I Ask This Of You!

I have Parkinson's diseases and thought it would be nice to have a place where the contents of updated news is found in one place. That is why I began this blog.

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 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.

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Thursday, November 15, 2018

Researchers find inhibiting one protein destroys toxic clumps seen in Parkinson's disease

November 14, 2018, Georgetown University Medical Center

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

A defining feature of Parkinson's disease is the clumps of alpha-synuclein protein that accumulate in the brain's motor control area, destroying dopamine-producing neurons. Natural processes can't clear these clusters, known as Lewy bodies, and no one has demonstrated how to stop the build up as well as breakdown of the clumps—until perhaps now.

A team of neurologists at Georgetown University Medical Center (GUMC) has found through studies in mice and human brains, that one reason Lewy bodies develop is that a molecule, USP13, has removed all the "tags" placed on  that mark the protein for destruction. Toxic heaps of alpha-synuclein accumulate, and are never taken away.
The findings, published in Human Molecular Genetics, show that inhibiting USP13 in mouse models of Parkinson's disease both eliminated Lewy bodies and stopped them from building up again. The "tag" that USP13 removes is called ubiquitin, which labels alpha-synuclein for degradation.
"This study provides novel evidence that USP13 affects development and clearance of Lewy body protein clumps, suggesting that targeting USP13 may be a therapeutic target in Parkinson's disease and other similar forms of neurodegeneration," says the study's lead investigator, Xiaoguang Liu, MD, Ph.D., an assistant professor of neurology.
There are three forms of motor disorders associated with build-up of alpha-synuclein. These "synucleinopathies" include Parkinson's, dementia with Lewy bodies, and multiple system atrophy.
Parkin is one of a family of ubiquitin ligase enzymes. Ubiquitination is a process in which molecules are labeled (or tagged) with ubiquitin and directed to cellular machines that break them down. USP13 is known as a de-ubiquitinating enzyme, which removes ubiquitin tags from protein. USP13 renders parkin ineffective via removal of ubiquitin tags (de-ubiquitination) from proteins. Loss of parkin function leads to genetically inherited forms of Parkinson's disease.
The study began with postmortem autopsies of individuals who donated their brains to research including 11 with Parkinson's disease and a control group of 9 without Parkinson's. The autopsies, which occurred 4 to 12 hours after death, found that the level of USP13 was significantly increased in the midbrain in Parkinson's disease patients, compared to the control participants.
"Overexpression of USP13 in post-mortem brains with Parkinson's disease was never discovered before this work. Its presence indicates that this molecule might reduce parkin's ability to tag proteins with ubiquitin or may strip ubiquitin away from certain molecules like alpha-synuclein, resulting in accumulation of toxic clumps in the brain," said Charbel Moussa, MBBS, Ph.D., the study senior investigator and director of GUMC Translational Neurotherapeutics Program.
Studies in mouse models of Parkinson's disease then demonstrated that knocking out the USP13 gene increased alpha-synuclein ubiquitination and destruction. Researchers also saw that USP13 knockdown protected the mice against alpha-synuclein-induced dopamine neuron death. The mice had improved motor performance; parkin protein was increased and alpha-synuclein was cleared.
Investigators also found that a newer therapy being studied in those with Parkinson's disease, nilotinib, worked better when USP13 was inhibited. Nilotinib is FDA approved for use in specific blood cancers.
"Our discovery clearly indicates that inhibition of USP13 is a strategic step to activate parkin and counteract alpha-synuclein de-ubiquitination, to increase toxic protein clearance" added Moussa. "Our next step is to develop a small molecule inhibitor of USP13 to be used in combination with nilotinib in order to maximize protein clearance in Parkinson's and other neurodegenerative diseases."
"To our knowledge, these data are the first to elucidate the role of USP13 in neurodegeneration," Liu says, suggesting that other neurodegeneration disorders that features  clumps, such as Alzheimer's , may have a similar pathology.
"Clearance of neurotoxic proteins, including alpha-synuclein, may depend on the balance between ubiquitination and de-ubiquitinating," she says.
Journal reference: Human Molecular Genetics

New advanced biomaterial to repair damaged nervous tissue

November 14, 2018, Universidad Politécnica de Madrid

Fluorescence microscopy images showing stem cells (green) implanted in a brain tissue (blue). The four figures at the right show the survival of non-encapsulated stem cells, and the figures at the right show the silk fibroin hydrogels-encapsulated stem cells. Credit: Front Cell Neurosci. 2018 Sep 6;12:296. doi: 10.3389/fncel.2018.00296

A team of researchers from the Centre for Biomedical Technology (CTB) at Universidad Politécnica de Madrid (UPM) in collaboration with the Universidad Complutense de Madrid (UCM), the Instituto Cajal and the Hospital Clínico San Carlos has developed an innovative treatment to repair damaged brain tissues. Thanks to the implantation of encapsulated stem cells in an innocuous biomaterial and fully biocompatible (silk fibroin), researchers have achieved the functional recovery of mice after suffering an induced brain stroke.
This encapsulation can increase the survival rate of stem  implanted in the  and, in addition to positively influencing the repair of damaged nerve tissue, it can prevent the extent of the damage.
A wide range of neurological disorders can cause permanent physical and cognitive disabilities. The nervous system has a limited capacity to recover after an injury, for instance after a stroke or brain trauma but also in neurodegenerative diseases such as Alzheimer's or Parkinson's in which there is a progressive deterioration of our brain.
Stem cell therapies have the therapeutic potential to protect and repair the damaged brain. However,  has difficulties, including a reduced survival rate in the brain after transplant. This a barrier to achieving the most suitable therapy.
In order to overcome this barrier, a team led by researchers from the Centre for Biomedical Technology, in collaboration with UCM, the Instituto Cajal and the Hospital Clínico San Carlos, has developed an innovative bioengineering strategy to repair the damaged brain tissue. To do this, the researchers implanted  encapsulated in fully biocompatible silk fibroin into mice with brain infarctions.
After the treatment, the mice experienced a significant improvement in their sensory and motor skills. Additionally, by using electrophysiological techniques, the researchers have shown improvement of brain reorganization in adjacent areas to the damaged zone. Silk fibroin considerably increased the survival of  implanted in the brain, preventing an extent of the damage after de induced stroke in animals.
Daniel González Nieto, a CTB-UPM researcher, says, "These results are a step forward in new treatments of neurologic disorders when using silk fibroin as a drug delivery vehicle, achieving a higher therapy performance and the functional improvement of patients."
More information: Laura Fernández-García et al. Cortical Reshaping and Functional Recovery Induced by Silk Fibroin Hydrogels-Encapsulated Stem Cells Implanted in Stroke Animals, Frontiers in Cellular Neuroscience(2018). DOI: 10.3389/fncel.2018.00296 

FoxFeed Blog: Visiting with Family Members Who Have Parkinson’s

Posted by  Rachel Dolhun, MD, November 15, 2018

If you are visiting family you haven't seen in a while, you may not be sure what to expect. If you see change, you may not know what's part of Parkinson's or what to do about it. Watch the video for tips you can use before and during your visit.

Ask the MD has been made possible through the leadership of members of our Parkinson's Disease Education Consortium in conjunction with The Albert B. Glickman Parkinson's Disease Education Program and Charles B. Moss Jr. and family. These partners' support allows us to furnish high-quality educational content to the Parkinson's community while maintaining our commitment to allocate donor dollars to high-impact research. Editorial control of all Michael J. Fox Foundation-published content rests solely with the Foundation.

FoxFeed Blog: LRRK2 Heads Back to Space

 Posted by  Krishna Knabe, November 14, 2018

On November 17, the second experiment led by The Michael J. Fox Foundation (MJFF) is scheduled to launch to the International Space Station (ISS). The project is part of our partnership with the Center for the Advancement of Science in Space (CASIS), which manages the ISS U.S. National Laboratory.
The MJFF-sponsored study will attempt to grow crystals of the protein LRRK2 in microgravity conditions, which can result in larger crystals. LRRK2 is a priority target for Parkinson's disease therapies, and the first LRRK2 inhibitor has already reached clinical trials. But we still lack an understanding of the atomic structure of this critical protein. Marco Baptista, PhD, Director, Research Programs at MJFF explains: "LRRK2 therapies have enormous potential for Parkinson's patients. Industry is forging ahead with LRRK2 inhibitors, but can't yet pursue structure-based drug design that fully leverages the insight of the drug's binding pocket. To do that we need to grow better crystals, which we are hopeful we can do on the ISS National Lab."
previous attempt to grow LRRK2 crystals aboard ISS last year was successful but the resolution wasn't high enough to get an accurate picture of the protein. The team published its results and used feedback from peers to modify the study protocol, which will take advantage of "real time" study monitoring aboard ISS. The team, which includes Paul Reichert of Merck and Sebastian Mathea and Stefan Knapp of Goethe University Frankfurt, will be able to monitor the progress of the ISS crew performing the study and provide feedback to improve the likelihood of success.
Tara Ruttley, associate chief scientist for Microgravity Research at NASA, notes that research aboard the ISS National Lab "provides a platform for us to think differently . . . to best benefit our lives on Earth." The MJFF team has done just that and hopes that, freed from the limitations of Earth's gravity, they will be able to unlock the mysteries of LRRK's structure.
MJFF's experiment will be aboard Northrop Grumman's commercial resupply mission to the ISS; the launch window is now scheduled to open at 4:01 a.m. EST Saturday, November 17 at Wallops Flight Facility in Wallops Island, Virginia. (It has been delayed from its original launch date of November 15 due to weather conditions.) In addition to scientific research, the rocket is carrying crew supplies and hardware to support the station's Expedition 57 and 58 crews.

FoxFeed Blog: Lights, Cameras, Music and Comedy at the #FoxGala to Raise Funds to End Parkinson's Disease

Posted by  Allison Boiles, November 13, 2018

Tracy Pollan and Michael J. Fox welcome the audience.

This year's host of The Michael J. Fox Foundation's (MJFF) annual "A Funny Thing Happened on the Way to Cure Parkinson's" gala, Denis Leary, put it best as he described the event on the red carpet: "I love this event. I love what it stands for. I love Michael."
Nearly 900 friends from near and wide gathered at the Hilton New York to celebrate raising $4.6 million for critical Parkinson's research. And as with every year, thanks to the MJFF Board of Directors, every penny of the millions raised will go directly to high-impact programs to bring an end to Parkinson's. To date, "Funny Thing" has raised nearly $80 million in total.
Guests of the #FoxGala were treated to a comical opening number from Denis Leary and standout, stand-up comedy from our star-studded lineup of Jim Gaffigan, John Mulaney and Michelle Buteau. Plus, iconic musician Steve Winwood brought the house to its feet with a few of his classic hits. And if that wasn't enough, Michael J. Fox and rock legend Joan Jett joined Steve on stage to close out the night with "Gimme Some Lovin'."
Long-time supporters of Michael and the Foundation came out for the evening including MJFF Board members Willie Geist and George Stephanopoulos, Katie Couric, Christopher Lloyd, Jennifer Grey, Clark Gregg and Susie Essman. View the gallery below to get an insider look. While on the red carpet, Willie spoke to his admiration for Michael:
"He walks the walk. There are a lot of opportunities when you're in the public eye or you have a platform to do things where you can put your name on it, or put your name on an invitation, or say I support that, but that's the end of it. He inspires me because he works at it. He is at the meetings, he is on the cutting edge of research talking to doctors, and getting the word out. He shows that the continued use of your celebrity or your platform can truly, truly make a difference in something like this as his Foundation has."
And in case you missed it, Michael and Tracy Pollan sat down with Entertainment Tonight for an exclusive interview about their marriage, navigating Parkinson's and the work of the Foundation. During the conversation, Michael discussed how he manages living with the disease:
"I'm really into acceptance, and acceptance means you resign to something. But you have to recognize it is what it is. Deal with it and move on. And when you do that, you can keep it in check -- it is what it is. Ninety-nine percent of the rest of my life is not Parkinson's, it's other stuff and that keeps me busy and I don't feel sorry for myself."
All of the people at the Gala.

Wednesday, November 14, 2018

The puzzle of a mutated gene lurking behind many Parkinson’s cases

NOVEMBER14, 2018

Why a defective gene is tied so strongly to Parkinson’s disease has baffled researchers. Now, a study led by Stanford scientists appears to have pieced together a major part of the puzzle.

Suzanne Pfeffer

Genetic mutations affecting a single gene play an outsized role in Parkinson’s disease. The mutations are generally responsible for the mass die-off of a set of dopamine-secreting, or dopaminergic, nerve cells in the brain involved in physical movement.
The pathogenic variants of the gene, LRRK2, share a common tendency: They cause the protein it encodes to run in constant overdrive, upsetting the delicate balance of a healthy cell.
What ties defective LRRK2 so strongly to Parkinson’s has puzzled researchers. Now, a study led by scientists at the School of Medicine appears to have pieced together a major part of that puzzle.
Suzanne Pfeffer, PhD, professor of biochemistry and the Emma Pfeiffer Merner Professor in Medical Sciences, is the senior author of the study, which waspublishedNov. 6 in eLife.  The lead authors are postdoctoral scholars Herschel Dhekne, PhD, and Izumi Yanatori, PhD.
Randomness of Parkinson’s disease 

Most cases of Parkinson’s are sporadic, meaning the condition seems to hit individuals at random rather than run in their families. But even in sporadic cases, genetic mutations can figure in.
Of the numerous LRRK2 variants suspected of predisposing people to Parkinson’s, so far five have been solidly identified as boosting Parkinson’s risk. Taken together, these LRRK2 mutations have been implicated in about 10 percent of inherited cases and 4 percent of sporadic cases among Caucasians. Just a single one of those mutations is responsible for about 40 percent of familial Parkinson’s cases and 13 percent of sporadic cases among Ashkenazi Jews. 
Drugs targeting the LRRK2 protein are already in clinical trials for Parkinson’s, despite the absence of a real understanding of its role in the disease.
Pfeffer and her colleagues have previously reported that mutant LRRK2 renders some classes of nerve cells deficient in their ability to create an important subcellular structure called the primary cilium, which acts analogously to a radio receiving tower, except that instead of sucking in waves of electromagnetic radiation, the primary cilium slurps up signaling substances from its surrounding environment.
It’s easy to imagine how a cell lacking such a receiving tower could go astray. But Pfeffer’s team wanted to know why the defect preferentially leads to Parkinson’s disease as opposed to a number of other neurodegenerative disorders.
A complicated molecular explanation

In the new study, the researchers unraveled a complicated molecular explanation: First, cells lacking primary cilia are unable to respond to a powerful chemical messenger known as sonic hedgehog. Second, the scientists learned, the types of cells that can’t make a decent primary cilium when their LRRK2 protein is in overdrive include a set of cholinergic nerve cells, so named because they secrete acetylcholine rather than dopamine or other substances that signal nerve cells.
These cholinergic cells have a close working relationship with the dopaminergic cells implicated in Parkinson’s disease. When the dopaminergic cells need some help, they pump out sonic hedgehog. Cholinergic cells with functioning primary cilia respond by triggering the secretion of a molecule that keeps dopaminergic cells healthy. Without that molecule, dopaminergic cells become more vulnerable to dying.  
So an LRRK2 protein in overdrive leads to no primary cilia, which leads to no response to the sonic hedgehog signal, which leads to no chemical help for the dopaminergic cells and, therefore, to their death.
Could the breakdown of that support system underlie the unrelenting loss of dopaminergic cells in Parkinson’s? Pfeffer’s lab is now hard at work studying that very question.
Another Stanford co-author is graduate student Rachel Gomez. Researchers from the University of Dundee in Scotland; the Parkinson’s Institute in Sunnyvale, California; and the Max Planck Institute of Biochemistry in Germany also contributed to the work. The work was funded by the National Institutes of Health (grantDK37332), the Michael J. Fox Foundation for Parkinson’s Research and the Medical Research Council.
Stanford’s Department of Biochemistry also supported the work.

The ABCs of Parkinson’s: ‘K’ Is for Knowledge


A continuation of the “ABCs of Parkinson’s” series.
When diagnosed with Parkinson’s disease (PD), or any disease, it is always beneficial to educate yourself about it. Ask yourself: Do they know what caused it? What are the symptoms? How can I best care for myself? Is there a cure?
Knowledge is a good and powerful thing. However, too much knowledge can be detrimental to your health.
Upon receiving a Parkinson’s diagnosis, each patient’s reaction will differ from another’s. You may want to know more. You may want to know little or nothing about the disease at first to allow yourself time to adjust or grieve. When you get to the point of wanting to know more about PD, tread carefully and cautiously. While there is a plethora of information out there to soothe those hungry for knowledge, not all sources are created equal.
Look for studies and research carried out by credible institutions and conducted relatively recently. You’ll find articles citing studies published five or more years ago, written as though the research is new. While the information may be still relevant, check if more up-to-date research is available. 
Many publications report on the findings from new studies. Take care not to overwhelm your brain. You don’t have to read all 112 articles on the research; a couple from your favorite publishers will be sufficient unless you are writing a research paper or testing your brain to see how much information it can hold.
Too much knowledge can cause unnecessary anxiety and stress. Parkinson’s is a unique disease for each patient and symptoms, medications, and the effects of treatments can vary from one individual to another.
I’d just finished reading a post on Facebook by a woman who was recently diagnosed with PD and wanted to know what to expect. The very first reply from a disgruntled caregiver who desperately needs a break would have scared the bejeebers out of me if that reply was the first bit of solicited advice I had received.
Go easy on the “knowledge” you give to a newbie. We are here to encourage them on their journey. The last thing they need at the onset of diagnosis is to have the living daylights scared out of them with all of the knowledge we’ve acquired.That wouldn’t be prudent. It wouldn’t be wise.
Note: Parkinson’s News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The opinions expressed in this column are not those of Parkinson’s News Today or its parent company, BioNews Services, and are intended to spark discussion about issues pertaining to Parkinson’s disease.

Analysis of Tiny Vesicles Released by Red Blood Cells May Help Identify Parkinson’s Patients, Study Shows


A new blood-based analysis that evaluates the levels and content of tiny vesicles released by red blood cells may help diagnose patients with Parkinson’s disease according to disease stage, researchers suggest.
Parkinson’s disease is linked to a broad spectrum of clinical manifestations and several molecular mechanisms.
This represents a challenge for the development and identification of useful biomarkers for diagnosis and disease progression, as well as to track the effectiveness of new treatments.
All human cells produce tiny vesicles containing fatty molecules, proteins, and genetic information, which they release to the surrounding environment. These so-called extracellular vesicles are produced both in healthy and disease conditions, and are used by cells to communicate among themselves.
Given the major role these extracellular vesicles may have, researchers hypothesized that their cargo could hold useful information on the biological state of the body, representing a possible new diagnostic tool.
To this end, Canadian researchers developed a new method of isolating extracellular vesicles from blood samples that would preserve their integrity, while still removing any potential contaminants.
Using flow cytometry, a technique that allows the visualization and sorting of cells and small particles according to their size and shape, the team could identify not only extracellular vesicles but also which cells originated them. After the vesicles were isolated, the team could analyze their content.
Following the assay’s optimization, the team analyzed blood samples collected from 60 Parkinson’s patients and 37 age- and sex-matched healthy volunteers.
They found that Parkinson’s patients had about 1.8 times more extracellular vesicles released by red blood cells than healthy controls. However, upon further analysis, the team found that only five patients were responsible for this significant difference, implying that the number of extracellular vesicles could not be used to differentiate between Parkinson’s patients and healthy controls.
The quantity of extracellular vesicles released by other blood cell types was similar between groups.
When researchers analyzed vesicle numbers in regards to patients’ disease severity status — measured by total scores on the Unified Parkinson Disease Rating Scale (UPDRS) — they found that at least 87% of the variation in the total number of red blood cell-derived vesicles was due to a variation in UPDRS scores.
To validate their results, the team used the same analysis approach in a new set of blood samples collected from 42 Parkinson’s patients. Once more, they found they could use the number of red blood cell-derived extracellular vesicles to distinguish between patients according to their UPDRS scores.
Analysis of the content of the isolated vesicles revealed a total of 818 proteins, eight of which were found in significantly different amounts between controls and patients, allowing researchers to group individuals according to stages of disease (control, mild Parkinson’s, and moderate Parkinson’s).
“Our study shed light on a potential biomarker indicative of disease stage, which is derived from 2 measures: the number of [red blood cells-derived extracellular vesicles] and the expression of 8 different proteins,” the researchers wrote.
Although the analysis and isolation of extracellular vesicles through flow cytometry may not be accessible to all laboratories, “identification of specific proteins that match clinical stages of Parkinson’s” could be performed using simple and less expensive techniques, according to the researchers.
“The ability to develop a biomarker that not only works as a diagnostic tool but a predictor of disease stages/course would represent a major breakthrough in the field, opening up to new therapeutic opportunities,” they concluded.

‘Reprogrammed’ stem cells implanted into patient with Parkinson’s disease

NOVEMBER 14, 2018        David Cyranoski

A man in his 50s is the first of seven patients to receive the experimental therapy.

Neurons derived from stem cells.Credit: Silvia Riccardi/SPL

Japanese neurosurgeons have implanted ‘reprogrammed’ stem cells into the brain of a patient with Parkinson’s disease for the first time.
The condition is only the second for which a therapy has been trialled using induced pluripotent stem (iPS) cells, which are developed by reprogramming the cells of body tissues such as skin so that they revert to an embryonic-like state, from which they can morph into other cell types. 
Scientists at Kyoto University use the technique to transform iPS cells into precursors to the neurons that produce the neurotransmitter dopamine. A shortage of neurons producing dopamine in people with Parkinson’s disease can lead to tremors and difficulty walking. 
In October, neurosurgeon Takayuki Kikuchi at Kyoto University Hospital implanted 2.4 million dopamine precursor cells into the brain of a patient in his 50s. In the three-hour procedure, Kikuchi’s team deposited the cells into 12 sites, known to be centres of dopamine activity. Dopamine precursor cells have been shown to improve symptoms of Parkinson’s disease in monkeys
Stem-cell scientist Jun Takahashi and colleagues at Kyoto University derived the dopamine precursor cells from a stock of IPS cells stored at the university. These were developed by reprogramming skin cells taken from an anonymous donor. 
“The patient is doing well and there have been no major adverse reactions so far,” says Takahashi. The team will observe him for six months and, if no complications arise, will implant another 2.4 million dopamine precursor cells into his brain.
The team plans to treat six more patients with Parkinson’s disease to test the technique’s safety and efficacy by the end of 2020. 
Takahashi says that if this trial goes well, they might have enough evidence for the treatment to be sold to patients as early as 2023, under Japan's fast-track approval system for regenerative medicines. “Of course it depends on how good the results are,” he says. 
In 2014, ophthalmologist Masayo Takahashi, Takahashi’s wife, created retinal cells from iPS cells that were used to treat eye disease.
doi: 10.1038/d41586-018-07407-9

United Neuroscience Strengthens Vaccine Pipeline with Novel Immunotherapy for Parkinson's Disease

November 13, 2018

Vaccine Targeted Against Aggregated Alpha-Synuclein Takes Aim at Parkinson's Disease

United Neuroscience (UNS), a clinical-stage biotech company pioneering a new class of medicine to treat and prevent brain disorders, today announced the presentation of pre-clinical evidence for UB-312, a Parkinson's disease vaccine candidate, at the Parkinson's UK Research Conference held in York, England, from Nov. 12 - 13. Dr. Hui Jing Yu, Medical Director of UNS, delivered the presentation "Anti-alpha synuclein active immunotherapy in Parkinson's disease," on Monday, Nov. 12 at 11:50 a.m. GMT. In this presentation, Dr. Yu highlighted the potential of the Company's technology to address brain disorders across a variety of therapeutic areas, including Alzheimer's disease and Parkinson's disease. 
Data presented demonstrate that the UB-312 vaccine presents numerous advantages over traditional vaccines when treating progressive disorders like Parkinson's disease. The vaccine was confirmed to selectively target and prevent accumulation of pathogenic forms of alpha-synuclein proteins in in vitro and in vivo mouse studies, as well as in post-mortem brain tissue from patients with Parkinson's disease, Dementia with Lewy bodies and Multiple System Atrophy.
"Parkinson's disease is the second most common neurodegenerative disorder after Alzheimer's disease, affecting approximately 7 million people worldwide," said Ajay Verma, Chief Medical Officer of UNS. "In fact, aggregated alpha-synuclein plays a prominent role in multiple disorders of cognition, movement and autonomic function. The ability of UB-312 antisera to target toxic alpha-synuclein species in several disorders will allow us to address multiple neurodegenerative conditions including Parkinson's disease." 
Chief Executive Officer Mei Mei Hu added that "Expansion of UNS' proprietary 'Endobody' vaccine technology platform to other targets affirms our goal of becoming a global leader in neurodegenerative disorders and asserts our vision of democratizing brain health." 
The proprietary platform technology of UNS, UBITh®, has successfully proven its efficiency and potential for a broad range of therapeutic applications starting with UB-311, the Company's Alzheimer's disease vaccine. UB-311 is currently in a Phase IIa study with top-line results expected by the end of the year.
"We are very pleased with the promising results of UB-312 in both in vitro and in vivo preclinical studies, which supports our efforts to develop a convenient and cost-effective treatment for Parkinson's disease," said Dr. Hui Jing Yu, Medical Director of UNS. "With this platform, and thanks to the wonderful opportunity to participate in the Parkinson's UK Research Conference, we will continue driving forward our efforts to improve the lives of millions of people suffering from neurodegenerative disorders."
About UB-312 in Parkinson's Disease
Active vaccination of human individuals against pathogenic forms of α-synuclein (αSyn) has yet to be safely and effectively achieved. UB-312-induced antibodies have been shown to preferentially bind pathogenic fibrillar αSyn strains and promote disaggregation while preserving motor function, body weight and survival in animal models of aggregated aSyn pathology. The proprietary platform technology of UNS, UBITh®, can generate site-specific B-cell epitope's antigens that overcome the frequent issue of self-tolerance, while inducing an optimal and targeted immune response. UNS has begun an observational study to establish a biomarker by phenotyping a trial-ready cohort of Parkinson's disease patients in the United Kingdom and will commence a Phase I study in The Netherlands in 2019 with UB-312. 
About Parkinson's UK
Parkinson's UK is the United Kingdom's leading charity supporting those with the condition. Its mission is to find a cure and improve life for everyone affected by Parkinson's through cutting edge research, information, support and campaigning. The Parkinson's UK Research Conference is held every two years and brings Parkinson's researchers together to share ideas and develop collaborations that translate into the development of truly transformational new treatments in the field and it is organized by the Parkinson's UK Research and Support Charity.  
About United Neuroscience
United Neuroscience (UNS) is a clinical-stage biotech company dedicated to the development of best-in-class immunotherapeutics for the brain. A global company headquartered in Dublin, Ireland, with operations in Taiwan and the United States, UNS was founded to address the social and economic burden of Alzheimer's and other neurodegenerative diseases and seeks to rapidly advance candidates into and through clinical trials with the goal of delivering breakthrough treatments to patients. For more information please visit
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SOURCE United Neuroscience