JULY 7, 2017 BY MAGDALENA KEGEL
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.
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Friday, July 7, 2017
Lauren Santye, Assistant Editor
Friday, July 07, 2017
Friday, July 07, 2017
A newly released paper offers the most comprehensive overview of exosomes to date, indicating its significant potential to detect and treat disease.
Exosomes are tiny biological nanoparticles ranging from 30 to 130 nanometers in size. They communicate between cells, carrying proteins, lipids, DNA, and RNA. They also help drive biological processes.
In a commissioned paper published in Trends in Molecular Medicine, investigators showed that the potential medical benefits of nanoparticles can be divided into 3 broad categories: detecting disease by acting as disease-specific biomarkers; activating immune responses to boost immunity; and treating diseases by acting as a vehicle for drugs to target tumors directly.
Thus far, several studies have demonstrated the potential benefits of exosomes including improvement of prostate cancer testing, a small-cell lung cancer trial; stem cell-derived exosomes to strengthen heart muscles; regeneration of muscle and tissue; Parkinson’s disease; and diabetes.
The authors believe that exosomes as becoming increasingly promising, but more research needs to be done before they can be translated into new techniques and treatments.
“Our survey of research into exosomes shows clearly that they offer enormous potential as a basis for detecting and treating disease,” said author Steve Conlan. “Further studies are necessary to turn this research into clinical outcomes, but researchers and funders should be very encouraged by our findings. Our own research in Swansea is investigating the use of exosomes and exosome-like synthetic nanoparticles in combatting ovarian and endometrial cancer.
“Progress in this field depends on partnership. As the authorship of our own paper illustrates, researchers in different countries are increasingly working together in nanohealth. Swansea University has wider links with Houston and Portuguese-based researchers in the field. It’s also important to build partnerships outside academia, in particular, with government and companies in the fast-growing sector.”
Free Webinar Hosted by University at Albany
Thursday, July 20, 2017, 9:00—10:00AM ET
University at Albany is hosting a free live webcast for medical and public health professionals, featuring guest speaker Guy J. Schwartz, MD, the Assistant Clinical Professor of Neurology at Stony Brook University Medical Center. Guy will be discussing in depth the psychiatric symptoms of Parkinson’s disease, their complex interaction and relationship with medical treatments of the disease, and the uphill battle that therapeutic treatment for these specific symptoms is currently facing.
According to the University at Albany website, attendees will learn the following:
- Recognize the biologic underpinnings of psychiatric symptoms of Parkinson’s disease;
- Identify at least three strategies to reduce the psychiatric adverse effects resulting from treatment for the disease; and
- Describe the impact on quality of life and care-giver burden resulting from the psychiatric symptoms of the disease.
Call us at 518.402.0330 or e-mail firstname.lastname@example.org if you need assistance.
NEUROSCIENCE NEWS JULY 6, 2017
Source: Bill Hathaway – Yale
•A potent mGluR5 SAM blocks Aβo/PrPC but not glutamate signaling
•The mGluR5 SAM rescues age-dependent memory loss in an AD mouse model
•Synapse density is restored by mGluR5 SAM treatment over 4 weeks
•mGluR5 SAM reveals a glutamate-independent AD role with a wide therapeutic index
Metabotropic glutamate receptor 5 (mGluR5) has been implicated in Alzheimer’s disease (AD) pathology. We sought to understand whether mGluR5’s role in AD requires glutamate signaling. We used a potent mGluR5 silent allosteric modulator (SAM, BMS-984923) to separate its well-known physiological role in glutamate signaling from a pathological role in mediating amyloid-β oligomer (Aβo) action. Binding of the SAM to mGluR5 does not change glutamate signaling but strongly reduces mGluR5 interaction with cellular prion protein (PrPC) bound to Aβo. The SAM compound prevents Aβo-induced signal transduction in brain slices and in an AD transgenic mouse model, the APPswe/PS1ΔE9 strain. Critically, 4 weeks of SAM treatment rescues memory deficits and synaptic depletion in the APPswe/PS1ΔE9 transgenic mouse brain. Our data show that mGluR5’s role in Aβo-dependent AD phenotypes is separate from its role in glutamate signaling and silent allosteric modulation of mGluR5 has promise as a disease-modifying AD intervention with a broad therapeutic window.
July 6, 2017, Desert News, Utah
The 12th annual Pedal Away Parkinson’s 10-mile family fun ride is set for Saturday, July 22, Gailey Park, 200 S. 300 West, at 8 a.m.
July 6, 2017
PET scan of a human brain with Alzheimer's disease. Credit: public domain
Researchers at the MRC Laboratory of Molecular Biology (LMB) have, for the first time, revealed the atomic structures of one of the two types of the abnormal filaments which lead to Alzheimer's disease. Understanding the structures of these filaments will be key in developing drugs to prevent their formation. The researchers, whose study is published today in Nature, believe the structures they have uncovered could also suggest how tau protein may form different filaments in other neurodegenerative diseases.
Alzheimer's, the most common neurodegenerative disease, is characterised by the existence of two types of abnormal 'amyloid' forms of protein which form lesions in the brain. Tau forms filaments inside nerve cells and amyloid-beta forms filaments outside cells. Tau lesions appear to have a stronger correlation to the loss of cognitive ability in patients with the disease.
Almost thirty years ago, scientists at the LMB (including Michel Goedert, one of the senior authors on this paper) identified tau protein as an integral component of the lesions found in Alzheimer's and a range of other neurodegenerative diseases. But, until now, scientists have been unable to identify the atomic structure of the filaments.
The researchers extracted tau filaments from the brain of a patient who had died with Alzheimer's disease. The filaments were then imaged using cryo-electron microscopy (cryo-EM). Senior author Sjors Scheres and colleagues developed new software in order to calculate the structure of the filaments in sufficient detail to deduce the arrangement of the atoms inside them.
Sjors Scheres said: "It's very exciting that we were able to use this new technique to visualise filaments from a diseased brain as previous work depended on artificial samples assembled in the laboratory. Amyloid structures can form in many different ways, so it has been unclear how close these lab versions resembled those in human disease.
"Knowing which parts of tau are important for filament formation is relevant for the development of drugs. For example, many pharmaceutical companies are currently using different parts of tau in tests to measure the effect of different drugs on filament formation; this new knowledge should significantly increase the accuracy of such tests."
Fellow senior author Michel Goedert said: "We have known for almost three decades that the abnormal assembly of tau protein into filaments is a defining characteristic of Alzheimer's disease. In 1998, the dysfunction of tau protein was shown to be sufficient for neurodegeneration and dementia. In 2009, the prion-like properties of assembled tau were identified. These properties allow the abnormal form to convert previously normal forms.
"Until now the high-resolution structures of tau or any other disease-causing filaments from human brain tissue have remained unknown. This new work will help to develop better compounds for diagnosing and treating Alzheimer's and other diseases which involve defective tau."
Dr Rob Buckle, chief science officer at the MRC, which funded the research, said: "This ground-breaking work is a major contribution to our understanding of Alzheimer's disease. Nearly thirty years ago scientists at the LMB were the first to discover that tau protein plays a key role in the disease. Knowing the basic structure of these filaments in diseased tissue is vital for the development of drugs to combat their formation.
"This research opens up new possibilities to study a range of other diseases where the accumulation of abnormal protein filaments plays a role, including Parkinson's disease, motor neuron disease and prion diseases."
More information: Anthony W. P. Fitzpatrick et al. Cryo-EM structures of tau filaments from Alzheimer's disease, Nature (2017). DOI: 10.1038/nature23002
Journal reference: Nature
Provided by: Medical Research Council
July 7, 2017
- By SARAH FAY CAMPBELL
As of July 1, several new conditions are eligible for treatment with cannabis oil, under Georgia’s expanded program allowing the use of a medicine derived from marijuana.
Anyone under hospice care, whether inpatient or outpatient, is eligible to be treated the cannabidiol oil, as long as a doctor signs the paperwork for the patient to receive a registration card from the state.
Other new conditions include severe autism in children and any form of autism in adults, the skin disease epidermolysis bullosa and severe or end-state Alzheimer’s, AIDs, peripheral neuropathy and Tourette’s syndrome.
Senate Bill 16, which expanded the state’s medical cannabis law, took effect July 1. Other conditions that were already approved are seizure disorders, Crohn’s disease, mitochondrial disease, cancer when it is severe or end-stage or when cancer treatment creates wasting illness or severe nausea or vomiting, and severe or end-stage Amyotrophic Lateral Sclerosis, multiple sclerosis, Parkinson’s disease and Sickle cell disease.
Amyotrophic Lateral Sclerosis was formerly called Lou Gehrig’s Disease, named for a baseball player who had ALS.
To receive a card allowing the possession and use of the oil, patients must have a doctor who will fill out the certification paperwork.
The oil can contain up to 5 percent THC, the primary ingredient responsible for the marijuana high. The primary active ingredient in the oil is cannabidiol, another compound found in marijuana. Under the law, the oil must be in a pharmaceutical container that states the percentage of THC.
Though the possession and use of the oil is legal for those with a registration card, the law doesn’t address how someone is to acquire the oil. The oil is not legally available in the state of Georgia, though some companies in Colorado will ship certain low-THC varieties.
Earlier versions of an expansion bill contained several additional conditions including chronic pain, post-traumatic stress disorder and autoimmune disease. Those conditions were in a version that passed the Georgia House of Representatives, but that bill was a no-go in the state Senate.
Cowetan Stefanie Anderson has chronic pain and fibromyalgia and has been following the expansion actions in Georgia.
She was disappointed that chronic pain was removed. “I’ve never had any interest in ‘drugs.’ But I’m so sick of feeling this awful, even on prescription meds,” she said.
Other Coweta women said they wished the state would allow the oil for the pain of arthritis and endometriosis, as well as bipolar disease, anxiety and depression.
Anderson is hopeful that fibromyalgia or chronic pain will one day be added to the state’s list of approved conditions. “I want to see if I can get relief,” she said.