Understanding the Relationship as Sanctuary

 November 22, 2019 by Dr. C.

The healing relationship holds a sacred place for people as they search for a path to well-being moments. This relationship offers every possibility for allowing those moments to occur. It is a safe place and a sanctuary that aims to facilitate and bear witness to the experience of well-being.

The healing relationship starts with an agreement to enter the compassion space for the purpose of exploring well-being. Some people enter the compassion space almost effortlessly and without a great deal of resistance. Some move to experience well-being in the compassion space quickly, while others take longer. Understanding how to sit with resistance and eventually let go is part of the relationship as sanctuary.

Resistance can be more intense with relationship sanctuary than with sanctuary formed in connection to a place. So many deep emotions — good and bad — are tied to the memories of our relationships. We enter the healing relationship with a “relationship stance” built upon our history. Within that stance is resistance to sanctuary.

Working with a healer or a guide as a form of relationship sanctuary can be helpful. An experienced guide can show you your resistance obstacles, teach you to move around them, and help you to experience a well-being moment.

Finding healing relationships while battling a chronic illness is tough, but necessary. We are by nature social creatures and our health benefits from nurturing relationships. I long for conversations that explore the sacredness of life rather than the sickness of strife. Chronic illness consumes much of my time, but it does not define me. I’ll always have time for stimulating discourse.

Everything seems so rushed these days. Henry David Thoreau said there was no need for people to travel so fast on those locomotives going 25 mph. I giggled, and then thought that we are still going fast. Relationships are affected by a technological train that steamrolls into our lives without conscious consent. Texts, tweets, and obligatory holiday visits give us brief glimpses of those we love as they go dashing about their lives.

I don’t dash any more. Well, maybe to that emergency bathroom call, but not much else. I remember when I used to dash, both mentally and physically. I can’t push hard like that anymore. Stress hit me hard with the progression I experienced following the ruin of stagnation.

My disease took a turn for the worse this summer. It wasn’t a big crash into a tree, but a noticeable bump in the road. The ruin of stagnation was part of the progression. Everything is more difficult than it was three months ago. It’s hard to share all of this in a way that doesn’t come across as a pity party.

The relationship as sanctuary is a compassion space for me to be heard, understood, welcomed, and embraced. My partner does this day in and day out without complaint. I get tired of being with myself more often than that.

Relationship as sanctuary has been my life’s work. I find that the more I learn, the less I seem to know. It’s an old saying, but it is deeply poignant when applied to the sacred quality within the healing relationship. It is the best thing that I do as a human being in my service to humanity.

***

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.

https://parkinsonsnewstoday.com/2019/11/22/relationship-sanctuary-healing/

Glassy Carbon Electrodes Safer Than Metal in MRIs, Study Suggests

NOVEMBER 22, 2019    BY MARISA WEXLER IN NEWS.

Implantable electrodes made of glassy carbon may be safer for use in MRI scans than traditional electrodes made of metal for people who undergo deep brain stimulation, a new study shows.

The study, “Glassy carbon microelectrodes minimize induced voltages, mechanical vibrations, and artifacts in magnetic resonance imaging,” was published in Microsystems & Nanoengineering.

In cases where Parkinson’s patients are not responding well to medication, deep brain stimulation (DBS) can be used to treat motor symptoms associated with this neurodegenerative disease. The treatment involves surgically implanting an electrode directly in the brain, then using that electrode to electrically stimulate specific brain regions.

Traditionally, electrodes used for DBS have been made of metal, most typically platinum. But metal electrodes pose a problem when a person needs to undergo an MRI scan. Such scans can be used to image the brain using powerful magnets, but those magnets can interact badly with metal electrodes.

Specifically, the electrodes can lead to large “white spots” on the MRI images themselves, which can limit the utility of the images. Plus, the magnetic fields generated in MRI can cause electrodes to vibrate, or they can generate electrical currents that make the electrode heat up. These circumstances run the risk of causing damage or irritation in the brain.

In the new study, researchers wondered if electrodes made of glassy carbon, instead of metal, would be resistant to these issues. Glassy carbon (GC) is basically a bunch of very thin layers of carbon pressed together.

The researchers previously had created GC-based electrodes designed for DBS, and in a previous study, they showed that these electrodes were more durable than traditional platinum ones.

“Inherently, the carbon thin-film material is homogenous—or one continuous material—so it has very few defective surfaces. Platinum has grains of metal which become the weak spots vulnerable to corrosion,” Sam Kassegne, PhD, a professor at San Diego State University (SDSU) and co-author of both studies, said in a press release.

The researchers tested their GC electrodes in an MRI; but, rather than using actual human brains, they implanted the electrodes in a substance sort of like Jell-O. The researchers demonstrated that, while the metal electrode created a bright white patch on the MRI images themselves, the CG was nearly invisible — suggesting that, in an actual brain, this type of electrode would interfere with imaging far less.

They measured the currents generated in these electrodes during an MRI scan, as well as how much they vibrated, and compared these measurements to similar measurements obtained using traditional metal probes.

They found that the current generated in the GC electrodes was about 10 times lower than that in the metal probes. Similarly, vibrations in the GC electrode were about 40 times weaker than those in the metal ones, Researchers noted, however, that “for both types of microelectrodes, the measurable forces were below the detection limit” — that is, the vibrations were very small for both, even if they were smaller for the GC electrode.

“Our lab testing shows that unlike the metal electrode, the glassy carbon electrode does not get magnetized by the MRI, so it won’t irritate the patient’s brain,” said Surabhi Nimbalkar, study co-author and doctoral candidate at SDSU.

Although the researchers noted that they did not directly assess heating of the electrodes, which may be an avenue for further study, they nonetheless concluded that “GC microelectrodes demonstrate superior behavior with respect to MR safety compared to [platinum]-based electrodes.”

“Since GC has recently been demonstrated to have a compelling advantage over other materials for neural stimulation (…), this MRI compatibility validated in this study offers an additional advantage for long-term in vivo use in clinical settings,” they wrote.

https://parkinsonsnewstoday.com/2019/11/22/glassy-carbon-electrodes-safer-mris-metal-study/

Dystonia Researchers Awarded Bachmann-Strauss Prize for Excellence

November 22, 2019    By Mary Chapman

Investigative collaborators from the University of Alabama at Birmingham (UAB) and the University of Rome Tor Vergata in Italy have been awarded the fifth annual Bachmann-Strauss Prize for Excellence in Dystonia Research.

The Michael J. Fox Foundation (MJFF) for Parkinson’s Research presented the awards recently to UAB’s David G. Standaert, MD, PhD, and John N. Whitaker professor and chairman of neurology, and to the University of Rome Tor Vergata’s Antonio Pisani, MD, PhD, associate professor of neurology.

The award is for significant contributions to dystonia research, and comes with an unrestricted grant of $100,000 to support further joint research. Also meant to motivate the next generation of investigators, the award is part of a partnership announced in 2014between the MJFF and the Bachmann-Strauss Dystonia & Parkinson Foundation (BSDPF).

“Drs. Pisani and Standaert have made significant strides in plotting the cellular dysfunction that leads to dystonia,” said Bonnie Strauss, BSDPF founder, MJFF board member, and a dystonia patient, in a press release. “This team has laid the groundwork for development and testing of new therapies to help those living with dystonia.”

A generally poorly understood movement disorder characterized by painful, protracted muscle contractions that cause abnormal movements and postures, dystonia is both a distinct disorder and a common symptom of Parkinson’s disease. Dystonia symptoms usually begin in one body region — such as the neck, face, vocal cords, arm, or leg — then may spread to other areas.

Having co-authored their first published work in 2006, Standaert and Pisani have collaborated on nine research papers detailing dystonia’s pathology. The investigators, who are also practicing clinicians, have examined the role and relationship of neurotransmitter activity in dystonia, and have profiled a dopamine imbalance and acetylcholine activity in a condition type that usually begins in adolescence.

“We are honored to receive the prestigious Bachmann-Strauss Prize,” Pisani said. “It means we are working in the right direction for our findings to be recognized with such an award, and that we can continue building knowledge toward new treatments and cures.”

Added Standaert: “This work with Antonio is a very productive collaboration that has been an engine for discovery. There is a tremendous need for more research in the field, and more researchers. I hope this recognition from Bachmann-Strauss and MJFF will demonstrate to young investigators that there is a support and encouragement for research in dystonia and will attract more of them to this field.”

The researchers will use award funds to collaboratively study multiple models of a genetic form of dystonia to better understand the mutation’s effect.

The Bachmann-Strauss prize is intended to honor current research, an individual’s past body of work, or both.

https://parkinsonsnewstoday.com/2019/11/22/collaborators-awarded-bachmann-strauss-prize-excellence-dystonia-research/

Mount Sinai researchers uncover new genetic drivers of Parkinson's disease

Nov 22, 2019

Defects in the STMN2 gene cause nine other genes related to Parkinson's disease to become overly active, a new study reports. (CC0 Creative Commons)

Only about 20% of Parkinson’s diagnoses can be tied to genetic mutations, making the disease difficult to address with targeted therapies. Researchers at the Mount Sinai Icahn School of Medicine hope to change that by using brain samples from Parkinson’s patients to identify gene networks that drive the disease.

A new study out of Mount Sinai takes that effort one step further.

The Mount Sinai scientists examined postmortem analyses from 83 patients in eight studies and identified the gene STMN2 as a key regulator of Parkinson’s disease. They went on to show that when the gene is knocked down in the brains of mice, nine other genes that had been previously tied to Parkinson’s became overly active. They published the finding in the journal Nature Communications.

"The new genes we identified suggest that new pathways should be considered as potential targets for drug development,” particularly for Parkinson's cases that have no known cause, said Zhenyu Yue, Ph.D., Professor of Neurology and Neuroscience at the Icahn School, in a statement.

The team focused in on the substantia nigra, the region of the brain that’s most negatively affected by Parkinson’s. They compared brain tissue from the 83 patients to tissue taken from 70 people who had been healthy. They then applied a statistical method called multiscale gene network analysis (MGNA) to both sample sets, which allowed them to identify gene networks associated with Parkinson’s.

n healthy people, the STMN2 gene is expressed in neurons that produce dopamine, the critical neurotransmitter that’s lacking in the brains of people with Parkinson’s. When they knocked down STMN2 in the substantia nigra of mice, the animals struggled to complete motor tasks, such as balancing on a rod. Their dopamine-producing neurons started to break down, and there was an increase in a toxic protein called alpha-synuclein in their brains, the Mount Sinai team reported.

The STMN2 gene is of great interest to researchers studying neurodegenerative diseases. Earlier this year, a Harvard team reported a newly discovered connection between STMN2 and TDP-43, a gene that’s mutated in some cases of amyotrophic lateral sclerosis (ALS). They’re now examining whether repairing the STMN2 gene can slow or stop the progression of ALS.

The next step for the Mount Sinai researchers is to validate their observations related to STMN2 and Parkinson’s disease in larger studies. “Our approach is expected to be improved with comprehensive longitudinal studies, increased sample size, and better diagnosis” of Parkinson’s, they wrote in the study.

https://www.fiercebiotech.com/research/mount-sinai-researchers-uncover-new-genetic-drivers-parkinson-s-disease

Accelerating Medicines Partnership launches data knowledge portal for Parkinson’s disease

November 22, 2019 

The Accelerating Medicines Partnership (AMP) program for Parkinson’s disease (PD) has launched a data portal to provide de-identified information collected from 4,298 PD patients and healthy controls to researchers working to develop effective therapies for the disease. The portal enables researchers to study complex data sets and perform genome-wide analyses at a scale previously impossible.

AMP PD is a public-private partnership between the National Institutes of Health, the U.S. Food and Drug Administration, with industry (Celgene, GSK, Pfizer, Sanofi and Verily) and non-profit (The Michael J. Fox Foundation for Parkinson’s Research) organizations and managed through the Foundation of the National Institutes of Health (FNIH). The goal of this partnership is to transform and accelerate drug development in PD by providing the expertise and support needed to determine which biomarkers show the greatest potential for predicting PD and the progression of the disease.

“AMP PD is a true example of the whole being greater than the sum of its parts,” said Walter Koroshetz, M.D., director, National Institute of Neurological Disorders and Stroke (NINDS). “The combination of many data sets could allow researchers greater power to analyze potential biomarkers for Parkinson’s disease. This effort follows other AMP programs which have the shared goal of changing the way we go about the business of studying disease.”

The AMP PD Knowledge Portal contains data from cerebrospinal fluid, RNA, plasma and DNA samples previously collected through programs including The Michael J. Fox Foundation for Parkinson’s Research (MJFF) and National Institute of Neurological Disorders and Stroke (NINDS) BioFIND Study, the Harvard Biomarkers Study of Brigham and Women's Hospital and Massachusetts General Hospital, the NINDS Parkinson's Disease Biomarkers Program, and MJFF’s Parkinson’s Progression Markers Initiative. Additionally, AMP PD provides a platform that can incorporate additional data sources and new types of data, including proteomics, a project already planned.

“One important part of this platform is that, in addition to providing a place for storing complex data, we are also providing the tools to analyze that data within the platform itself,” said Debra Babcock, M.D., Ph.D., program director at NINDS and co-chair of the AMP PD Steering Committee. “In this way, we are bringing scientists to the data, which will increase opportunities for collaboration.”

Over the past 18 months, AMP PD scientific teams have worked to ensure that the data added into the portal was accurate and described in a consistent way. This crucial step, called data harmonization, allows information gathered from different programs to be compared, and it also provides best practices for how to integrate new data provided by the community into the platform. One of the unique features of these data is that they are longitudinal – it will allow researchers to analyze data from across an individual’s lifespan or disease course.

Through a single data use agreement, researchers can today apply for access to the knowledge portal and interact with the entire data set here.

“The AMP model has provided a unique platform for bringing together diverse patient cohorts, advances in technology and scientific expertise to study Parkinson’s disease on a scale that has not been attempted before,” said David Wholley, Senior Vice President, Research Partnerships, FNIH. “With the AMP PD Knowledge Portal, we are helping the scientific community worldwide to fast-track discoveries that we hope will ultimately help Parkinson’s disease patients and their families.”

About AMP PD: The Parkinson’s disease initiative is a part of the Accelerating Medicines Partnership, a joint venture between the National Institutes of Health, the U.S. Food and Drug Administration, six industry partners and one non-profit organization, managed by the Foundation for the NIH, to identify and validate promising biomarkers for Parkinson’s disease.

NINDS is the nation’s leading funder of research on the brain and nervous system. The mission of NINDS is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease.

About the Foundation for the National Institutes of Health: The Foundation for the National Institutes of Health (FNIH) creates and manages alliances with public and private institutions in support of the mission of the NIH. The FNIH works with its partners to accelerate biomedical research and strategies against diseases and health concerns in the United States and across the globe. Established by Congress in 1990, the FNIH is a not-for-profit 501(c)(3) charitable organization. For additional information about the FNIH, please visit fnih.org.

About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

https://www.nih.gov/news-events/news-releases/accelerating-medicines-partnership-launches-data-knowledge-portal-parkinsons-disease

Increased use of antibiotics may predispose to Parkinson's disease

NOVEMBER 22, 2019   by University of Helsinki

Higher exposure to commonly used oral antibiotics is linked to an increased risk of Parkinson's disease according to a recently published study by researchers form the Helsinki University Hospital, Finland.

The strongest associations were found for broad spectrum antibiotics and those that act against against anaerobic bacteria and fungi. The timing of antibiotic exposure also seemed to matter.

The study suggests that excessive use of certain antibiotics can predispose to Parkinson's disease with a delay of up to 10 to 15 years. This connection may be explained by their disruptive effects on the gut microbial ecosystem.

"The link between antibiotic exposure and Parkinson's disease fits the current view that in a significant proportion of patients the pathology of Parkinson's may originate in the gut, possibly related to microbial changes, years before the onset of typical Parkinson motor symptoms such as slowness, muscle stiffness and shaking of the extremities. It was known that the bacterial composition of the intestine in Parkinson's patients is abnormal, but the cause is unclear. Our results suggest that some commonly used antibiotics, which are known to strongly influence the gut microbiota, could be a predisposing factor," says research team leader, neurologist Filip Scheperjans MD, Ph.D. from the Department of Neurology of Helsinki University Hospital.

In the gut, pathological changes typical of Parkinson's disease have been observed up to 20 years before diagnosis. Constipation, irritable bowel syndrome and inflammatory bowel disease have been associated with a higher risk of developing Parkinson's disease. Exposure to antibiotics has been shown to cause changes in the gut microbiome and their use is associated with an increased risk of several diseases, such as psychiatric disorders and Crohn's disease. However, these diseases or increased susceptibility to infection do not explain the now observed relationship between antibiotics and Parkinson's.

"The discovery may also have implications for antibiotic prescribing practices in the future. In addition to the problem of antibiotic resistance, antimicrobial prescribing should also take into account their potentially long-lasting effects on the gut microbiome and the development of certain diseases," says Scheperjans.

The possible association of antibiotic exposure with Parkinson's disease was investigated in a case-control study using data extracted from national registries. The study compared antibiotic exposure during the years 1998-2014 in 13,976 Parkinson's disease patients and compared it with 40,697 non-affected persons matched for the age, sex and place of residence.

Antibiotic exposure was examined over three different time periods: 1-5, 5-10, and 10-15 years prior to the index date, based on oral antibiotic purchase data. Exposure was classified based on number of purchased courses. Exposure was also examined by classifying antibiotics according to their chemical structure, antimicrobial spectrum, and mechanism of action.

More information: Tuomas H. Mertsalmi et al. Antibiotic exposure and risk of Parkinson's disease in finland: A nationwide case‐control study, Movement Disorders (2019). DOI: 10.1002/mds.27924

Provided by University of Helsinki 

https://medicalxpress.com/news/2019-11-antibiotics-predispose-parkinson-disease.html

Royal recognition for neuroscience research at the University of Sheffield

21-NOV-2019   UNIVERSITY OF SHEFFIELD

• The University of Sheffield has been awarded the Queen's Anniversary Prize for innovation in neuroscience
• The prize is the highest national honour that recognises outstanding work by UK universities and colleges that demonstrate quality and innovation in their research
• Sheffield has been recognised for improving patient outcomes for people living with neurodegenerative diseases such as Parkinson's Disease and Motor Neurone Disease 

Neuroscience research at the University of Sheffield has been recognised by Her Majesty The Queen for delivering real benefits in improving patient outcomes for people living with some of the most devastating neurodegenerative diseases.

The Sheffield Institute for Translational Neuroscience (SITraN) based at the University of Sheffield was awarded a Queen's Anniversary Prize today (21 November 2019) at St James's Palace.

The prize awarded to SITraN is unique in the honours system and only bestowed upon a UK college or university which demonstrates new and innovative approaches to its research and development that have delivered benefits to the public at local, national and global levels. 

SITraN's vision is to harness the rapidly emerging, exciting developments in neuroscience to translate into new treatments and improved quality of life for patients with neurodegenerative disorders such as Parkinson's Disease, Motor Neurone Disease (MND), Dementia and Alzheimer's Disease and Multiple Sclerosis (MS).

Achievements highlighted by the award include:

• a new orthotic device, 'HeadUp', for patients living with MND who suffer from muscle weakness in their neck
• ground-breaking clinical stem cell clinical trials for MS patients
• research which has improved the life-expectancy and quality of life for those living with MND
• the discovery of a biomarker linked to the development of Alzheimer's Disease for the first time, which has the potential for earlier diagnosis and has sparked the development of new therapies
• drug discovery programmes to develop new treatments for Parkinson's Disease
• new gene therapy experimental medicine studies for MND which are showing promising early results. 

Professor Dame Pamela Shaw, Director of SITraN, said: "Receiving this award is a great honour. It gives recognition to our research teams who have made enormous scientific progress in treating some of the most devastating neurological diseases, making a real difference to patients' lives.

"We hope that this award will inspire confidence for patients and their families, research partners and donors as we continue to make discoveries that deepen the understanding of neurological diseases and open up the potential for new treatments and therapies."

SITraN - which will celebrate its 10th anniversary in 2020 - is considered a world-leader in neuroscience research. Its work forms part of the University of Sheffield's Neuroscience Institute, which aims to bring academics together from across varied specialties to translate scientific discoveries from the lab into pioneering treatments that will benefit people living with neurodegenerative diseases.

Professor Koen Lamberts, President and Vice-Chancellor of the University of Sheffield, said: "It's wonderful to see the Queen's Anniversary Award recognising the University of Sheffield as a centre for excellence in neuroscience research and teaching which has the power to transform people's lives.

"As well as making life-changing discoveries today, SITraN is nurturing the next generation of talented neuroscience students, whose research will lead to pioneering treatments for those living with neurological diseases in the future."

Chair of the Royal Anniversary Trust, Sir Damon Buffini, said: "The prizes are granted every two years by the Queen and are the most prestigious national honour awarded to UK universities and colleges for their work.

"Entries in the scheme are invited in any subject area and are subjected to rigorous independent assessment in a process managed by the Royal Anniversary Trust. Recommendations for the Queen's approval are made on the Prime Minister's advice. 

"The criteria are demanding and look for outstanding excellence in the chosen field, for innovation and for evidence of real public benefit. Competition is strong and the award is a mark of high quality in education and training which is widely recognised internationally as well as in the UK."

###

Notes to editors:

• Find more information about the Royal Anniversary Prizes here: https://www.queensanniversaryprizes.org.uk/
• The awards were announced at a ceremony at St. James's Palace in the City of Westminster on Thursday 21 November 2019. 

The University of Sheffield

With almost 29,000 of the brightest students from over 140 countries, learning alongside over 1,200 of the best academics from across the globe, the University of Sheffield is one of the world's leading universities.

A member of the UK's prestigious Russell Group of leading research-led institutions, Sheffield offers world-class teaching and research excellence across a wide range of disciplines.

Unified by the power of discovery and understanding, staff and students at the university are committed to finding new ways to transform the world we live in.

Sheffield is the only university to feature in The Sunday Times 100 Best Not-For-Profit Organisations to Work For 2018 and for the last eight years has been ranked in the top five UK universities for Student Satisfaction by Times Higher Education.

Sheffield has six Nobel Prize winners among former staff and students and its alumni go on to hold positions of great responsibility and influence all over the world, making significant contributions in their chosen fields.

Global research partners and clients include Boeing, Rolls-Royce, Unilever, AstraZeneca, Glaxo SmithKline, Siemens and Airbus, as well as many UK and overseas government agencies and charitable foundations.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

https://www.eurekalert.org/pub_releases/2019-11/uos-rrf112119.php

Tiny Crystals May Help Scientists Trace Causes of Brain Inflammation in Parkinson’s, Study Reports

NOVEMBER 21, 2019 BY CATARINA SILVA, MSC 

Tiny and traceable man-made crystals, known as quantum dots, may be useful in carrying toxins to select cells in the brain, allowing researchers to better understand Parkinson’sneurodegenerative processes by being able to model and visualize them, researchers in Canada report.

Their study, “Quantum dot conjugated saporin activates microglia and induces selective substantia nigra degeneration,” was published in NeuroToxicology.

Microglia, primary immune cells of the brain and spinal cord, are known to contribute to the inflammation that underlies Parkinson’s neurodegeneration, which severely affects a brain area involved in motor control called the substantia nigra.

A key aspect of Parkinson’s research is to understand new and targeted ways of modulating microglia’s behavior, with a goal of influencing the survival or neurons or nerve cells. Such an ability would help to address the precise link between neurons and microglial cells.

Quantum dots, or nanoscale crystals, can be specifically taken up by microglia cells and may be useful as a direct way of targeting these cells. The nanoparticles also glow a particular color after being illuminated by ultraviolet light, allowing scientists to trace the molecules inside cells and study their cellular behavior.

Researchers at Carleton University investigated whether microglia within the substantia nigra of mice would take up quantum dots alone, and quantum dots carrying an immunotoxin called saporin. The latter works by inactivating ribosomes — cells’ protein builders — which compromises protein synthesis and leads to cell death. The scientists also studied how these nanoparticles affected microglia status (i.e., whether it is active or inactive).

Animals were given a four-minute infusion directly into their substantia nigra of either quantum dots alone, or of one of two doses of quantum dots conjugated with saporin. Within a week post-infusion, the mice’s balance and coordination were assessed.

Using imaging technology, researchers observed that quantum dots alone were selectively taken up by microglia and activated them. Microglia activation is a hallmark of inflammation in the context of neurodegenerative disorders. Despite their activated state, however, microglia had minimal effects on neurons and other neuronal support cells like astrocytes.

But in mice whose quantum dots were administered together with saporin, scientists observed a significant dose-dependent reduction in the number of nigral — meaning “of the substantia nigra” — neurons that produce dopamine, as well as impaired motor coordination six days after the infusion.

Quantum dots conjugated to saporin also increased the levels of a molecular mediator of inflammation, called WAVE2. This protein “is critical for the changes in activation state morphology of microglia,” the scientists wrote

The researchers believe that quantum dots carrying saporin could be a new and targeted way of modeling Parkinson’s-related inflammation, and evaluating new therapies aiming to treat it.

“[Quantum dots] might be a viable route for toxicant delivery and also has an added advantage of being fluorescently visible,” they wrote.

“Future work using this model should attempt to establish various degrees of neuronal loss. This model could then be used to test neuro-recovery or protective agents at differing stages of [the disease],” the researchers added.

https://parkinsonsnewstoday.com/2019/11/21/fluorescent-cystals-help-model-parkinsons-brain-inflammation-study-suggests/

Human Participants In Experimentation On The Brain? They Better Be Treated Well.

Nov 21, 2019 Elizabeth Fernandez

The MRI of a patient suffering from Dystonia, who received implants within the brain.  UNIVERSAL IMAGES GROUP VIA GETTY IMAGES

Some diseases of the brain are incredibly hard to treat. Parkinson’s Disease. Alzheimer’s. Severe depression. Cutting edge neurotechnologies may help people suffering from these diseases. Sometimes this comes in the form of a brain implant - sometimes, electroconvulsive therapy. These therapies involve exerting control over the central nervous system. Developing these therapies, however, involves human experimentation. Because of this, the National Institutes of Health Brain Research Through Advancing Innovative Neurotechnologies (BRAIN) Initiative not only focuses on developing new technologies but also on the ethics of these technologies - particularly, how the participants of the studies will be affected. BRAIN’s working group recently developed a set of ethical guidelines, some of which have not been widely considered before. 

Neurotechnologies that control the central nervous system can come in various forms. Invasive devices can be implanted within the brain, under the skull or below the dura. The most common of these is DBS, or deep brain stimulation. In this treatment, an electrode is placed within the brain. This can help a patient, even if they had previously not responded to other treatments, such as medication. DBS can treat things such as Parkinson’s disease, epilepsy, and obsessive-compulsive disorder, and is being investigated for the treatment of Alzheimer’s, obesity, and chronic pain. Other types of neurotechnologies can help with prostheses or spinal cord injuries. In addition, there are various types of noninvasive procedures, such as electric, magnetic or sonic stimulation of the brain. 

“Cutting-edge science requires cutting-edge ethics,” said Khara Ramos, Ph.D., who co-authored the report and who is the Director of Neuroethics at the National Institute of Neurological Disorders and Stroke. In order for research to move forward, research participants are needed. Three ethical standards were outlined in the report that protect these participants. 

Firstly, the risks and benefits must be weighted. The benefit of the new technology must be larger than the risk to the individual participants. Experimentation involves some risk, and these risks should be minimized. The surgery itself could lead to hemorrhage, a seizure or infection. The implant could move. There is a privacy risk if people don’t fully understand what data is being recorded. And there is even a risk that the participant’s personality may be altered by the implant. Some of these changes may be permanent. 

This brings us to the second ethical point: informed consent. Patients need to understand what the treatment entails and what the risks are. They should know the alternatives and should not be pressured to participate. This becomes complicated when the patient cannot consent because of an inability to communicate. “Because neural device research affects the brain in predictable and unpredictable ways, facilitating informed consent by considering participants’ values, interests, and preferences may be especially important,” says Ramos and co-authors.

A patient undergoes surgery to implant an electrode in the brain as a treatment for Parkinson's ... [+]UNIVERSAL IMAGES GROUP VIA GETTY IMAGES

The final ethical point, and one that has not been investigated in depth before, is what happens after the trial is over? Participants often think that the cost of their care after the trial is over will be covered, but this is not always the case. Imagine if the battery of the implant needs to be replaced after the trial. Who pays? What if the patient is benefiting from the implant? Who covers the cost of treatment after the trial ends? Health insurance many times will not cover expenses like this, so the authors encourage researchers to plan for care of the participants even after the trial is completed. 

“Such studies are only possible because research participants generously contribute,” says Ramos and co-authors. Their interests should be guarded, both during and after the trial.

https://www.forbes.com/sites/fernandezelizabeth/2019/11/21/human-participants-in-experimentation-on-the-brain-they-better-be-treated-well/#61302c2d2d55