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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.
Please discuss this with your doctor, should you have any questions, or concerns. Never do anything without talking to your doctor. I do not make any money from this website. I volunteer my time to help all of us to be informed. Please No advertisers, and No Information about Herbal treatments. Please no advertisements.
This is a free site for all.
Thank you.


Saturday, February 17, 2018

Camden Parkinson’s group lightens life’s stresses with laughs

 Feb 16, 2018



CAMDEN — Whether you’re coping with a chronic condition like Parkinson’s or just the temporary affliction known as winter, nothing lightens the load like a good laugh. The next meeting of Camden’s Parkinson’s Support Group, set for Tuesday, March 6, from noon to 2 p.m. at the Anderson Inn at Quarry Hill, aims to prove the point.
During the first half of the March meeting, participants will forgo the usual informative presentation in favor of a little group “humor therapy,” gathering around Quarry Hill’s big-screen TV for an hour-long video marathon of some of the funniest film clips ever made.
After the presentation, attendees will divide into smaller groups to discuss insights and perspectives.
The Parkinson’s Support Group meets at Quarry Hill on the first Tuesday of each month between noon to 2 p.m . Participation is free and open to all those living with Parkinson’s as well as their family members and caregivers. Attendees are welcome to bring bag lunches; Quarry Hill provides beverages and desserts.
FMI: contact Cassie Walters at 596-3978 or via email at ckwalters66@gmail.com.

https://knox.villagesoup.com/p/camden-parkinsons-group-lightens-lifes-stresses-with-laughs/1725713?source=rss

Are hallucinations caused by medication or the disease itself?

February 15, 2018   Ann Miner




“I have a question,” said he. “What about hallucinations in Parkinson’s? Is that a normal malady or is it caused by medications?”
Was he asking about hallucinations or dementia? They are not the mutually inclusive. Hallucinations are often caused by certain medicines. My Burt had a patch on his neck to help prevent nausea. That medication caused him to hallucinate. His visions were harmless and kind of sweet. “I’m watching those two mice playing in the corner,” he would say. Or, “That spider was almost up onto my bed, and you scared him away.”
One time, when I asked him what he was doing he said he was watching the game on the TV. Okay, but the TV was not turned on. However, his cousin’s husband saw evil and scary things, such as demons in certain pictures on the wall, that were brought on by a certain medication for PD.
Parkinson’s can also give rise to cognitive deficits. According to Dr. Norman Doidge, in his book, “The Brain’s Way of Healing,” any neurological condition that restricts mobility can weaken the brain. As people become immobile, the lack of activity in the brain — that is they see less, hear less, and process less new information — can cause the brain to atrophy from the lack of stimulation.
Dementia can be caused by inactivity or atrophy of the brain. Unfortunately, regardless of the cause, Parkinson’s patients develop cognitive deficits at rates higher than the normal population. Cognitive problems can progress into dementia in advanced cases: PD patients have a six-times normal risk of dementia.
As part of chronic Parkinson’s disease and its treatment, psychotic behaviors occur in over 50 percent of patients. These problems include illusions (perceptual errors), hallucinations (false perceptions), delusional thinking and even suspicious and paranoid behaviors.
Life-style changes, medication adjustments and new, specifically anti-psychotic treatments, are available. Learn more by registering now for a free Expert Briefing webinar taking place on Feb. 27 from 10-11 p.m. by calling 1-800-473-4636 or emailing helpline@parkinson.org.
Future Expert Briefings include:Marijuana and PD: What Do We Really Know?
Living Alone: Home Safety and  Management in PD
Have we discussed attitude in this column? To quote a favorite teacher in college, “I’m here to tell you” that attitude makes all the difference in the world as to how we feel physically. For instance, my daughter and I live together. She is a remarkable woman, who senses that I need more help than I really do. She often says, “Wait, let me do that for you.” 
She had helped me in so many areas that I began to think of myself as an infirm little old lady. Yes, dearie.
Then she went on an extended stay to Italy last summer. As she was making travel plans, I began to worry about how I would handle everything on my own. Then I was reminded that I lived on my own for 22 years before I married my Burt.
At the end of her three-month hiatus, I saw that I had myself back, and I felt 15 years younger. My physical energy is surprisingly strong for an infirm little old lady.
As a Parkinson’s patient, you will have your off times, and they can dampen your spirit. I encourage you to find something every day that makes you happy, makes you smile, makes you remember how good it feels to feel good. Desert living allows us to awaken to sunshine most mornings, and that alone is a blessing. Take an attitude check. Let the sun’s rays work their magic.
For now, take long steps and keep looking up.
Ann Miner lives in Apple Valley. She writes non-fiction, and children’s books. Contact her at eannminer@yahoo.com.
http://www.vvdailypress.com/news/20180215/are-hallucinations-caused-by-medication-or-disease-itself

To hear the beat, your brain may think about moving to it




BY  
, FEBRUARY 16, 2018


A brain region linked to movement is integral to recognizing rhythms


FEELING OFFBEAT  Briefly disrupting a brain region involved in planning movement with a magnetic pulse hinders a person’s ability to follow a rhythmic beat. (The black square in this heat map indicates the site of highest pulse stimulation.)

If you’ve ever felt the urge to tap along to music, this research may strike a chord.
Recognizing rhythms doesn’t involve just parts of the brain that process sound — it also relies on a brain region involved with movement, researchers report online January 18 in the Journal of Cognitive Neuroscience. When an area of the brain that plans movement was disabled temporarily, people struggled to detect changes in rhythms.

The study is the first to connect humans’ ability to detect rhythms to the posterior parietal cortex, a brain region associated with planning body movements as well as higher-level functions such as paying attention and perceiving three dimensions.

“When you’re listening to a rhythm, you’re making predictions about how long the time interval is between the beats and where those sounds will fall,” says coauthor Jessica Ross, a neuroscience graduate student at the University of California, Merced. These predictions are part of a system scientists call relative timing, which helps the brain process repetitive sounds, like a musical rhythm.

“Music is basically sounds that have a structure in time,” says Sundeep Teki, a neuroscientist at the University of Oxford who was not involved with the study. Studies like this, which investigate where relative timing takes place in the brain, could be crucial to understanding how the brain deciphers music, he says.

Researchers found hints of the relative timing system in the 1980s, when observing that Parkinson’s patients with damaged areas of the brain that control motion also had trouble detecting rhythms. But it wasn’t clear that those regions were causing patients’ difficulty with timing — Parkinson’s disease can wreak havoc on many areas of the brain.

 Ross and her colleagues applied magnetic pulses to two different areas of the brain in 25 healthy adults. Those areas — the posterior parietal cortex and the supplementary motor area, which controls movement — were then unable to function properly for about an hour.
Suppressing activity in the supplementary motor area caused no significant change in participants’ ability to follow a beat. But when the posterior parietal cortex was suppressed, all of the adults had trouble keeping rhythm. For example, when listening to music overlaid with beeps that were on the beat as well as off the beat, participants frequently failed to differentiate between the two. This finding suggests the posterior parietal cortex is necessary for relative timing, the researchers say.

The brain has another timing system that was unaffected by the suppression of activity in either brain region: discrete timing, which keeps track of duration. Participants could distinguish between two notes held for different amounts of time. Ross says this suggests that discrete timing is governed by other parts of the brain. Adults also had no trouble differentiating fast and slow tempos, despite tempo’s connection to rhythm, which might imply the existence of a third timing system, Ross says.

Research into how the brain processes time, sound and movement has implications for understanding how humans listen to music and speech, as well as for treating diseases like Parkinson’s.

Still, many questions about the brain’s timing mechanisms remain (SN: 07/25/15, p. 20): What are the evolutionary origins of different timing mechanisms? How do they work in conjunction to create musical perception? And why do most other animals seem to lack a relative timing system?

Scientists are confident that they will have answers — all in good time


https://www.sciencenews.org/article/hear-beat-your-brain-may-think-about-moving-it

'I was worried people would see the disability not the man': Watkins breaks silence on diagnosis

February 16, 2018  -  Alexandra Smith

Former NSW deputy premier John Watkins.  Photo: Janie Barrett


John Watkins wasn’t ready to be an old man.
He was busy. The former deputy premier was head of Alzheimer's NSW and the chair of three boards. He was still active in the Labor Party and even briefly considered running for the federal seat of Bennelong after he was approached by the ALP.
John Watkins has kept his condition a secret since his diagnosis seven years ago.  Photo: Janie Barrett
"I was worried people would see the disability not the man," he says. “I hadn’t wanted to talk about it until now because of the embarrassment, the perceived stigma, the feeling that people might think you are no longer useful.”
The diagnosis was slow. Watkins first noticed a minor symptom at an event just before he left politics. It started with a small shake in his hand which he put down to an essential tremor. His grandmother had had an essential tremor, the most common form of tremor but it is not Parkinson’s.
It was three years until his neurologist confirmed Parkinson’s.
“I remember when I was first diagnosed and I wasn’t particularly upset about it, other than the mystery of where it was going. I remember thinking that I was just glad it wasn’t a progressive fatal disease like Alzheimer’s which I was surrounded by at the time.”
John Watkins underwent a seven-hour operation last month, having a pacemaker-like device permanently attached to his brain. Photo: Janie Barrett
Watkins stepped down from Alzheimer's NSW last year. Not through ill health, but because the organisation was reborn as the national body Dementia Australia. He had been at Alzheimer's NSW since quitting state politics in 2008 and very briefly toyed with a return to politics when a byelection was called in Bennelong last year in the wake of the citizenship crisis.
“The party came to me and I hadn’t completely thought it through but then I spoke to Kristina Keneally, who is a very good friend, and when she said she was interested I was really keen and happy to support her,” he says. “I think politics is over for me.”
Until then, Watkins had been managing his Parkinson's with medication. His neurologist had suggested brain surgery – deep brain stimulation – about 18 months earlier but Watkins was not interested.
“Brain surgery? I thought, no thanks, that’s not for me,” Watkins says. But his thinking changed late last year as he found simple things – rolling over in bed or getting into a car – becoming a major struggle.
“I didn’t want to be an old man, I wanted to be around and active for my kids and grandkids and I still wanted to be useful, there was still things I want to do,” he says.
He agreed to undergo deep brain stimulation and his surgeon operated last month. It was a seven-hour operation to attach a pacemaker-like device permanently to his brain.
Deep brain stimulation is used to treat a range of human movement disorders, including tremor, dystonia , Tourette’s syndrome and Parkinson’s disease. Wires are implanted by a neurosurgeon into the brain and then run under the skin to an implanted battery, placed in the chest or abdominal wall.
The rechargeable battery produces a continuous impulse to the brain 24 hours a day to alleviate symptoms. The voltage can be adjusted by the patient with a small handheld device to control tremors.
Watkins says he was a good candidate for the treatment and was told it was likely to be effective. He was fit and healthy, had no illnesses such as diabetes and was not depressed – a side effect for about 20 per cent of people with Parkinson’s and often one of the first symptoms of the disease. “Once I spoke seriously about it with my surgeon, I took the opportunity.”
The surgery has been life changing. The improvements, he says, have been “dramatic”.
“I am not in any pain, I am not on any medication. It is amazing to not have to have a sleep every day, there is no uncontrollable movement in my limbs,” he says. “It really has been incredible. I can roll over in bed and hop in and out of a car and I don’t feel like I have played two games of football all the time.”
He also realises his reluctance to speak about his Parkinson’s was based on his assumptions, not those of others.
“I used to be quite embarrassed about the tremor and would worry people would make judgments. But now I realise it was me judging others, not them judging me. But by talking about it now, I hope I can give some people the confidence to take the step and hopefully gain the benefit I have been blessed with.”

http://www.smh.com.au/nsw/i-was-worried-people-would-see-the-disability-not-the-man-watkins-breaks-silence-on-diagnosis-20180216-p4z0kn.html

Friday, February 16, 2018

Amyloid Protein Transmission Through Neurosurgery

NEUROSCIENCE NEWS  FEBRUARY 15, 2018
Source: UCL.


Researchers report, in a number of cases, amyloid beta pathology may have been transmitted by contaminated instruments used in neurosurgeries up to three decades previously.

A separate review of the medical literature supported the discovery by identifying four other case studies with similar pathology and past surgical history. As these patients were all men with a history of head trauma, research teams had previously speculated that those were correlated. NeuroscienceNews.com image is in the public domain.


Amyloid beta pathology – protein deposits in the brain – might have been transmitted by contaminated neurosurgical instruments, suggests a new UCL-led study.

For the paper, published today in Acta Neuropathologica, researchers studied the medical records of four people who had brain bleeds caused by amyloid beta build-up in the blood vessels of the brain.

They found that all four people had undergone neurosurgery two or three decades earlier as children or teenagers, raising the possibility that amyloid beta deposition may be transmissible through neurosurgical instruments in a similar way to prion proteins which are implicated in prion dementias such as Creutzfeldt-Jakob disease.

Amyloid beta is best known for being one of the hallmark proteins of Alzheimer’s disease, but the researchers did not find evidence of Alzheimer’s in this study.

“It is well known that the abnormal proteins seen in Creutzfeldt-Jakob disease have been transmitted between patients by certain medical and surgical procedures. We have been investigating whether the same can be true for amyloid beta,” said the study’s lead author, Professor Sebastian Brandner (UCL Institute of Neurology).

The researchers looked in the pathology archive at the National Hospital for Neurology and Neurosurgery for biopsy and autopsy materials of young adult patients with confirmed amyloid beta pathology, which can lead to brain bleeds or harmful plaques, in the brain’s blood vessels. These deposits of the amyloid protein occur increasingly frequently in older individuals but only very rarely in younger people.

Four cases were identified – three of them were in their 30s, and one was aged 57 – all of whom had experienced brain bleeds caused by amyloid deposits in brain blood vessels. None had any known genetic causes that predispose to this pathology in younger people.

A separate review of the medical literature supported the discovery by identifying four other case studies with similar pathology and past surgical history. As these patients were all men with a history of head trauma, research teams had previously speculated that those were correlated.

The new study suggests otherwise, as all patients had a history of childhood neurosurgery, three were women and only one had a history of head trauma.

In a comparison group of 50 people of similar ages from the same archives, the researchers did not find any amyloid beta pathology and only three had a recorded history of childhood neurosurgery.

Previous work in laboratory animals has shown that tiny amounts of abnormal amyloid beta protein can stick to steel wires and transmit pathology into the animals’ brains, but this paper is the first to suggest the same may be possible in humans.

The new study follows reports in recent years of amyloid beta pathology in brain blood vessels following treatment with cadaver-derived human growth hormone in childhood.

“We have found new evidence that amyloid beta pathology may be transmissible. This does not mean that Alzheimer’s disease can be transmitted, as we did not find any significant amount of pathological tau protein which is the other hallmark protein of Alzheimer’s disease,” said Professor Brandner.

“Our findings relate to neurosurgical procedures done a long time ago. Nevertheless, the possibility of pathological protein transmission, while rare, should factor into reviews of sterilisation and safety practices for surgical procedures,” he said.

“Neurosurgery is becoming increasingly common in older individuals. As amyloid beta pathology increases in brains with age, this raises the potential for onward transmission of protein pathology to other individuals in the same hospital,” said the study’s first author, Dr Zane Jaunmuktane (UCL Institute of Neurology).

As this study was small and retrospective, the authors hope their findings stimulate others to explore these ideas further. They are currently expanding their study by looking at more archives across the UK.

“There are several reasonable alternative explanations for our findings that we cannot yet rule out. Further research is required to clarify things. A large epidemiological study would be particularly useful,” said co-author Professor Simon Mead (MRC Prion Unit at UCL).
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Funding: The study was conducted by researchers at UCL, UCLH, Centro Hospitalar Universitario do Porto, Centro Hospitalar de Lisboa Ocidental and the University of Leuven, and was funded by the National Institute for Health Research University College London Hospitals Biomedical Research Centre and the Queen Square Dementia Biomedical Research Unit.
Source: Chris Lane – UCL
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Open access research in Acta Neuropathologica.


Abstract

Evidence of amyloid-β cerebral amyloid angiopathy transmission through neurosurgery
Amyloid-β (Aβ) is a peptide deposited in the brain parenchyma in Alzheimer’s disease and in cerebral blood vessels, causing cerebral amyloid angiopathy (CAA). Aβ pathology is transmissible experimentally in animals and through medical procedures in humans, such as contaminated growth hormone or dura mater transplantation in the context of iatrogenic prion disease. Here, we present four patients who underwent neurosurgical procedures during childhood or teenage years and presented with intracerebral haemorrhage approximately three decades later, caused by severe CAA. None of these patients carried pathogenic mutations associated with early Aβ pathology development. In addition, we identified in the literature four patients with a history of neurosurgical intervention and subsequent development of CAA. These findings raise the possibility that Aβ pathology may be transmissible, as prion disease is, through neurosurgical procedures.

http://neurosciencenews.com/amyloid-transmission-neurosurgery-8499/

Link Between Hallucinations and Dopamine Not Such a Mystery

NEUROSCIENCE NEWS  FEBRUARY 16, 2018
Source: Columbia University Medical Center.


Researchers report elevated dopamine levels may make those with schizophrenia rely more on expectations, which results in them experiencing auditory hallucinations.




The researchers designed an experiment that induces an auditory illusion in both healthy participants and participants with schizophrenia. They examined how building up or breaking down sensory expectations can modify the strength of this illusion. They also measured dopamine release before and after administering a drug that stimulates the release of dopamine. NeuroscienceNews.com image is in the public domain.



Researchers at Columbia University Irving Medical Center (CUIMC) and New York State Psychiatric Institute (NYSPI) found that people with schizophrenia who experience auditory hallucinations tend to hear what they expect, an exaggerated version of a perceptual distortion that is common among other people without hallucinations. Those with hallucinations and other psychotic symptoms are known to have elevated dopamine, the main area of focus for available treatments for psychosis, but it was unclear how this could lead to hallucinations. The researchers found that elevated dopamine could make some patients rely more on expectations, which could then result in hallucinations.

The findings, published recently in Current Biology, explain why treatments targeting the production of dopamine could help alleviate this condition.

“Our brain uses prior experiences to generate sensory expectations that help fill in the gaps when sounds or images are distorted or unclear,” said Guillermo Horga, MD, PhD, assistant professor of clinical psychiatry at CUIMC and a research psychiatrist at NYSPI. “In individuals with schizophrenia, this process appears to be altered, leading to extreme perceptual distortions, such as hearing voices that are not there. 

Furthermore, while such hallucinations are often successfully treated by antipsychotic drugs that block the neurotransmitter dopamine in a brain structure known as the striatum, the reason for this has been a mystery since this neurotransmitter and brain region are not typically associated with sensory processing.”

The researchers designed an experiment that induces an auditory illusion in both healthy participants and participants with schizophrenia. They examined how building up or breaking down sensory expectations can modify the strength of this illusion. They also measured dopamine release before and after administering a drug that stimulates the release of dopamine.

Patients with hallucinations tended to perceive sounds in a way that was more similar to what they had been cued to expect, even when sensory expectations were less reliable and illusions weakened in healthy participants. This tendency to inflexibly hear what was expected was worsened after giving a dopamine-releasing drug, and more pronounced in participants with elevated dopamine release, and more apparent in participants with a smaller dorsal anterior cingulate (a brain region previously shown to track reliability of environmental cues).

“All people have some perceptual distortions, but these results suggest that excess dopamine can exacerbate our distorted perceptions,” said Dr. Horga. “Novel therapies should aim to improve the processing of contextual information by targeting the dopamine system or downstream pathways associated with modulation of perceptual processing, which likely include the dorsal anterior cingulate cortex.”
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Funding: Funding for this study was provided by grants K23-MH101637 (PI: Horga), P50-MH086404 (PI: Abi-Dargham), R21-MH099509 (PI: Abi-Dargham), and R01MH068073 (PI: Balsam) from the National Institute of Mental Health. Dr. Cassidy was supported by a post-doctoral fellowship from the Fonds de Recherche du Québec, Santé. Dr. Horga was additionally supported by a grant from the Sidney R. Baer Jr. Foundation. The authors declare no competing financial interests.
The other contributors from CUIMC and NYSPI are Clifford M. Cassidy, PhD, Peter D Balsam, PhD, Jodi J. Weinstein, MD, Rachel J. Rosengard, BA, and Anissa Abi-Dargham, MD.
Source: Eian Kantor – Columbia University Medical Center
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Open access research in Current Biology.
doi:10.1016/j.cub.2017.12.059


Abstract

A Perceptual Inference Mechanism for Hallucinations Linked to Striatal Dopamine

Highlights
•Auditory hallucinations are linked to a perceptual bias toward uncertain expectations
•Elevated striatal dopamine function relates to the same pattern of perceptual bias
•Volume of dorsal anterior cingulate relates to the same pattern of perceptual bias

Summary
Hallucinations, a cardinal feature of psychotic disorders such as schizophrenia, are known to depend on excessive striatal dopamine. However, an underlying cognitive mechanism linking dopamine dysregulation and the experience of hallucinatory percepts remains elusive. Bayesian models explain perception as an optimal combination of prior expectations and new sensory evidence, where perceptual distortions such as illusions and hallucinations may occur if prior expectations are afforded excessive weight. Such excessive weight of prior expectations, in turn, could stem from a gain-control process controlled by neuromodulators such as dopamine. To test for such a dopamine-dependent gain-control mechanism of hallucinations, we studied unmedicated patients with schizophrenia with varying degrees of hallucination severity and healthy individuals using molecular imaging with a pharmacological manipulation of dopamine, structural imaging, and a novel task designed to measure illusory changes in the perceived duration of auditory stimuli under different levels of uncertainty. Hallucinations correlated with a perceptual bias, reflecting disproportional gain on expectations under uncertainty. This bias could be pharmacologically induced by amphetamine, strongly correlated with striatal dopamine release, and related to cortical volume of the dorsal anterior cingulate, a brain region involved in tracking environmental uncertainty. These findings outline a novel dopamine-dependent mechanism for perceptual modulation in physiological conditions and further suggest that this mechanism may confer vulnerability to hallucinations in hyper-dopaminergic states underlying psychosis.

http://neurosciencenews.com/dopamine-hallucinations-8508/

Dodgers, Gibson to raise funds for Parkinson's disease





https://youtu.be/QuA_XRKPBxo


GLENDALE, Ariz. -- The Dodgers will mark the 30th anniversary of the 1988 World Series championship Opening Week by partnering with World Series hero Kirk Gibson in the fight against Parkinson's disease.
The 60-year-old Gibson, diagnosed with the illness in 2015, will throw out the ceremonial first pitch on Opening Day at Dodger Stadium on March 29, highlighting an Opening Week fundraiser for the Kirk Gibson Foundation, the Los Angeles Dodgers Foundation and the Dodgers.

Gibson's foundation raises money and awareness for the disease. Proceeds from the Opening Day 50-50 raffle and silent auction will go to the Gibson Foundation, and the Dodgers Foundation will auction off 88 limited-edition Gibson-autographed bobbleheads and game-worn jerseys from the March 30 game against the Giants, when Gibson bobbleheads will be given to the first 40,000 ticketed fans in attendance.
"I'd like to thank the Dodger organization, the Los Angeles Dodgers Foundation and Dodger fans for their support of the Kirk Gibson Foundation and Parkinson's disease research. We're going to be able to help a lot of people through the money raised during Opening Week," said Gibson. "I'm honored to help kick off the Dodgers' 60th anniversary celebration, and am looking forward to re-living many magical moments at Dodger Stadium on Opening Day and on my bobblehead night."
Opening Day presented by Bank of America is sold out, but limited tickets are still available through the purchase of mini plans at Dodgers.com/miniplans. Single-game tickets are still available for Friday's game at Dodgers.com/promotions, which will also feature Friday Night Fireworks presented by Denny's, as well as the rest of the Dodgers' season-opening series vs. San Francisco. Single-game game tickets, mini-plans, group tickets and suites are all available now at Dodgers.com/tickets.
https://www.mlb.com/news/dodgers-kirk-gibson-fighting-parkinsons/c-266506344

Scientists improve DNA transfer in gene therapy

February 15, 2018  -    Deutsches Primatenzentrum (DPZ)/German Primate Center

Parkinson's disease, Huntington's disease, cystic fibrosis - these and many other fatal hereditary human diseases are genetically transmitted. Many cancers and cardiovascular diseases are also caused by genetic defects. Gene therapy is a promising possibility for the treatment of these diseases. With the help of genetically modified viruses, DNA is introduced into cells in order to repair or replace defective genes. By using this method, scientists have discovered a quicker and more efficient treatment for the cells.

Parkinson's disease, Huntington's disease, cystic fibrosis -- these and many other fatal hereditary human diseases are genetically transmitted. Many cancers and cardiovascular diseases are also caused by genetic defects. Gene therapy is a promising possibility for the treatment of these diseases. With the help of genetically modified viruses, DNA is introduced into cells in order to repair or replace defective genes. By using this method, scientists from the German Primate Center (DPZ) -- Leibniz Institute for Primate Research have discovered a quicker and more efficient treatment for the cells. For this purpose, the scientists changed the so-called HEK293 cell line that is used for the production of therapeutic viruses. The cells then produced a protein called CD9 in large quantities. In addition, they modified the viruses used for gene transfer in such a way that CD9 is integrated into their envelope membrane. These genetic manipulations resulted in a faster and more efficient infection of the target cells. The resulting higher transfer rate of DNA into the target cells promises new and improved gene therapy treatment. The study was published in the journal Molecular Therapy.
The ability of viruses to introduce their genetic material into the host cells is used as a tool in gene therapy. These "gene taxis" consist of modified viruses, the so-called viral vectors. They are equipped with fully functional genes to replace the defective disease-causing genes in the cells. However, the prerequisite for this is that the viruses recognize and infect the corresponding cells. This is the point where the research of the junior research group Medical RNA Biology at the German Primate Center comes in.
Transport bubbles in the cell should increase the efficiency of gene therapy
"In our study, we wanted to find out if it was possible to improve the infection rate of viral vectors and how," says Jens Gruber, head of the junior research group and senior author of the study. "At the moment, the infection rates, depending on the target cells, are often around 20 percent, which is not enough for certain therapies." To change that, the researchers looked at the production of the so-called exosomes to find out how to use this mechanism in order for the virus vectors to become more efficient. Exosomes are small membrane vesicles filled with proteins, RNA or other molecules. They are used for the transportation of cell components and for intercellular communication. "Our hypothesis was that we could improve the production of viruses and their efficiency by boosting exosome production in the cells," explains Jens Gruber explaining the relevance of the transport vesicles for the study.
In order to produce large quantities of the CD9 protein, Jens Gruber and his team genetically engineered the HEK293 cell lines that are used for the production of viral vectors. This protein is known for its function in cell movement, cell-cell contact, and membrane fusion. The assumption was that it could also play a role in exosome production. In addition, scientists incorporated the CD9 protein into the envelope membrane of viral vectors. "We were able to observe two things," Jens Gruber summarizes the results. "Firstly, in comparison to the untreated HEK293 cells, exosome production in the HEK293-CD9 cells increased significantly, which suggests a crucial role of the protein in exosome formation. Secondly, the incorporation of the CD9 protein in the viral membrane has significantly improved the transfer of DNA. This was observed in an increased number of infected target cells that carried the desired gene without the implementation of additional virus vectors."
80 percent infection rate
The increased amount of CD9 in the virus resulted in a higher infection rate that amounted to approximately 80 percent. The protein appears to have a direct impact on exosome production and virus efficiency, which has previously not been described. "The results of our study provide us with a better understanding of exosome formation as well as virus production in cells," says Jens Gruber. "These findings can be used to make currently used virus-based gene therapies more efficient. In future, one might be able to completely abstain from using viruses and only use exosomes to transport genetic material into target cells."
Story Source:
Materials provided by Deutsches Primatenzentrum (DPZ)/German Primate CenterNote: Content may be edited for style and length.

Journal Reference:
  1. Kai O. Böker, Nicolas Lemus-Diaz, Rafael Rinaldi Ferreira, Lara Schiller, Stefan Schneider, Jens Gruber. The Impact of the CD9 Tetraspanin on Lentivirus Infectivity and Exosome SecretionMolecular Therapy, 2017; DOI: 10.1016/j.ymthe.2017.11.008

https://www.sciencedaily.com/releases/2018/02/180215105723.htm

Hartford HealthCare Pioneers New Technology For Patients with Parkinson's Disease and Essential Tremor

HARTFORD, Conn.Feb. 16, 2018 /PRNewswire

Hartford HealthCare's Ayer Neuroscience Institute has pioneered the most advanced Deep Brain Stimulation technology for patients with Parkinson's disease and essential tremor, becoming the first in Connecticut and among the first in New England to offer the Infinity Deep Brain Stimulation (DBS) System.


Dr. Patrick Senatus discusses deep brain stimulation for patients with Parknison's and Essential Tremor.


On February 8, Dr. Patrick Senatus, Neurosurgery Director at the Chase Family Movement Disorders Center at the Hartford HealthCare Ayer Neuroscience Institute, implanted the Abbott Infinity Deep Brain Stimulation (DBS) System. The new technology allows for even more targeted treatment and reduces potential side effects.
Deep Brain Stimulation is a surgical procedure in which wires are connected from the brain to a pacemaker-like battery pack implanted in the chest. DBS is not a cure for movement disorders, but it can dramatically decrease symptoms, restore mobility and improve patients' quality of life.
According to Abbott, the Infinity system is the first in the U.S. to feature a directional lead designed to precisely customize therapy that may maximize patient outcomes and reduce side effects. The lead offers eight independent electrode segments through which physicians can precisely steer electrical current toward structures of the brain that control movement.
"The technology we've used in the past can be limited in that it stimulates an entire contiguous field within the brain including areas we sometimes may not want to stimulate. This can cause unwanted effects such as slurred speech, tingling in the hands, twitching of muscles or double vision," said Chase Family Movement Disorders Medical Director Dr. Joy Antonelle de Marcaida. "The new system potentially decreases the likelihood of that because we can direct stimulation in a more focused manner."
The system is also the world's only DBS system operating on a Bluetooth iOS software platform. Clinicians can streamline the programming process by using the software platform on an iPad Mini mobile device. Patients can manage their symptoms with their Abbott Infinity DBS System iPod Touch mobile digital device controller.
"With the original system the physician was always knee to knee with the patient during programming because there was a wire attached. The new system is more in line with modern technology. Patients are more comfortable with it. They can change some of the parameters discretely on their own with the provided iPod Touch device, such as increasing or decreasing voltage or turning the stimulator on or off if need be," de Marcaida said.
The Chase Family Movement Disorders Center has locations in VernonCheshire and Meriden.
"Being first in Connecticut and surrounding states to utilize the Abbott system is another example that the Chase Family Movement Disorders Center is truly a leading edge destination program with its early adoption of new technologies, interventions, medications and involvement in clinical research that improve outcomes for our patients," said de Marcaida.
SOURCE Hartford HealthCare

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