How these extraordinary images could help cure Parkinson's

Pictures of the brain entered into competition by scientists may help in fight against condition

• Parkinson's UK invited brain scientists to submit images of their research
• Winning entry shows the links between nerve cells the disease destroys
• Competition honours scientist, 34, who died from Parkinson's last year

By DAMIEN GAYLE FOR MAILONLINE

PUBLISHED: 03:31 EST, 12 November 2014 | UPDATED: 09:57 EST, 12 November 2014

These remarkable, vivid images are the winning entries in a competition set up to visualise research into Parkinson's disease.

The charity Parkinson's UK invited British brain scientists to submit pictures captured in the course of their research to help 'create a full and vivid picture of Parkinson's research'.

The winning entry, which shows green branches between nerve cells glowing like the filaments in a plasma globe, was titled Nerve Superhighway, by Rowan Orme, from the University of Keele.

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Nerve Superhighway: Rowan Orme's winning entry, which shows green branches called axons between nerve cells, which break down in individuals who are suffering from Parkinson's disease

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Waterlilies: Nicola Drummond's bright pink, green and blue image of the build-up of protein that is thought to kill nerve cells and trigger the effects of Parkinson's, which won second place in the competition. The protein is called α–Synuclein, the University of Edinburgh scientist explained

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Tangled Web: The third placed picture, by Joel Beevers of Oxford University, shows skin cells reprogrammed into stem cells and then grown into the types of brain cells that Parkinson's kills

'The green branches between the nerve cells are axons,' he said. 'They act like superfast broadband connections, allowing millions of communications every second. 

'These connections break down in Parkinson's.'

The competition was open to researchers employed at a United Kingdom university, NHS Trust or other research institution.

Parkinson's UK dedicated it to the memory of Jonathan Stevens, a scientist who died from the disease last year aged just 34.

Dr Stevens was a prolific blogger, sharing both scientific writing and photography, and the charity called him on of its 'most creative research supporters'.

Parkinson's is caused by the loss of nerve cells in the brain that produce the chemical dopamine, which helps to control mood and movement.

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Ocean: Nicola Drummond also submitted this shortlisted image. She said: 'The α–Synuclein protein, in red, has been captured in this image in an area of the brain called the cerebellum. Understanding how α–Synuclein clumps together, and causes nerve cells to die, will hopefully lead to the development of new treatments for Parkinson’s'

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Berry burst: Another entry from Nicola Drummond shows a close up of nerve cells in the brain. She said: 'The cells can be kept alive for several months allowing researchers to carry out lots of different tests. They want to work out why the pink α–Synuclein protein, which is normally harmless, clumps together in Parkinson’s, and how this event cascades into the death of nerve cells'

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The Odyssey: Hugo Fernandes, of the University of Oxford, said of his entry: 'These cells are at the start of a remarkable journey from skin cells to nerve cells. They can tell us a huge amount about what’s going wrong in the brains of people with Parkinson’s. This technique could be the answer to replacing the nerve cells that are lost in the condition'

EVERY HOUR SOMEONE IS TOLD THEY ARE SUFFERING PARKINSON'S 

Every hour, someone in the UK is told they have Parkinson's.

It affects 127,000 people in the UK - which is around one in 500 of the population.

Parkinson's is a degenerative neurological condition, for which there currently is no cure. 

The main symptoms of the condition are tremor, slowness of movement and rigidity.

Parkinson's UK is the UK'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. 

There is no cure for the disease, but medication and brain stimulation can alleviate symptoms.

First runner up in Parkinson's UK's competition went to Waterlilies by Nicola Drummond of Edinburgh University.

The beauty of her bright pink, green and blue microscope image belies the deadly effect it depicts. 

It shows the build-up of protein that is thought to kill nerve cells, triggering the effects of Parkinson's.

'What looks like the pink flowers of waterlilies is actually a protein called α-Synuclein building up in the nerve cells of the brain,' she said.

'It is thought to play a major role in the death of nerve cells in Parkinson's.'

Third place went to Joel Beevers of Oxford University for his so-called Tangled Web, which visualises one of the latest breakthroughs in Parkinson's research.

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Energise: Dr Amy Reeve, of Newcastle Universit, said of her entry: 'These are mitochondria, the batteries of our cells. Brain cells demand a lot of energy, so finding ways to keep these batteries working is a vital aspect of Parkinson’s research'

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Galaxy: Federico Zambon, of the University of Oxford, said of his entry: 'Nerve cells which produce a chemical called dopamine have been created from the skin cells of people with Parkinson’s. The green staining confirms the cells they’ve made are nerve cells, and the enzyme responsible for producing dopamine in the cellscan be seen in red'

His deep red and pink image shows skin cells reprogrammed to become stem cells that can be grown into the same kind of nerve cells that Parkinson's destroys. 

Just last week scientists in Sweden said experiments using the technique on rats heralded a 'huge breakthrough' towards developing treatments for the disease.

Mr Beevers said: 'Skin cells from people can be reprogrammed to turn into stem cells which can develop into almost any type of cell in your body.

'Here they're grown into the type of brain cells that die in Parkinson's.' 

Parkinson’s UK Research Director, Dr Arthur Roach, said of the winners: 'Beautiful images like "Waterlillies" would be at home in the Tate, but are in fact the product of tireless researchers working to unpick what’s going awry in the hundreds of millions of nerve cells to cause people to develop Parkinson’s.

'As well as being visually arresting, the images give us unique insights into how we could intervene and stop Parkinson’s, or even prevent the condition in the first place.' 

Brian Stevens, Jonathan Stevens’ father, who judged the entries with his family, said: 'Judging this extraordinarily complex research was a sheer privilege. 

'Jonathan would be honoured that this competition was held in his memory. 

'He was an avid supporter of Parkinson’s research, and communicating its progress to inspire other people with Parkinson’s.' 

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Fireball: This second entry by Hugo Fernandes was also shortlisted. He said: 'What looks like an angry ball of fire is actually an image revealing the journey of adult skin cells being converted into neurons from Parkinson's patients in the lab. Once the nerve cells are created their potential as a tool in Parkinson’s research is huge'

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Purple haze: Heather Booth, of the University of Oxford, said: 'In Parkinson’s the nerve cells that produce dopamine die off in an area of the brain called the midbrain. No one knows why. This image is of midbrain nerve cells created in the lab, which will help to uncover this mystery'

Read more: http://www.dailymail.co.uk/health/article-2831190/How-extraordinary-images-help-cure-Parkinson-s-Pictures-brain-entered-competition-researchers-help-fight-against-condition.html#ixzz3IsLTACAX
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What is Lewy Body Dementia?

FoxFeed Blog

Barbara and Lee Mendel of Denver, Colorado

Posted by  Rachel Dolhun, MD, November 11, 2014

Memory problems and dementia are on the minds of many aging people— not just those with Parkinson’s disease.

Dementia is a description rather than a diagnosis. It refers to memory problems and difficulty in understanding or expressing knowledge. Dementia can include impaired judgment, reduced language skills or confusion severe enough to interfere with daily function. 

Alzheimer’s disease is the most common cause of dementia. Cognitive decline can be associated with later stages of Parkinson’s disease or Lewy body dementia (LBD).

It can be tricky to separate dementia associated with Parkinson’s disease (PD) from LBD because both have motor symptoms and memory problems. Doctors rely on timing and certain symptoms to differentiate the two. When significant memory problems develop within one year of the onset of Parkinson’s motor symptoms, LBD is more likely.

Also, people with both conditions can have hallucinations and fluctuating levels of alertness and confusion, but these symptoms are often more pronounced in LBD.

Treatment for dementia associated with PD and with LBD is the same. Medications called acetylcholinesterase inhibitors, such as rivastigmine (Exelon), are commonly used to treat memory problems. Doctors may prescribe specific medications targeting hallucinations or adjust Parkinson’s medications. 

Both Parkinson’s disease and Lewy body dementia are characterized by clumps of protein called Lewy bodies. Research is focused on determining the reason for the clinical differences between these diseases.

https://www.michaeljfox.org/foundation/news-detail.php?what-is-lewy-body-dementia

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Learning to Laugh and Let Go: One Couple’s Journey with Parkinson’s and Dementia

Posted by  Lauren Shoor, June 03, 2013

While thumbing through their passports, Barbara and Lee Mendel of Denver, Colorado, recalled travels as a couple: to Africa on safari and, most recently, to Mexico. But there’s one journey their passports can’t document—living with Lee’s Parkinson’s disease and Lewy Body Dementia (LBD), a type of Parkinson’s-related cognitive dysfunction.

Ten years ago, Lee was diagnosed with Parkinson’s. On a road trip to Oregon four years ago, Barbara started noticing “strange things.” Lee kept misreading road signs on the drive, and couldn’t keep the scores straight when they played golf or gin rummy. Soon they learned the cause: Lee had Lewy Body Dementia.

LBD is marked by a decline in memory and/or intellectual functioning severe enough to interfere with one’s daily social or professional life. It can include difficulty with executive reasoning (involved in multitasking and problem-solving), changes in personality and mood, loss of attention, and visual hallucinations.

The Mendels were devastated by the news. “Life really changed at that moment,” Barbara says. At first, they didn’t want to admit the truth to themselves or to others. But, with time, they would both learn to adapt. As they became more open with friends and family about Lee’s dementia, they’ve been surprised—by the reactions and lack of knowledge. Even within the Parkinson’s community, many have never heard of Lewy Body Dementia and resist talking about the cognitive challenges for people with PD. Others often want to attribute symptoms of Lee’s dementia to simply growing older, Barbara says. “This is why it’s so helpful when someone else says, ‘I noticed this in Lee, too.’ It can be a lonely world as a caregiver, and it makes such a difference when you start talking about it.”

Like Parkinson’s, Lewy Body Dementia is progressive. While Lee has always been a fun person, Barbara says, his child-like side has become more pronounced. She admits getting frustrated. “But if I can laugh about it, he laughs, too. You have to keep your sense of humor. And I remind myself, ‘It’s not him, it’s the disease.’”

While they feel lucky Lee doesn’t have hallucinations, they have experienced scary moments. Within the last few months, Lee was a victim of fraud, sharing their personal and financial information on the phone. Barbara wonders, “What would have happened if I wasn’t there to intervene? I can’t put him in a bubble.”

She wants to do whatever she can to help raise awareness across the Parkinson’s community—and beyond—about Parkinson’s-related cognitive dysfunction. The Mendels have learned to speak up among their friends, when they have noticed potential signs of either disease. Their philosophy is the sooner you know what you’re facing, the sooner you can do something about it. For Lee, staying active both physically and socially has been essential to maintaining his quality of life.

“If there were a better treatment than what’s available now, we’d go for it in a heartbeat,” Barbara says. “While it might not be able to help my husband, it could help others like him. That’s something we both want.”

She continues, “Today, I look at Lee with even more respect. I see how he’s been able to adjust—to living with Parkinson’s and dementia. But he’s still having fun and hasn’t lost his great self-image. Now that is a special man.”

https://www.michaeljfox.org/foundation/news-detail.php?learning-to-laugh-and-let-go-one-couple-journey-with-parkinson-and-dementia

Stem Cell Transplants for Parkinson's, Closer

Tue Nov 11, 2014 

TEHRAN (FNA)- A major breakthrough in the development of stem cell-derived brain cells has put researchers on a firm path towards the first ever stem cell transplantations in people with Parkinson’s disease. A new study presents the next generation of transplantable dopamine neurons produced from stem cells.

These cells carry the same properties as the dopamine neurons found in the human brain.

The experiments, performed in rat models of Parkinson's disease, reveal that the latest version of stem cell-derived dopamine cells fully mimic the characteristics and function of the dopamine neurons that are lost in Parkinson's disease. The potentially unlimited supply of transplantable cells, sourced from stem cell lines, opens the door to clinical application on a much broader scale. The results are published in the leading journal in the field, Cell Stem Cell.

"This study shows that we can now produce fully functioning dopamine neurons from stem cells. These cells have the same ability as the brain's normal dopamine cells to not only reach but also to connect to their target area over longer distances. This has been our goal for some time, and the next step is to produce the same cells under the necessary regulations for human use. Our hope is that they are ready for clinical studies in about three years," says Malin Parmar, who led the study conducted at Lund University and at MIRCen in Paris as part of the EU networks NeuroStemCell and NeuroStemcellRepair.

Brain cell transplants with fetal dopamine cells obtained from human embryos have already been performed on a few occasions, with varying results. In the past decade, the EU network TRANSEURO has been working hard to get a new and improved trial underway. That moment is now here. In the coming months a small number of patients will be transplanted with fetal cells in Lund, Sweden and Cambridge, UK.

The fetal dopamine cells that will be used within TRANSEURO, however, carry some restrictions. Firstly, there is the ethical concern of taking tissue from aborted fetuses. There is also the issue of availability of fetal cells, which is often scarce. The logistics surrounding the gathering of cells for any specific transplantation is partly down to luck and circumstance. These concerns will be resolved as the stem cell-derived dopamine cells become available in the clinic, making the treatment accessible for larger patient groups.

The collaborative efforts within EU networks NeuroStemcellRepair and TRANSEURO have put cell therapy on a faster track towards reaching patients. Getting stem cells to become functioning dopamine neurons, the method of delivering them to a specific target, and learning how to get them to integrate in the brain, are all extremely complicated processes. The sharing of ideas and data has been integral to the success of these networks, says Professor Elena Cattaneo, coordinator for NeuroStemcellRepair.

"Collaborative research of this nature is so much more than the results it produces, especially if we consider its potential for expanding the boundaries of knowledge and dissolving cultural barriers. From this perspective, basic research and collaboration among nations stand out once more as something the scientific community should never distance itself from."

http://health.einnews.com/article/233977696/IbmKfoMPgYcw19ax?n=2&code=ga_qGBxHZ2aVYO4P

Parkinson's disease drugs caused Robin Williams suicide says pal Rob Schneider

Parkinson's disease drugs caused Robin Williams' suicide, says Rob Schneider

Jason Kempin, Valeric Macon/Getty Images

Comedian Rob Schneider blamed the suicide of his longtime friend Robin Williams on the Parkinson's disease drugs he was taking to control his tremors.

Schneider, who has been friends with Williams for 20 years, made the remarks on Twitter, writing:

"Now that we can talk about it. #RobinWilliams was on a drug treating the symptoms of Parkinson's. One of the side effects is suicide! The evil pharmaceutical industry admits [that] over 100,000 people in the USA die a year from 'prescription' drugs!!"

Schneider has since deleted that tweet. Rob made the comments shortly after Robin's widow, Susan Schneider (no relation), revealed that Williams had been diagnosed with Parkinson's disease shortly before his tragic Aug. 11 suicide.

Levodopa (also called L-dopa) is the most commonly prescribed drug for Parkinson's disease. Potential side effects include mood disorders and depression.

Susan said Robin, who had previously struggled with drug addiction and substance abuse, had been clean and sober before his suicide. "Robin's sobriety was intact," his wife wrote in a statement. "And he was brave as he struggled with his own battles of depression, anxiety, as well as early stages of Parkinson's Disease, which he was not yet ready to share publicly.”

Williams managed his depression with antidepressants, exercise and cycling, and was reportedly extremely upset that Parkinson's would impede his ability to ride his bike and work out.

Parkinson's is a degenerative neurological disease that leads to shaking (tremors) and difficulty walking and moving. There is no known cure, but symptoms can be controlled with drugs. Sadly, there's a close link between depression and Parkinson's disease.

Research shows that 20 to 40 percent of Parkinson’s patients suffer from depression at some point, Philly.com reported. Studies also show that people with a history of midlife depression are more likely to get Parkinson's disease and that Parkinson’s can cause depression even in people who weren't previously depressed.

Comedian Wayne Brady recently revealed that Robin Williams' suicide threw him into a deep depression. "You don't want to move," said Brady. "You're like, 'I am just going to sit right here and I want to wallow in this."

Wayne has since sought treatment and is doing well.

http://www.examiner.com/article/parkinson-s-disease-drugs-caused-robin-williams-suicide-says-pal-rob-schneider

Robin Williams was on antidepressants: Had depression, paranoia, Parkinson's

Robin Williams was on antidepressants when he committed suicide, according to a coroner's report. While Williams' depression was widely publicized after his suicide, it was unclear (until now) whether he was taking antidepressants when he hanged himself on Aug. 11.

An autopsy revealed Williams had struggled with severe depression, anxiety, paranoia and Parkinson's disease in the months leading up to his suicide, the Washington Post reported Nov. 9.

The autopsy revealed he had the tetra-cyclic antidepressant mirtazapine in his blood at the time of his death. A potential side effect of mirtazapine is an increase in suicidal tendencies. There were no illegal drugs or alcohol found in Robin's system.

Mild depression can be managed with exercise, meditation and herbal supplements, said psychologist Sonja Lyubomirsky, author of The How of Happiness. However, severe clinical depression like the kind Williams had require more serious treatments, including prescription drugs and therapy.

Williams' widow, Susan Schneider, said she had spoken with Robin the night before his suicide, and he seemed to be in a healthy mental state. After his death, Schneider revealed Robin had recently been diagnosed with Parkinson's disease.

Williams' friend of 20 years, comedian Rob Schneider (no relation to Robin's widow), has blamed Parkinson's drugs for causing Williams' death. Levodopa (also called L-dopa) is the most commonly prescribed drug for Parkinson's disease. Potential side effects include mood disorders and depression.

Williams managed his depression and stress through exercise and cycling, and was reportedly extremely upset that Parkinson's would impede his ability to ride his bike and work out.

Parkinson's is a degenerative neurological disease that leads to shaking (tremors) and difficulty walking and moving. There is no cure, but symptoms can be controlled with drugs. Sadly, there's a close link between depression and Parkinson's disease.

Comedian Wayne Brady recently revealed Robin Williams' suicide threw him into a deep depression. "You don't want to move," said Brady. "You're like, 'I am just going to sit right here and I want to wallow in this." Wayne has since sought treatment and is doing well.

http://www.examiner.com/article/robin-williams-took-depression-drugs-before-suicide-suffered-from-paranoia

Resources for Prescription Assistance

Help with dignity

NeedyMeds
The mission of NeedyMeds has been to make information about assistance programs available to low-income patients and their advocates at no cost. Databases such as Patient Assistance Programs and Disease-Based Assistance, government programs and other types of assistance programs are the crux of the free information we offer online.

http://www.needymeds.org/index.htm

RxAssist
RxAssist offers a comprehensive database of pharmaceutical companies’patient assistance programs which provide free medications to people who cannot afford to buy their medicine. RxAssist also provides practical tools, news and articles so that health care professionals and patients can find the information that they need. All in one place.

http://www.rxassist.org

Rx Outreach 
Rx Outreach is managed by Express Scripts Specialty Distribution Services, Inc. (ESSDS), a fully-licensed mail order pharmacy that is committed to making the use of prescription drugs safer and more affordable. Rx Outreach is not a prescription insurance program nor an Internet pharmacy.

ESSDS developed Rx Outreach to provide a safe, affordable, and easy way for people of all ages to get medicines they need. The program offers prescription medicines to uninsured individuals and families, as well as those who have limited prescription drug coverage. Customer Service: 1-800-769-3880. http://rxoutreach.org

Partnership for Prescription Assistance Program
1-888-4PPA-NOW (1-888-477-2669) Their mission is to increase awareness of patient assistance programs and boost enrollment of those who are eligible. The Partnership for Prescription Assistance offers a single point of access to more than 475 public and private patient assistance programs, including more than 180 programs offered by pharmaceutical companies.

https://www.pparx.org

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http://www.parkinson.org/Parkinson-s-Disease/Treatment/Medications-for-Motor-Symptoms-of-PD/Resources-for-Prescription-Assistance

Changes in 'Parkinson's walk' predict dementia

6 November, 2014

“Subtle changes in the walking pattern of Parkinson’s patients could predict their rate of cognitive decline,” The Times reports after new research compared the gait of people with Parkinson’s disease with those of healthy volunteers.

Parkinson’s disease is a condition with three classic features: a tremor, stiff rigid muscles and slow movements, notably a slow, shuffling walk. It also has other symptoms, including Parkinson’s dementia, though it can be difficult to predict who will go on to develop dementia.

Researchers wanted to see if comparing the differences in gait (walking pattern) and cognition (thinking) between 121 people newly diagnosed with Parkinson’s disease and 184 healthy adults would provide any clues.

As may be expected, the study found measures of both gait and cognition were poorer in people with Parkinson’s compared with healthy adults.

They then compared people with Parkinson’s who mainly had gait problems with those who mainly had tremor problems.

Though there was no difference in cognitive abilities between the two groups, in those who mainly had gait problems there was a link between this and their cognitive function. That is, if a person had more problems with gait, they tended to have more cognitive problems.

This study will help doctors further understand how gait may be associated with cognition in people with Parkinson’s. It suggests that progression in gait problems may be associated with cognitive decline.

While there is currently no cure for dementia, knowing that someone is at a higher risk could help explain often upsetting changes in mood and behaviour, and enable early access to treatment.

Where did the story come from?

The study was carried out by researchers from Newcastle University and was funded by the National Institute for Health Research.

It was published in the peer-reviewed open-access journal, Frontiers in Aging Neuroscience, so the article is free to access online.

The Times’ reporting is accurate. But the Daily Mail’s coverage is misleading and confusing, as its headline asks, “Could your walk signal dementia?”

This study is specific to Parkinson’s disease and people with this condition who go on to develop dementia. It is not relevant to the population at large or to other types of dementia, such as Alzheimer’s.

What kind of research was this?

This was a case-control study examining the differences in gait (walking pattern) and cognition (mental abilities) between people newly diagnosed with Parkinson’s disease (the cases) and a comparison group of healthy older adults (the controls).

Parkinson’s disease is a neurological condition with an unknown cause, where not enough of the chemical dopamine is produced in the brain. This causes characteristic symptoms of:

• a resting tremor – shaking when the person is relaxed
• rigidity – stiff and inflexible muscles
• slow movements – someone with Parkinson’s classically walks with slow shuffling steps, and they are generally slower in all movements

As well as these classic symptoms, there are a variety of others, and usually Parkinson’s has some mental health effects, including dementia and depression.

While treatments such as Levodopa can help improve symptoms, there is no cure for Parkinson’s and the condition usually progresses.

It has been observed that in people who have a predominant tremor (TD), symptoms progress more slowly than those with predominant postural instability and gait disorder (PIGD).

These people who predominantly have problems with walking and balance tend to demonstrate greater decline, not only in terms of movement, but also cognition.

This study aimed to quantitatively measure the differences in movement and cognition between cases and controls. The researchers expected to see a specific association between movement and cognition in people with the different predominant type of Parkinson’s.

What did the research involve?

The researchers included 121 people (average age 67) who had been diagnosed with Parkinson’s disease in the past four months. They were matched by age and sex to 184 healthy controls, who were able to walk independently and had no specific cognitive or mental health problem.

The Movement Disorder Society (MDS)-revised Unified Parkinson’s Disease Rating Scale, which is a well-validated scale, was used to measure disease severity. It was also used to determine which features were predominant – TD (53 people) or PIGD (55 people).

Gait was measured by asking people to walk at their comfortable walking pace for two minutes around a 25m oval walkway. Researchers observed five variables: pace, rhythm, variability in step, asymmetry and posture.

Separately, a range of validated assessment scales were used to measure six domains of cognitive function: global cognition, attention, visual memory, executive function, visuospatial function and working memory.

A range of other tests were performed, including a timed chair stand to assess slow movements and muscle strength. This involved participants being asked to stand up from a seated position with their arms folded across their chest and sit down five times, as quickly as possible.

Balance was measured using the activities balance self-confidence scale, and physical fatigue and depression were also measured.

What were the basic results?

All gait variables were significantly different between healthy controls and people with Parkinson’s.

People with Parkinson’s walked more slowly, walked less symmetrically, made shorter steps, and overall had a more variable gait.

The only measures that were not different were step velocity variability, swing time and step width. As expected, gait measures were poorer for those with Parkinson’s characterised as PIGD compared with TD.

When looking at cognition, cognitive outcomes were significantly poorer for people with Parkinson’s compared with controls, with the exception of a measure of attention (choice reaction time).

Cognition was no different between the TD and PIGD types of Parkinson’s, with the exception of one measure of executive function (semantic fluency), which was poorer in people with PIGD.

The researchers found some association between gait and cognition in both people with Parkinson’s and controls. In the group with Parkinson’s, four measures of gait (pace, rhythm, variability and postural control) were correlated with measures of cognition, such as poorer measure of gait and poorer cognition.

Two of these measures (pace and postural control) were also associated with cognition in controls. In both people with Parkinson’s and the controls, the strongest association was between pace and attention.

Looking at the different types of Parkinson’s, associations between measures of gait and cognition were evident in people with PIGD, but not TD.

How did the researchers interpret the results?

The researchers say their observations provide a basis for understanding the complex role of cognition in Parkinson’s gait.

Conclusion

Parkinson’s is a neurological disease with characteristic features of tremor, rigidity and slow movements, as well as a variety of other classic symptoms, including Parkinson’s dementia.

This case-control study demonstrates how measures of both gait (walking) and cognition are, as would be expected, poorer in people newly diagnosed with Parkinson’s disease compared with healthy controls.

The study also demonstrates that in Parkinson’s disease, people with a predominant postural instability and gait disorder (PIGD) unsurprisingly have poorer measures of gait than people with predominant tremor disorder (TD).

Though there was little difference in cognitive measures between people with PIGD and TD, in those with PIGD there was a correlation between measures of their gait and cognitive function.

This suggests that progressive gait problems may be associated with progressive cognitive decline in people with Parkinson’s disease, though the specific biological mechanisms behind this link were not investigated by this study. The researchers now plan to investigate this link further.

The researchers also acknowledge several limitations with their study, including the relatively small sample size – involving only around 50 people with each subtype of Parkinson’s. This means these are small numbers on which to base firm conclusions about the differences between the two subtypes.

There are also other measures the study may not have been able to take into account, including the influence of medication (some had started Levodopa, some not) and depression.

Overall, this study helps doctors to further understand how gait may be associated with cognition in people with Parkinson’s, and that predominant gait problems may also be an indicator of more cognitive problems.

While there are no current preventative or treatment implications of these findings in terms of Parkinson’s, early recognition of people who may be at risk of dementia is likely to be beneficial.

 http://www.nursingtimes.net/home/behind-the-headlines/changes-in-parkinsons-walk-predict-dementia/5076531.article

Parkinson's stem cell therapy works in rats

Dopamine-making neurons derived from human embryonic stem cells. — Jeannie Liu in the lab of Jan Nolta at the University of California, Davis.ENTS

By Bradley J. Fikes10:04 A.M.NOV. 9, 2014
A rat model of Parkinson's disease has been successfully treated with neurons derived from human embryonic stem cells, according to a study led by Swedish scientists. It’s a promising sign for scientists at The Scripps Research Institute and Scripps Health who hope to perform similar therapy on Parkinson’s patients, using artificial embryonic stem cells.

In rats and people, neurons that make the neurotransmitter dopamine are essential for normal movement. The cells are destroyed in Parkinson's, leading to the difficulty in movement that characterizes the disease.

Researchers transplanted dopamine-producing cells grown from human embryonic stem cells into the brains of rats whose own dopamine-making neurons had been destroyed. The rats were immune-suppressed so they would not reject the cells. Within five months, the transplanted cells boosted dopamine production to normal levels, restoring normal movement in the rats.

The study was published Thursday in the journal Cell Stem Cell. The senior author was Malin Parmar of Lund University in Lund, Sweden.

Parkinson's embryonic stem cell therapy

The results support the Scripps approach of using the artificial embryonic stem cells, called induced pluripotent stem cells, said Jeanne Loring, who heads the Center for Regenerative Medicine at The Scripps Research Institute in La Jolla. Loring is part of a group called Summit 4 Stem Cell that's raising funds to treat eight Parkinson's patients with their own IPS cells.

Particularly significant is the study's comparison of the effects of dopamine-making neurons derived from fetal cells to that of embryonic stem cells, Loring said by email.

"In the 1980s and 1990s, there were several clinical trials that showed that grafts of fetal brain containing the precursors of dopamine neurons could reverse the effects of Parkinson's disease in some patients," Loring said. "We, and the others developing stem cell therapies, based our plans on the results of those studies, but no one had ever directly compared fetal tissue and human pluripotent stem cell-derived dopamine neurons in an animal model of PD."

Induced pluripotent stem cells appear to have much the same capacity as human embryonic stem cells to generate different tissues and organs.

There has been uncertainty about how similar they are to each other, specifically whether the IPS process produces mutations. But recent studies have found the cell types are extremely similar, including a study also published in Cell Stem Cell on Thursday. That study compared IPS cells with embryonic stem cells produced by SCNT, or somatic cell nuclear transfer, the same process used to create Dolly the sheep.

Evan Snyder, a stem cell scientist at the Sanford-Burnham Medical Research Institute in La Jolla, said by email that the work is well-done, but represents an "incremental advance."

"From what I see so far, the work is done in a very meticulous fashion and answers the question of whether hESCs (human embryonic stem cells) can give rise to neurons that worked as well as the old fetal tissue used to do," Snyder said. "However, unless you are a PD maven, it really is just an incremental advance.

"The techniques are not new. the method for making the cells has been out there for a while,' he said. "The model is only a rat, not a monkey. So there would need to be a lot of work before going into humans -- like whole monkey studies, as we are doing."

• Snyder is researching Parkinson's treatment derived from another type of stem cell, grown from parthenogenetic, or unfertilized human egg cells. The research is being performed in monkeys, which have a nervous system more similar to humans than do rats. International Stem Cell, based in Carlsbad, plans to commercialize the therapy if successful.

  Both the parthenogenetic and induced pluripotent methods have advantages and drawbacks. Induced pluripotent stem cells can be created from the patient's own cells, typically skin cells. This minimizes the chance of immune rejection. However, such a patient-customized therapy incurs additional expenses over a therapy made for many patients. The parthenogenetic stem cells are immune-matched to large numbers of patients, but rejection is still a possibility.

  The complete study is available at: utsandiego.com/parkesc.

  http://www.utsandiego.com/news/2014/nov/09/parkinsons-embryonic-rats/2/?#article-copy