TOXIC CAUSES OF PARKINSON'S DISEASE. 8th December 2010 - New review There are now fourteen known toxic causes of Parkinson's Disease : pesticides (Paraquat, Rotenone, Maneb), solvents (Trichloroethylene, Toluene, N-Hexane, Carbon disulfide), MPTP, Mercury, Manganese, Copper, Carbon monoxide, Lead, Cyanide. Although Agent Orange is widely claimed to be a toxic cause of Parkinson's Disease, not even one study in the entire medical literature has ever shown that to be true. Toxicity has the potential to be the sole cause of Parkinson's Disease. To very varying extents, toxicity can also be a partial cause of Parkinson's Disease. Symptoms normally develop when toxic exposure occurs or soon after, or gradually increase over time as exposure to toxicity persists. Symptoms do not develop years or decades after exposure as is often claimed. In fact, there is a tendency for toxic effects to decline over time, but with some toxic substances that can take years.
ROTIGOTINE (NEUPRO) 21st February 2011 - New research Movement Disorders [2011] 26 (1) : 90-99 (Trenkwalder C, Kies B, Rudzinska M, Fine J, Nikl J, Honczarenko K, Dioszeghy P, Hill D, Anderson T, Myllyla V, Kassubek J, Steiger M, Zucconi M, Tolosa E, Poewe W, Surmann E, Whitesides J, Boroojerdi B, Chaudhuri KR) Complete abstract People with Parkinson's Disease who had unsatisfactory early-morning motor symptom control were given either rotigotine (2mg-16mg rotigotine every 24 hours) or a placebo. Neupro® (Rotigotine Transdermal System) is a dopamine agonist that is applied to the skin in order to continuously deliver rotigotine over a 24-hour period. For more information go to Neupro. Movement symptoms had improved in comparison to the use of a placebo, but not greatly as was claimed by the researchers. Sleep had also improved in comparison to a placebo.
In April 2008, Neupro was withdrawn from use in the U.S.A. because specific batches of Neupro had deviated from their specification. Oxidative Stress, Defective Nucleoli Likely a Cause of Parkinson's Disease. Parkinson’s disease may be caused by oxidative stress within cells due to defective nucleoli. Dopamine producing neurons are particularly sensitive to oxidative stress. The researchers present evidence showing defective nucleoli within dopamine producing neurons lead to oxidative stress and damage, resulting in symptoms mimicking those of Parkinson’s disease, such as palsy shaking. Genetically modified mice with dopamine-producing neurons only capable of forming defective nucleoli were studied by the researchers.
These mice exhibited movement impairment very much like those seen with Parkinson’s disease patients. The research further found that reduced mTOR enzyme activity was a likely cause of defective nucleoli and oxidative stress within cells. With a new model to study, cellular cues to monitor and promising new details revealed, the path to understanding and treating Parkinson’s disease is clearing. “Defective nucleoli apparently cause oxidative stress in cells. Research Notes: IPX066 Completes Enrollment in ASCEND-PD Phase III Trial. Genetic polymorphisms involved in dopaminergic neurotransmission and risk for Parkinson's disease in a Japanese population. Genetic polymorphisms involved in dopaminergic neurotransmission and risk for Parkinson's disease in a Japanese population Parkinson's disease (PD) is characterized by alterations in dopaminergic neurotransmission. Genetic polymorphisms involved in dopaminergic neurotransmission may influence susceptibility to PD.
Methods: We investigated the relationship of catechol-O-methyltransferase (COMT), monoamine oxidase B (MAOB), dopamine receptor (DR) D2 and DRD4 polymorphisms and PD risk with special attention to the interaction with cigarette smoking among 238 patients with PD and 369 controls in a Japanese population. Results: Subjects with the AA genotype of MAOB rs1799836 showed a significantly increased risk of PD (odds ratio (OR) = 1.70, 95% confidence interval (CI) = 1.12 - 2.58) compared with the AG and GG genotypes combined. The AA genotype of COMT rs4680 was marginally associated with an increased risk of PD (OR = 1.86, 95% CI = 0.98 - 3.50) compared with the GG genotype. Comments. Scientist converts human skin cells into functional brain cells. A scientist at the Gladstone Institutes has discovered a novel way to convert human skin cells into brain cells, advancing medicine and human health by offering new hope for regenerative medicine and personalized drug discovery and development.
In a paper being published online July 28 in the scientific journal Cell Stem Cell, Sheng Ding, PhD, reveals efficient and robust methods for transforming adult skin cells into neurons that are capable of transmitting brain signals, marking one of the first documented experiments for transforming an adult human's skin cells into functioning brain cells.
"This work could have important ramifications for patients and families who suffer at the hands of neurodegenerative diseases such Alzheimer's, Parkinson's and Huntington's disease," said Lennart Mucke, MD, who directs neurological research at Gladstone. "Dr. The work was done in collaboration with Stuart Lipton, M.D., Ph.D., who directs the Del E. Dr. Dr. Ding's work extends Dr. Dr. MANF in the News: Amarantus BioSciences Announces Positive Data Comparing the Trophic Factors MANF and GDNF. Fasudil - Van Andel investigate drug to halt Parkinsons progression. GRAND RAPIDS, Mich. — Researchers from Michigan State University's College of Human Medicine, Van Andel Research Institute and the Translational Genomics Research Institute are investigating a drug that has the potential to not only alleviate Parkinson's symptoms but also halt the disease's progression.
A $400,000 grant from the Michael J. Fox Foundation for Parkinson's Research – part of $2.4 million in funding the foundation awarded this week to institutions nationwide – will fund the research project. Researchers are focusing on the drug Fasudil, which is currently approved in Japan to improve blood flow to the brain in stroke victims and has shown similar positive outcomes in U.S. clinical trials. In 2009, investigators from the Translational Genomics Research Institute in Arizona and Arizona State University reported that a form of Fasudil had the potential to help improve learning and memory and reduce the risk of Alzheimer's disease. Exercise has numerous beneficial effects on brain health and cognition, review suggests. Public release date: 25-Jul-2011 [ Print | E-mail Share ] [ Close Window ] Contact: Donna Krupadkrupa@the-aps.org 301-634-7209American Physiological Society Bethesda, Md. (July 25, 2011)—It's no secret that exercise has numerous beneficial effects on the body.
However, a bevy of recent research suggests that these positive effects also extend to the brain, influencing cognition. In a new review article highlighting the results of more than a hundred recent human and animal studies on this topic, Michelle W. Voss, of the University of Illinois at Urbana-Champaign, and her colleagues show that both aerobic exercise and strength training play a vital role in maintaining brain and cognitive health throughout life.
The article, "Exercise, Brain and Cognition Across the Lifespan," is published in the online edition of the Journal of Applied Physiology. Methodology Results Importance of the Findings Study Team In addition to Dr. NOTE TO EDITORS: The abstract and article are available online. Brain training increases dopamine release - Startpage. Oxford BioMedica Announces Interim Data from Highest (5x) Dose Cohort in ProSavin Phase I/II Study in Parkinson's Disease. ProSavin® for the treatment of Parkinson’s disease (PD) Oxford BioMedica Announces Interim Data from Highest (5x) Dose Cohort in ProSavin Phase I/II Study in Parkinson's Disease 04 Aug 2011 -- Positive interim review of fourth patient cohort by Data Monitoring Committee -- Oxford, UK | August 4, 2011 | Oxford BioMedica plc ("Oxford BioMedica" or "the Company") (LSE: OXB), the leading gene-based biopharmaceutical company, today announces positive interim data from the on-going Phase I/II trial of ProSavin® for the treatment of Parkinson’s disease (PD).
The first three patients in the current six-patient cohort were treated with a 5x dose of ProSavin®, the scaled equivalent to the maximum dose in pre-clinical studies, and have reached their three-month assessment. Highlights of fourth patient cohort at three months (n=3, 5x dose) Graphene neural implants being developed to treat Alzheimer’s, Parkinson’s and more. Neural implants have the potential to treat disorders and diseases that typically require long-term treatment, such as blindness, deafness, epilepsy, spinal cord injury, and Alzheimer's and Parkinson's. However, implantable devices have been problematic in clinical applications because of bodily reactions that limit device functioning time.
Graphene neural implants could be made to last longer (perhaps 5 years) and could be smaller than current implants. Mark Ming-Cheng Chen (Wayne State has an NSF grant) is studying the potential of graphene, a novel carbon material, in the development of a reliable, high-performance, long-term implantable electrode system to improve quality of life using nanotechnology Cheng hypothesizes that graphene might be better suited to long-term treatment than platinum and iridium oxide, two of the most popular materials now used to make implantable electrodes. If you liked this article, please give it a quick review on ycombinator or StumbleUpon. New clue to Parkinson's: Shape of key protein surprises researchers. A new study finds that a protein key to Parkinson's disease has likely been mischaracterized.
The protein, alpha-synuclein, appears to have a radically different structure in healthy cells than previously thought, challenging existing disease paradigms and suggesting a new therapeutic approach. "Our data show that alpha-synuclein was essentially mistakenly characterized as a natively unfolded protein that lacked structure," said Dennis Selkoe, the Vincent and Stella Coates Professor of Neurologic Diseases at Brigham and Women's Hospital and Harvard Medical School and senior author of the paper, published online August 14 in the journal Nature. "We think this discovery has fundamental importance for understanding both how alpha-synuclein normally functions and how it becomes altered in Parkinson's. " When it comes to proteins, function follows form. A protein consists of a chain of chemical building blocks (amino acids), typically folded into an exquisite three-dimensional structure. New discovery may eliminate potentially lethal side effect of stem cell therapy.
Like fine chefs, scientists are seemingly approaching a day when they will be able to make nearly any type of tissue from human embryonic stem cells. You need nerves or pancreas, bone or skin? With the right combination of growth factors, skill and patience, a laboratory tissue culture dish promises to yield therapeutic wonders. But within these batches of newly generated cells lurks a big potential problem: Any remaining embryonic stem cells -- those that haven't differentiated into the desired tissue -- can go on to become dangerous tumors called teratomas when transplanted into patients.
Now researchers at the Stanford University School of Medicine have developed a way to remove these pluripotent human embryonic stem cells from their progeny before the differentiated cells are used in humans. ("Pluripotent" describes cells that are able to become all types of adult tissue.) Drukker is the senior author of the research, which will be published online Aug. 14 in Nature Biotechnology. Traumatic brain injury increases risk of Parkinson's disease, researchers say; Threat doubles with exposure to the pesticide paraquat.
Traumatic brain injury has entered the public's consciousness as the silent, signature wound brought back by many of our military warriors from Iraq and Afghanistan. But such injuries don't only happen in warfare, they happen to civilians too. Think car crashes, a slip and fall, two football players colliding helmet to helmet. While most people know the results of a traumatic brain injury -- ranging from a simple headache to long-term problems with memory and thinking, depending on the severity -- few are aware that such an injury can also increase one's risk later in life for Parkinson's disease, the neurodegenerative disorder that affects roughly 1 percent to 2 percent of the population over the age of 65. Now scientists at UCLA have found the mechanism for this elevated, long-term risk of Parkinson's: the loss of a specific type of neuron. While traumatic brain injury was known to be a risk factor for Parkinson's, no one knew why.
Other authors of the study included Dr. Genetic variation found to protect against Parkinson's disease. An international team of researchers led by neuroscientists at Mayo Clinic in Florida has found a genetic variation they say protects against Parkinson's disease. The gene variants cut the risk of developing the disease by nearly 20 percent in many populations. The study, published in the online Aug. 31 issue of Lancet Neurology, also reports the discovery of different variants of the same gene, LRRK2 -- the most important Parkinson's risk gene found to date -- that double Parkinson's risk in Caucasians and Asians. Parkinson's disease is a common movement disorder that affects 1 to 2 percent of people over age 65. The researchers say that although the relative influence of the variants in this study on risk is small, given the late-onset nature of Parkinson's, any variation that can delay the disease is important.
In addition, the finding provides evidence that Parkinson's disease is influenced by multiple genetic risks that act together to cause disease. Ny ledtråd om Parkinsons sjukdom. När forskarna vid Harvard Medical School undersökte proteinet alfa-synuclein, som spelar en nyckelroll i utvecklandet av Parkinsons sjukdom, hade man inte förväntat sig det resultat man fick. Det visade det sig nämligen att proteinet verkade ha en helt annan struktur än man tidigare trott. Forskare har länge antagit att alfa-synuclein förekommer i en lång rak kedja i friska celler, en så kallad monomer.
I stället visade det sig att proteinets naturliga skepnad är form av fyra identiska monomer-kedjor som är förbundna i en viss struktur, kallad tetramer. Upptäckten har enligt forskarna stor betydelse för hur framtida behandlingar mot sjukdomen bör utformas. Genom att få proteinet att behålla sin naturliga struktur hoppas forskarna kunna förhindra nervceller från att brytas ned, och på så sätt stoppa sjukdomsförloppet av Parkinsons sjukdom. Kanske till och med förhindra att sjukdomen överhuvudtaget utvecklas. – Det är intressanta och överraskande resultat.
Impax and GSK Announce Positive Topline Results of ASCEND-PD Phase III Study of IPX066 in Advanced Parkinson's Disease.