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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.
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Friday, May 1, 2015
Thursday, April 30, 2015
PARKINSON'S DISEASE NEWS
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  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
|Immunohistochemistry for alpha-synuclein showing positive staining (brown) of an intraneural Lewy-body in the Substantia nigra in Parkinson's disease. Credit: Wikipedia|
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.
Explore further: Mitochondria are altered in human cell model of Parkinson's disease
More information: Dopaminergic control of autophagic-lysosomal function implicates Lmx1b in Parkinson's disease, Nature Neuroscience, DOI: 10.1038/nn.4004
Wednesday, April 29, 2015
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.
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