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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.


Friday, May 1, 2015

Studies in Cell Transplantation show beneficial effects for variety of serious conditions


Last updated: 
Five studies from the current special issue of Cell Transplantation 24(4) devoted to work presented at the 21st meeting of the American Society for Neural Therapy and Repair (ASNTR) in 2014, a society for scientists focused on understanding the causes of, and developing cell and gene therapy and biopharmaceuticals for neurological injury and disease, are currently freely available on-line.*
MSCs promote improvement in patient with complete spinal cord injury
Complete spinal cord injury (SCI) leads to profound disability and, with long-term complications, even death. This study demonstrated the potential of transplanted bone marrow nucleated cells (BMNCs) to restore feeling and function to the lower body. Over a two year period, researchers assessed the safety and efficacy of combined intravenous/intrathecally administered autologous (self-donated) BMNCs and multiple lumbar puncture administered mesenchymal stem cell (MSC) injections in treating a patient with complete SCI. Results suggested that the treatment had the potential to produce "clinically meaningful improvements for SCI patients" as this patient experienced a restored ability to control his body trunk, a restoration of bladder and anal sensation, and gained the ability to stand with a standing frame and walk with the support of hip and knee ortheses.
Citation: Jarocha, D.; Milczarek, O.; Wedrychowicz, A.; Kwiatkowski, S.; Majka, M. Continuous Improvement After Multiple Mesenchymal Stem Cell Transplantations in a Patient With Complete Spinal Cord Injury. Cell Transplant. 24(4):661-672; 2015.
Bone marrow MSC culture enhances human neural stem cells 
"Rapid loss of stemness capacity in purified prototype neural stem cells (NSCs) remains a serious challenge to basic and clinical studies aimed at repairing the central nervous system," wrote a team of researchers from the Harvard Medical School and the Boston Veteran's Administration Health System. The researchers tested human NSCs and human MSCs to find out if bone marrow-derived MSCs could enhance the "stemness" of human NSCs. They speculated that the a biological pathway called Notch-1 might be a major mechanism through which hNSCs and hMSCs communicate to 'modulate' their stemness biology through direct interactions, offering a potential strategy for hNSC stemness enhancement. After their experiments in co-culturing hNSCs and hMSCs they found that enhancement of the stemness of hNSCs occurred through Notch-1 signaling. "Our finding provides mechanistic leads for devising effective regimens to sustain and augment stemness of in vitro established hNSC and hMSC lines for use in basic science as well as translational and clinical applications," concluded the researchers.
Primate model of Parkinson's disease study shows role for upgrading endogenous neurons
The possibilities for having the brain help heal itself when afflicted by neurological disorders such as Parkinson's disease (PD) is an area of interest. In this study, researchers observed primates modeled with PD and assessed changes in the numbers of neurons expressing the enzyme tyrosine hydroxylase (TH), a precursor for dopamine. They discovered "a close relationship" between PD symptom severity and striatal DA neuron numbers. The possibility of increasing the numbers of these neurons as compensation for their depletion in PD by artificial means "could prove beneficial for PD treatment, especially for individuals in the early disease stages," they concluded.
Citation: Bubak, A. N.; Redmond, D. E.; Elsworth, J. D.; Roth, R. H.; Collier, T. J.; Bjugstad, K. B.; Blanchard, B. C.; Sladek, J. R. A Potential Compensatory Role for Endogenous Striatal Tyrosine Hydroxylase-Positive Neurons in a Nonhuman Primate Model of Parkinson's Disease. Cell Transplant. 24(4):673-680; 2015.
Human pluripotent stem cells hold promise for Parkinson's disease 
Recent studies have shown that human pluripotent stem cells (PSCs) may hold promise for treating Parkinson's disease (PD). Transplanted fetal neural tissue has been shown to provide improvements in PD, but the source of this tissue is limited and controversial. Looking for alternatives and proof of concept, the researchers studied the benefits of using human pluripotent stem cells (hPSCs) and neural stem cells (NSCs) to engraft into animal models of PD. "In this study we showed for the first time the successful engraftment and safety of NSCs derived from human parthenogenetic stem cells following transplantation in rodent and non-human primate PD models," concluded the researchers. "In both models, transplantation of hpNSCs led to improvement of DA (dopamine) levels, which could be explained by the multimodal actions of the NSCs, to include neuroprotection and cell replacement."
Citation: Gonzalez, R.; Garitaonandia, I.; Crain, A.; Poustovoitov, M.; Abramihina, T.; Noskov, A.; Jiang, C.; Morey, R.; Laurent, L. C.; Elsworth, J. D.; Snyder, E. Y.; Redmond, D. E.; Semechkin, R. Proof of Concept Studies Exploring the Safety and Functional Activity of Human Parthenogenetic-Derived Neural Stem Cells for the Treatment of Parkinson's Disease. Cell Transplant. 24(4):681-690; 2015.
Anti-tumor effect of secreted factors studied for effect on glioblastoma-like cells
Researchers studied the possible anti-tumor effects of the secreted factors from MSCs on four glioblastoma stem-like cells (GSLCs) and found that MSCs "have an intrinsic ability to inhibit the cell cycle, induce senescence (halt cell division) and prevent differentiation of GSLCs." "Glioblastoma multiform (GBM) is the most malignant type of brain tumor that is still incurable, due to its characteristic highly infiltrative growth and resistance to therapy," said the researchers. "The highly tumorigenic subpopulation of cells with stem cell-like properties are presumably the cause for GBM recurrence." The researchers hypothesized that the secreted factors from the MSCs could cause an alteration in the GLSCs' behavior and did in fact observe that they cause cell cycle arrest. They also found that the MSCs also increased the sensitivity of GSLCs to chemotherapy.
"At the 22nd annual meeting of the ASNTR, we are pleased to announce the publication of studies on a myriad of topics ranging from neurotrauma to developmental neurobiology to neurodegenerative conditions in Cell Transplantation," said Dr. Paul Sanberg, Senior Vice President of Research and Innovation at the University of South Florida and co-founder of the ASNTR. "We are pleased to host another conference devoted to excellence in neural research and therapy." 
Citation: Kološa, K.; Motaln, H.; Herold-Mende, C.; Koršič, M.; Lah, T. T. Paracrine Effects of Mesenchymal Stem Cells Induce Senescence and Differentiation of Glioblastoma Stem-Like Cells. Cell Transplant. 24(4):631-644; 2015.
Adapted by MNT from original media release

http://www.medicalnewstoday.com/releases/293210.php?tw

Thursday, April 30, 2015

Hacked Kinect controller game changer for Parkinson's


Date:
April 30, 2015
Source:
Brunel University
Summary:
Microsoft's Kinect games controller has been hacked by researchers to relieve one of the most distressing symptoms of Parkinson's - freezing of gait. Many patients are afflicted by freezing of gait where suddenly, in mid-stride, the muscles freeze and they are left unable to move forward or they simply fall over.
Microsoft's Kinect games controller has been hacked by researchers at Brunel University London to relieve one of the most distressing symptoms of Parkinson's -- freezing of gait.
Scientists at Brunel University London have developed a system for Parkinson's sufferers to counter two of the most common and distressing symptoms of the degenerative disease.
Many patients are afflicted by freezing of gait (FOG) where suddenly, in mid-stride, the muscles freeze and they are left unable to move forward or they simply fall over.
Previous research shows that giving visual clues such as projecting lines ahead on the floor "unfreezes" the muscles but current equipment has to be worn.
But Dr Konstantinos Banitsas and PhD candidate Amin Amini Maghsoud Bigy have turned Microsoft's Kinect computer games controller into a system that can be installed into a patient's own home.
Linked to a ceiling mounted laser, the Kinect can not only project prompt lines when the software detects a FOG incident but if a patient falls, the system not only detects that but also automatically triggers a video conferencing call.
Said Dr Banitsas: "All the other systems require a patient to wear sensors and power packs where our solution is unobtrusive and covers a whole room.
"By mounting the laser guide marker on the ceiling it can provide the visual clues in any direction. And it is only activated when a FOG incident occurs instead of having to be worn constantly.
"The system has already passed proof of concept stage and we will shortly begin patient trials."

Story Source:
The above story is based on materials provided by Brunel UniversityNote: Materials may be edited for content and length.
Brunel University. "Hacked Kinect controller game changer for Parkinson's." ScienceDaily. ScienceDaily, 30 April 2015. <www.sciencedaily.com/releases/2015/04/150430082712.htm>.

http://health.einnews.com/article/262900155/RxsjZsVT3LyTOmVi

NEW GENETIC CAUSE OF PARKINSON'S DISEASE


PARKINSON'S DISEASE NEWS
http://www.viartis.net/parkinsons.disease/news.htm
30th April 2015 - New research

A new genetic cause of Parkinson's Disease has been discovered called CHCHD2. CHCHD2 is associated with the development of Parkinson's Disease. Most genetic causes of Parkinson's Disease do not inevitably cause Parkinson's Disease but make the person affected more likely to develop Parkinson's Disease.
The full name of the genetic cause is : Coiled-coil-helix-coiled-coil- helixdomain containing 2. The gene is on the Chromosome 7p11.2. The function of the gene is to mediate oxygen-dependent expression of cytochrome c oxidase subunit 4-2 gene expression. The researchers do not know how this function inclines somebody towards Parkinson's Disease. The type of inheritance is autosomal dominant, which means that if the abnormal gene is inherited from only one parent you can get the disease. Often, one of the parents may also have the disease. This gene is associated with an increased likelihood of Parkinsons' Disease.
There are now at least 32 known genetic causes of Parkinson's Disease : PARK 1 to 3, PARK 4 to 20, Tyrosine Hydroxylase deficiency, Aromatic L-amino acid decarboxylase deficiency, CHCHD2, CYP2D6, DRD2. DRD3, GLIS1, LINGO1, MAPT, NRA42, PITX3, RIT2, STH. Details of individual genes can freely accessed at http://www.ncbi.nlm.nih.gov/gene

Reference : The Lancet Neurology [2015] 14 (3) : 274-282 (M.Funayama, K.Ohe, T.Amo, N.Furuya, J.Yamaguchi, S.Saiki, Y.Li, K.Ogaki, M.Ando, H.Yoshino, H.Tomiyama, K.Nishioka, K.Hasegawa, H.Saiki, W.Satake, K.Mogushi, R.Sasaki, Y.Kokubo, S.Kuzuhara, T.Toda, Y.Mizuno, Y.Uchiyama, K.Ohno, N.Hattori)


Complete abstract : http://www.ncbi.nlm.nih.gov/pubmed/25662902

http://www.viartis.net/parkinsons.disease/news/150430.pdf mail@viartis.net
©2015 Viartis

Study identifies key factor in neural death that causes Parkinson's disease

Immunohistochemistry for alpha-synuclein showing positive staining (brown) of an intraneural Lewy-body in the Substantia nigra in Parkinson's disease. Credit: Wikipedia

April 27,2015

In studying the molecular biology of brain development, a team of researchers led by Ludwig Stockholm director Thomas Perlmann has discovered how disruption of a developmental mechanism alters the very nerve cells that are most affected in Parkinson's disease. They have also explained how such disruption induces a lethal dysfunction in the internal, house-keeping processes of such neurons. The results of their study, which took nearly four years to complete and involved the exquisitely targeted manipulation of mouse genes to generate a unique model of the disease, are published in the current issue of the journal Nature Neuroscience.
"Our model, in many important ways, mimics the manifestation of Parkinson's in humans and has illuminated what appears to be a key mechanism of neural decline in this devastating disease," says Perlmann.
An incurable neurological disorder, Parkinson's disease (PD) typically begins in patients as a mere tremor and progresses to a debilitating loss of control over movement and cognitive dysfunction, eventually leading to dementia and death. These symptoms are caused by the gradual wasting away of dopaminergic (DA) neurons, which respond to the neurotransmitter dopamine and are primarily clustered in the midbrain. They are critical to control of voluntary movement and the regulation of emotion.

The causes of their wholesale death in PD, however, remain something of a mystery. DA neurons of patients often contain odd clots of proteins named Lewy bodies. But it isn't clear whether these clumps cause neuronal death or are themselves an attempt by the cell to deal with a deeper dysfunction in breaking down and recycling the components of misfolded and malfunctioning proteins.
Perlmann and his colleagues were studying Lmx1a and Lmx1b, a pair of closely related transcription factors—proteins that control the expression of genes—involved in the development of DA neurons. These developmentally vital transcription factors persist even after the neurons have matured. To find out what they do in mature neurons, the researchers painstakingly engineered mice in a manner that permitted them to delete the Lmx1a/b genes in DA neurons alone, and to do so at a time of their choosing.
"When we looked at the DA neurons that lacked the Lmx1a/b genes, those in adult mice had many of the same abnormalities you see in various stages of PD," says Perlmann. "The nerve fibers that extend out from these neurons to others were degenerating, as were the nerve terminals, and this was happening long before the neurons died." Further, the engineered mice were shown in behavioral tests to have poor memory and motor control, both of which are symptoms of PD.
The researchers found that midbrain DA neurons from patients with PD express far lower levels of the Lmx1b protein than do their non-PD counterparts. So the researchers looked into how the loss of Lmx1a and b was affecting the neurons. They found that Lmx1b, in particular, controls the expression of a number of genes central to a process known as lysosomal autophagy by which cells break down abnormally folded protein molecules so that they don't poison the cell. This process is believed to be compromised in PD.
Treating young mice with a compound that boosts autophagy reversed the neural degeneration induced by loss of Lmx1b. In sum, the studies suggest the loss of Lmx1b expression is probably involved in the development of PD, that it induces a decline in the function of DA neurons by undermining autophagy and that this gradually sickens and then kills the DA neuron.
Perlmann and his colleagues are now using their unique animal model to research the details of Lmx1b's regulation of autophagy—such as the networks of genes it activates. The researchers are also looking into ways to prevent the loss of Lmx1b in PD and if such approaches could be of benefit in treating the disease. The process of autophagy also has relevance in cancer.

More information: Dopaminergic control of autophagic-lysosomal function implicates Lmx1b in Parkinson's disease, Nature Neuroscience, DOI: 10.1038/nn.4004
http://medicalxpress.com/news/2015-04-key-factor-neural-death-parkinson.html

Wednesday, April 29, 2015

PAN Priority Remains in Updated Draft of 21st Century Cures



On April 29, a bipartisan group of House Energy & Commerce Committee members released a second 21st Century Cures Initiative discussion draft.
The Parkinson’s Action Network (PAN) is excited that the draft includes the Advancing Research for Neurological Diseases Act, a provision that would create a data collection system for neurological diseases at the Centers for Disease Control and Prevention. The stand-alone bill (H.R. 292/S. 849), spearheaded in the House of Representatives by Reps. Burgess (R-TX) and Van Hollen (D-MD), is a top priority for the Parkinson’s’ community. Please show your continued support by urging your Members of Congress to support the Advancing Research for Neurological Diseases ActEmail today!
As you may recall, Chairman Upton (R-MI) released an initial draft of 21st Century Cures in January. On Thursday, April 30, the Health Subcommittee of the Energy & Commerce Committee will hold a hearing to discuss the updated draft.
The updated 21st Century Cures draft also includes provisions to:
  • Increase funding for the National Institutes of Health;
  • Incorporate the patient perspective in the discovery, development, and delivery process;
  • Foster development of treatments for patients facing serious or life-threatening diseases; and
  • Modernize clinical trials.
PAN staff is currently reviewing the entire draft and plans to continue working with the Committee as the process continues. Please stay tuned for updates

Go to: (To Read More)
http://parkinsonsaction.org/wp-content/uploads/2014/10/PAN-2.23.15-Senate-HELP.pdf

http://parkinsonsaction.org/pan-priority-remains-in-updated-draft-of-21st-century-cures/

A Parkinson's Diagnosis at Any Age Has Unique Challenges


Resources for Individuals and Physicians Offer Advice From Those Who've Been There 

TORONTO, ON--(Marketwired - April 29, 2015) - Learning you've got Parkinson's disease, a chronic neurodegenerative condition, when you're not yet 30 years old, can be a shocking and very emotional experience. Even at 50, it can wreak havoc on your future plans -- physically, mentally, financially, socially and emotionally. Parkinson Society Canada has funded two educational resources -- one for patients and one for physicians -- to help address the unique needs of individuals who are newly diagnosed with Young-onset Parkinson's disease (YOPD), developed by a National Research Program grant recipient. 
Although the average age to develop Parkinson's is around 60, young-onset Parkinson's (before age 40) occurs in five to 10 per cent of people diagnosed. Twenty percent of those newly diagnosed are under the age of 50. Some challenges in living with Parkinson's disease are universal, regardless of age, and there are a number of additional issues specific to younger people. 
The first is often the shock of a diagnosis of YOPD. "I think when you get the diagnosis, your life sort of stops," recalls one of the contributors to the booklet on advice for other patients. "You have to deal with your kids, you have to deal with your job, you have to deal with getting up every day and all the things you're supposed to do and then deal with this at the same time. And there's no instruction book on how to do that."
These latest resources help to fill that gap. Written by Michael Ravenek, PhD and associate professor at Western University, the two booklets, Young-onset Parkinson's disease: Advice for those newly diagnosed from individuals currently living with YOPD (2nd ed.) and Young-onset Parkinson's disease: Advice for physicians from individuals living with YOPD (2nd ed.) provide advice on personal topics such as when to reveal your condition to your employer, planning finances for possible disability or early retirement, sharing your diagnosis with young children, teenagers and parents, and sexuality, among several others issues.
With funding from Parkinson Society Canada and the Canadian Institutes of Health Research, Ravenek interviewed 39 people living with YOPD to write the initial editions of the two booklets. Feedback was later gathered from across the country from others with YOPD and their families, as well as health professionals to inform the second editions.
Helping those with young-onset Parkinson's disease 
"There is a big gap in information available to those who face everyday life challenges combined with the unexpected and unique aspects of living with YOPD.' says Grace Ferrari, National Manager, Professional & Public Education, Parkinson Society Canada. "We are very pleased to provide these additional resources in both digital and printed formats, in English and French, to support families, people with Parkinson's and their physicians."
The physician booklet highlights specific areas of the physician-patient interaction that all physicians should consider in their encounters with individuals with YOPD. Both booklets contain a sample "log" for daily medication, meals and exercise, along with a place to record "Questions for my next doctor's appointment," to help make the most of self-care efforts and doctor/patient interactions, respectively.
To find out more about living with Parkinson's disease and programs and services available near you, call 1-800-565-3000 or visit www.parkinson.ca. Use the interactive mapto find support groups, access to local programs and support groups for newly diagnosed, Young-Onset, exercise and more. Join the conversation on Twitter @ParkinsonCanada and follow Parkinson Society Canada on Facebook.
http://health.einnews.com/article/262631684/Z62GdZgmGBEYzaTv

Molecular Medical Food for Parkinson's Disease Produces 80% Improvement on all Symptoms Based on a Case Study Involving a Parkinson's Patient

BELMONT, Calif., April 29, 2015 (GLOBE NEWSWIRE) 
-- via PRWEB -
Xicepta Sciences, Inc., a biotech company in Belmont, CA, launches a molecular medical food, Agitan X, for Parkinson's disease that produces 80% improvement on all symptoms based on the company's case study involving a Parkinson's disease patient. Agitan X contains embryonic peptides from vaccine-grade chicken egg extract with microRNA nucleotides and peptides that replenishes what the disease has depleted in the sufferer's body. It also contains other natural ingredients including Amino Acids and Dopamine properties.
The core research and biotechnology of the embryonic peptide was developed by Dr. Gheorghe Mihaescu, an international expert in the fields of Experimental Immunology in Oncology, Steroid Biochemistry, Radio-assay Methodologies, and Geriatric Nutrition. Dr. Mihaescu has authored 32 published scientific papers in the aforementioned fields and has also performed human clinical studies on the benefits of the embryonic peptides. He also holds 15 invention patents, which have been recognized and prized by the European scientific community at the prestigious Brussels and Geneva Conventions.
The effectiveness of Agitan X in alleviating the disease's symptoms can be attributed to the neuroregenerative function of the factors and the miRNA strands that can be found in the embryonic peptides. These factors cross easily and intact from digestion in the large intestine to the blood stream where they interact and contribute to the renewal of the neural cell life cycle. The rest of the products' natural ingredients are designed to enhance the effectiveness of Agitan X.
Research shows that Parkinson's disease results from lack of dopamine and the degeneration of brain neurons. The symptoms include among others tremors, physical imbalance, muscle rigidity, drooling, and loss of energy. Overtime patients may also exhibit dementia-like symptoms and depression. All of Agitan X's ingredients are formulated to address the disease's symptoms as well as induce cell and tissue repair.
In a case study conducted by Xicepta Sciences, Agitan X was given to Patient A who suffered from Parkinson's disease for over eight years and has degenerated into what may be considered at the last stage of the disease. He exhibited symptoms such as extreme tremors, stuttering, gait imbalance, forgetfulness, depression and has in fact entertained suicidal ideation. Within 30 days after taking Agitan X , Patient A exhibited significant improvement in all areas of Parkinson's disease's core symptoms. After another 45 days, Patient A has gained approximately 80% improvement in all diagnostic axis. Patient A also reported that he now sleeps better, is in much happier mood, has gained back his normal gait and musculature, and even resumed riding his Harley Davidson motorcycle.
Xicepta Sciences is a founder-funded company and it is currently seeking an A-Round funding in order to perform additional studies and bring the product to the global market. Xicepta Sciences owns the exclusive rights to the trade and use of the patented embryonic peptide technology which took over 10 years to test and perfect. Agitan X is available for sale at xicepta.com.
For more information or to schedule an interview regarding the topic, please contact Dr. Soledad M. Manaay, President and CEO of Xicepta Sciences, Inc. at 650-771-7676 or at dr(dot)manaay(at)xicepta(dot)com.

This article was originally distributed on PRWeb. For the original version including any supplementary images or video, visit http://www.prweb.com/releases/2015/04/prweb12681294.htm
http://health.einnews.com/article/262611397/LxxkTlUmMaBcXQWc