collaborate with people with Parkinson's and care partners.  We are stronger together."
The advisory council's newest members, elected for a term of three years, represent a wide range of communities, professions and volunteer experiences.  They include the following individuals:
Caryn Balaban, M.P.H., of Phoenix, AZ: a retired healthcare marketing executive, who is care partner to her husband who lives with Parkinson's.
Daniel DeWitt, Psy.D., of Grand Rapids, MI: a licensed psychologist who has expertise caring for individuals with chronic illnesses.
David Malarkey, D.V.M., Ph.D., of Cary, NC: a veterinary pathologist and research scientist whose scientific career spans 25 years and 100 published papers.
Dana Seyfried, M.A., of Roslyn, NY: a professional who works in animal welfare and a former marketing manager, who is care partner to her father who lives with Parkinson's.
Robert "Kelly" Sweeney, of Portland, OR: a retired business development and program manager, whose career in the technology industry spanned nearly 40 years.
To learn more and see our full list of advisors, visit
About Parkinson's Disease
Parkinson's disease is a progressive neurological disorder that affects nearly one million people in the US and over 10 million worldwide.  Parkinson's is the second most common neurodegenerative disease after Alzheimer's and is the 14th leading cause of death in the US. It is associated with a loss of motor control (e.g., shaking or tremor at rest and lack of facial expression) as well as non-motor symptoms (e.g., depression and anxiety).  Although promising research is being conducted, there is currently no cure for Parkinson's disease.

About the Parkinson's Foundation
The Parkinson's Foundation is working toward a world without Parkinson's disease.  Formed by the merger of the National Parkinson Foundation and the Parkinson's Disease Foundation, the mission of the Parkinson's Foundation is to invest in promising scientific research that will end Parkinson's disease and improve the lives of people with Parkinson's, and their families, through improved treatments, support and the best care.  For more information, visit or call (800) 4PD-INFO (473-4636) or (800) 457-6676.

Contact: Melissa Barry
Director of Communications
Parkinson's Foundation
Phone: (212) 923-4700

SOURCE Parkinson's Foundation

African-Americans More Likely Than Whites to Receive Parkinson’s Care in Hospital, Study Reports


African-Americans are more likely to receive care for Parkinson’s disease in a hospital emergency room and have more hospital stays than whites, according to a U.S. study.
Blacks also more likely to be treated for stroke in a hospital than whites, researchers said.
Another finding was that both African-Americans and Hispanic-Americans are more likely than whites to be treated for multiple sclerosis in hospitals than doctor’s offices or clinics.
The research dealt with differences in the rates at which African-Americans, Hispanic-Americans and whites with neurological conditions receive treatment at doctor’s offices versus hospitals. Whites have a higher rate of treatment in doctor’s offices.
“Our findings demonstrate that there are substantial racial and ethnic disparities in neurologic health care access and utilization in the United States,” Dr. Altaf Saadi of Massachusetts General Hospital and Brigham and Women’s Hospital in Boston, said in a news release. “These disparities are concerning not only because racial and ethnic minorities represent 28 percent of Americans, but because all Americans should have equitable access to health care regardless of who they are, where they live, or what resources they have.”
Researchers used Medical Expenditure Panel Survey information from 2006 to 2013 to find where patients with neurological diseases were treated. The information included patients’ demographic characteristics, including race; the health conditions they reported; their neurology-disease-related visits; and their healthcare costs.
Of the 279,103 people who took part in the survey, 6 percent, or 16,936, reported a neurological  condition. They included 397 with Parkinson’s, 399 with multiple sclerosis, 2,236 with epilepsy, 3,338 with cerebrovascular disease, and others with different disorders.
Two percent of all the survey participants, or 5,890, said they had visited neurologists in doctor’s offices or clinics. Together, they reported making 13,685 such visits.
African-Americans were about 30 percent less likely than whites to see a neurologist in an office, even when the researchers adjusted the data for demographic, insurance, and health-status differences. Hispanics were 40 percent less likely than whites to see a neurologist in an office.
Similarly, African-Americans with a neurological disorder were more likely to receive care in a hospital emergency room and to have more hospital stays than whites. African-Americans also had higher hospital treatment expenditures than whites.
“Previous research has shown that having neurologists involved in the care of people with neurologic conditions reduces serious side effects and hospitalizations for acute problems,” Saadi said. “So unequal access to outpatient [doctor’s office] care may be resulting in unnecessary medical and financial costs.”
One factor that could play a role in races’ different treatment-setting patterns is divergent cultural beliefs about aging and disease. Another is that non-English speakers could be reluctant to go to doctor’s offices because of the language challenge. Still another is lack of doctor’s offices in many minority communities.
More studies are necessary to understand race-related treatment-setting disparities, and find ways to eliminate them, researchers said.
“Solutions could include initiatives to education hospital staff about bias and multicultural care, increase the proportion of underrepresented minorities in the field of neurology, improve patient education about neurologic disorders and change institutional practices to provide more equitable care,” Saadi said.

Big hunt for small molecule to treat neurodegenerative diseases

May 24, 2017 by Robin Tricoles

Daniela Zarnescu: "Flies make a great model that has been used to study development. Their genes are incredibly similar to humans'. About 70 percent of human disease genes are conserved in the fly genome." Credit: Bob Demers/UANews

Late last year, University of Arizona colleagues Daniela Zarnescu and May Khanna sped west on Interstate 8 bound for a brain-research conference in San Diego. Khanna is a biochemist who works with small molecules. Zarnescu is a molecular and cellular biologist who works with flies.

"I was talking with Daniela on the way to the meeting," Khanna recalls, "and I said, 'Daniela, I want a target that's never been done before. We're coming up with a small molecule that you can test on your flies.'"

That small molecule Khanna was referring to would bind with TDP-43, a  that has been implicated in the development of neurodegenerative diseases such as , or ALS—Zarnescu's and Khanna's focus. That binding, in turn, could open the door to therapeutic drugs to treat the disease.
However, finding the optimal small molecule, one that would bind with TDP-43 and that would be a safe and effective treatment for ALS, is a tall order. It's not impossible to fill, thanks to advances in genomic sequencing, the elegance and simplicity of the fly model, and the power of supercomputers. 
"Flies make a great model that has been used to study development and, in the past several years, has been used to study human diseases," says Zarnescu, associate professor of cellular and molecular biology. "Their genes are incredibly similar to humans'. About 70 percent of human disease genes are conserved in the fly genome."
About 10 percent of ALS cases are inherited, or familial. The other 90 percent are known as sporadic cases. Familial ALS has helped scientists study a pedigree; that is, it has helped researchers identify familial mutations. Many genes linked to ALS have been identified that way, Zarnescu says.
"But what is interesting is that in some of the sporadic cases, you also find similar mutations, so there is a clear genetic basis to the disease," she says.
To complicate matters, researchers suspect that environmental factors, such as cigarette smoke and toxic chemicals, contribute to the development of .
The Common Denominator
No matter, the presence of TDP-43 seems to be a common denominator in most if not all people with ALS. That is, TDP-43 is found within clumps of proteins, known as cellular aggregates, which form in the brain cells of those with ALS."If you take postmortem samples from people with ALS, and if you look at what's in those cellular aggregates, you find TDP-43-positive aggregates in 9 percent of patients," Zarnescu says. "I call that significant."
In a normal situation, the majority of the protein resides in the nucleus, where it takes care of , Zarnescu explains. But in disease states, it emerges from the nucleus and forms cytoplasmic aggregates.
"These are a hallmark of neurodegeneration, whether it's ALS, dementia, or Alzheimer's or Parkinson's," Zarnescu says.
"Essentially, proteins aggregate and form these huge areas in cells that act like kitchen sinks where other things go and then stick. It's like a huge traffic jam, a huge clog. They're essentially altering gene expression and protein function in a very dramatic way."
At first glance, it might seem that researchers would be trying to eliminate these aggregates, but studies show that these aggregates may be protective at some stage as they are originating from what are known as RNA stress granules.
These stress granules, composed of proteins and RNAs, form in the cells' cytoplasm when cells are under stress, whether the stress is environmental or caused by mutations, Zarnescu says.
Although their exact functions are not yet fully understood, Zarnescu explains that the granules won't allow certain RNA  to be translated into proteins, their final fate. 
"If the stress goes away, then these RNA granules dissolve, and the RNAs are freed, and the translation starts over again," Zarnescu says. "It's like a pause for protection."
If the stress doesn't go away, the aggregates persist and they undergo an evolutionary process, she says. That evolutionary process leads to the accumulation of protein aggregates seen after death.
"This is the process that many of us are trying to understand—and what May and I are working on together," Zarnescu says. "We don't want to get rid of these aggregates because they are protective in the initial stage. This is a physiological mechanism that we need to survive."
Finding the molecule
That is why Khanna, an assistant professor of pharmacology, and Zarnescu want to find that small molecule—a molecule that will remodel the aggregates before they get out of control. "You want to release the RNAs, you don't want to sequester them forever because that's how you lead to changes in gene expression and eventually motor neuron death," Zarnescu says.
But how does one find such a small molecule?
"I drove back from San Diego by myself with no music, nothing, and I started to think about the problem," says Khanna, an assistant professor of pharmacology.
Khanna says she knew solving the problem would start with harnessing tremendous computing power. To come up with just the right molecule, she would need to sort through more than 1 million target molecules in silico. She also knew she would need Zarnescu's impeccable fly model and other collaborators, including Vijay Gokhale, UA director of Computer Aided Drug Discovery, and her students, who would help select those target molecules while learning about drug discovery firsthand.
"May is actually teaching us how  bind to TDP-43," Zarnescu says. "She goes to her supercomputer and says, 'Here's a good molecule.' We find something in the fly, go back to her, and tell her what proteins and RNA we might be thinking about. She does her structural magic, and then she goes to the supercomputer. The supercomputer tells her what molecules might be even better, and then we come back to the fly and test, and we're going to go through a few iterations like that."
Will Khanna recognize a sound candidate when she sees one?
"The way I think of proteins is mountains and valleys," Khanna says. "These are like the pockets in proteins, and you want the small molecule to fit in there. That's the docking. We want them to prohibit other things to bind to them.
"The little molecule needs to fit on this groove or pocket and not allow something else to come in and dock there. You need to hit important regions. These regions you're hitting is like Achilles' heel. You hit his heel with an arrow and you kill him. You hit these regions and you inhibit these reactions."

Provided by: University of Arizona

Skin color no shield against skin cancer

May 23, 2017

Human skin structure. Credit: Wikipedia

Sidney Brown thought the mole on his nose was just an annoying pimple. He didn't consider that it could be a cancerous tumor, because, Brown thought, "skin cancer is something white people get."The misconception that people with more pigment—called melanin—in their  cells are protected from cancer-causing ultra-violet rays nearly cost Brown his life.

Brown's  turned out to be a melanoma, the least common form of , but also the deadliest. While most people associate skin cancer with sun exposure, melanomas are more likely to be caused by genetics than the sun's ultraviolet radiation, and far more likely to develop on sun-protected areas of the body in blacks, Hispanics and Asians.
May is Melanoma/Skin Cancer Detection and Prevention Month, the occasion for numerous messages about the importance of limiting time in the sun and using sunscreen. While those protective actions are important, they can mislead people into making the same dangerous mistake Brown made.
"The misconception that the sun is responsible for all cases of melanoma leads to lower survival rates because of delayed diagnosis, particularly among people of color," explains Arthur Rhodes, MD, MPH director of the Rush Melanoma Surveillance Clinic. Rhodes estimates that only ten to 15 percent of melanomas are caused by excessive sun exposure, typically in heavily freckled and sun-damaged skin.
'Anyone - regardless of skin color - may develop melanoma'
Brown, who is black and a father of two, wasn't worried about the mole on his nose until it began to change. "It started out flat. I didn't really pay much attention to it, because I had an oily face and pimples on my nose anyway," he says."So when I saw the black mark, I didn't think much about it. But then it kept irritating me, itching. Then it grew into a lump." His primary care doctor referred him to Rhodes, who quickly diagnosed the mole as cancerous. "He explained that once a mole starts growing up, it is also spreading cancer cells down through the body. That can be too late for many, but catching mine in time saved my life." Brown recalls2016 American Academy of Dermatology study, "Racial Disparities in Melanoma Survival," showed that while melanoma incidence is higher in whites, death rates are relatively higher among people of color.
"Far too often, black, Hispanic, and Asian patients with melanoma cancer tell us they believed that melanoma was only a danger for sun-seeking whites," the researchers write in their report of the study findings. "But anyone - regardless of skin color - may develop melanoma, in both sun-exposed and sun-protected sites. Not noticing or ignoring a new or changing mole in a sun-protected site can be fatal."
Early diagnosis key to survival
Melanomas develop from skin cells called melanocytes, which reside in the superficial layer of the skin called the epidermis. Melanocytes in the epidermis produce pigment (melanin) that gives the skin its color and protects skin cells from the damaging effects of the sun's ultraviolet radiation.
Abnormal varieties of melanocytes cause common skin growths known as moles. Most moles are harmless, but unique varieties of atypical moles may develop into melanoma.
While less common than other types of skin cancer, melanomas are deadlier, because the malignant cells can spread even though the tumor is relatively small and not bleeding or causing pain or itching. This capacity to metastasize underlies the importance of early detection, especially among people of color.
Rhodes stresses the need for monthly self-examination and examination in difficult-to-see areas on the body in family members, seeking the presence of a new mole, or a change in a pre-existing mole - a change in size, shape or color. Some of the most aggressive forms of melanoma may occur on areas that receive little or no direct sunlight.
Melanoma is reason for sole searching
A delayed diagnosis is common for melanomas in these difficult-to-self-examine sites. "Early diagnosis results in a cure, while delayed diagnosis may be deadly," Rhodes warns.
"Half of all melanomas in non-whites occur on the palms of the hands, soles of the feet, nailbeds, mucous membranes, perianal area, genitalia, and other areas that are not exposed to the sun, areas that are difficult-to-self-examine and commonly ignored."
Melanoma in a relatively hidden site will tend to thicken without symptoms or signs, leading to a delayed diagnosis that may result in a higher melanoma death rate, especially for people of color, including blacks, Hispanics, and Asians.
Since Rhodes removed his cancerous melanoma ten years ago, Brown has been counseling friends and family to pay closer attention to their skin. "Dark-skinned people think it's nothing," Brown says.
"A lot of times we get moles, and we don't think anything about it. Don't accept that it can't be something; go see what it is. Don't say 'Eh, (melanoma is) something that white people get.'"
Melanoma Risk Factors
According to the Rush Department of Dermatology, a variety of physical, historical, and genetic traits increase the risk for developing melanoma, including the following:
  • Having a mole present within the first two weeks of life (a birth mole) (10-fold increased risk)
  • Having a personal history of melanoma (nine-fold increased risk) 
  • Having a family history of  (eight-fold increased risk)
  • Having numerous moles and/or atypical moles (eight-fold to 40-fold increased risk)
  • Having had a Spitz tumor removed (eight-fold increased risk)
  • Having had an atypical nevus removed (seven-fold increased risk)
  • Having had at least 2 moles removed in the past (five-fold increased risk)
  • Prior treatment for psoriasis with more than 200 PUVA treatments (psoralen pills and ultraviolet A radiation) (five-fold increased risk)
  • Having had a basal cell cancer or squamous cell cancer (four-fold increased risk)
  • Presence of dense sun-induced freckles (three-fold increased risk) 
  • Immune suppression related to disease or medication (three-fold increased risk)
  • Having red hair (two-fold increased risk)
  • Having Parkinson disease (two-fold increased risk)
  • Multiple sunburns in early childhood (two-fold increased risk)