Parkinson’s podcast: Genetics and Parkinson’s disease

RESOURCES & TOOLS 

 

Author: Geoffrey ChangPublished: 14 January 2016

Will genetics helps us crack the Parkinson’s code? January’s podcast looks at the fascinating relationship between genetics and Parkinson’s disease

In the latest Portland Countdown podcast, regular hosts Dave Iverson and Jon Palfreman invite special guest Dr Christine Klein – an expert in Parkinson’s genetics – to discuss how the latest research in genetics is helping us to better understand the underlying structure of Parkinson’s disease.

In the 30-minute interview, Dr Klein explains how inherited forms of Parkinson’s are revealing more about the condition than we ever knew before.

The aim of the Portland Countdown series is to give listeners new perspectives on the latest advances in Parkinson’s research and treatment.

The shows, developed by the World Parkinson Coalition, are aired online on the first Tuesday of every month from June 2015 to September 2016 – when the 4th World Parkinson Congress takes place in Portland, Oregon, US. The podcasts are free and available for download.

Click on: 

https://soundcloud.com/world-parkinson-coalition/08-genetics-and-pd

http://parkinsonslife.eu/parkinsons-podcast-genetics-and-parkinsons-disease/?utm_source=Parkinson%27s+Life&utm_campaign=4e2859345e-EPDA_Parkinson_s_Life_newsletter_5&utm_medium=email&utm_term=0_8624a2371b-4e2859345e-153908349

Parkinson's Disease: High Levels Of Uric Acid In Blood May Reduce Risk

January 17, 2016

New research suggests high levels of urate in the blood could help protect against Parkinson's disease.  Pixabay

Men with high levels of urate in their blood, also known as uric acid, may be less likely to develop Parkinson’s disease, according to new research published in Neurology.

Urate forms when the body breaks down chemicals called purine. Purines are natural substances found in the body’s cells, though they can also be found in some food and drinks, including liver, anchovies, mackerel, dried beans and peas, and beer. And it's these purines researchers suspect are capable of slowing the disease down."These results suggest that urate could protect against Parkinson's or slow the progression of the disease in its very early stages before symptoms are seen," study author Xiang Gao said in a statement. "The findings support more research on whether raising the level of urate in people with early Parkinson's may slow the disease down."

Doctor's diagnose as many as 60,000 new cases of Parkinson's disease each year. The neurodegenerative brain disorder, which reportedly affects up to 1 million people in the U.S, strikes 50 percent more men than women, according to Florida Hospital. The average age of onset is 60.

For the study, researchers collected data from more than 90,000 men and women participating in three ongoing studies, 1,267 of which had not been diagnosed with Parkinson's. Participants were given blood tests in order to measure their urate levels, finding of that nearly 1,300 sample, 388 developed the motor system disorder after the studies began. The researchers combined these results with three previous studies on the topic in order to conduct a proper meta-analysis.

Normal levels of urate can range from 3.5 to 7.2 milligrams per deciliter, according to the study. Men with the lowest level of urate had levels of less than 4.9 mg/dL, while those with the highest levels had 6.3 to 9.0 mg/dL. And researchers found men who had the highest levels of urate were nearly 40 percent less likely to develop Parkinson’s disease than those with lower levels.

Among the men who developed the disorder during the study, 45 of them had the highest level of urate and 58 had the lowest level of urate. But among the healthy men, 111 were in the group with the highest level of urate and 107 were in the group with the lowest level. Researchers did not observe this relationship between higher urate concentrations and risk of developing Parkinson’s disease in women.

While the study does not prove a causal relationship between high levels of urate and the motor system disorder, it does suggest the chemical could be "protective against Parkinson ’s disease risk or could slow disease progression during the preclinical stage of disease," Gao said.

This is an exciting idea, given urate levels can be raised easily and inexpensively. However, Gao warns excessively high levels of urate can lead to its own set of health problems, like kidney stones and gout.

Source: Gao X, O’Reilly E, Schwarzschild M, Ascherio A. Prospective Study of Plasma Urate and Risk of Parkinson Disease In Men and Women. Neurology. 2016.

http://www.medicaldaily.com/parkinsons-disease-high-levels-uric-acid-blood-may-reduce-risk-369870

````````````````````````````````````````````````````````````````````````````````````````````````````

High Uric-Acid Levels, Lower Risk of Parkinson's?

WEDNESDAY Jan. 13, 2016, 2016 

Men with high levels of uric acid in their blood may be less likely to develop Parkinson's disease, a new study suggests.

Researchers compared about 400 people in ongoing studies who developed Parkinson's disease and more than 1,200 people in the same studies who did not develop the movement disorder.

Men with the highest levels of uric acid (also called urate) were nearly 40 percent less likely to develop Parkinson's disease than those with the lowest levels, according to the study published online Jan. 13 in the journal Neurology.

"These results suggest that urate could protect against Parkinson's or slow the progression of the disease in its very early stages before symptoms are seen," study author Dr. Xiang Gao, of Pennsylvania State University, said in a news release from the American Academy of Neurology.

"The findings support more research on whether raising the level of urate in people with early Parkinson's may slow the disease down," Gao added.

Among men who developed the disease, 45 had the highest level of urate and 58 had the lowest level. Among men without the disease, 111 had the highest level of urate and 107 had the lowest level, according to the report.

There was no association between urate levels and Parkinson's disease risk in women, the study found.

Urate is formed when chemicals called purines -- found in food -- are broken down in the body. Previous research has suggested that urate may help protect brain cells.

It's easy and inexpensive to boost people's urate levels, but it must be done with care because extremely high levels can cause kidney stones and gout, Gao said.

He explained that the study does not prove that high levels of urate protect against Parkinson's disease, only that such levels are associated with a lower risk. Further research is needed to learn more about this association and why high levels of urate are not associated with lower risk of Parkinson's disease in women, Gao added.

More information

The U.S. National Institute of Neurological Disorders and Stroke has more about Parkinson's disease.

http://health.einnews.com/article/306229073/nXij0hy9rxzNhjBW

Healthy Living: Duopa and Parkinson's

Healthy Living: Duopa and Parkinson's: Patients with advanced Parkinson’s disease can have an increasingly tough time regulating their medication. Please click Healthy Living
to watch video.

January 13, 2016

Patients with advanced Parkinson’s disease can have an increasingly tough time regulating their medication.

Now, they may have a better way to keep their drugs and their daily lives more consistent.

Tonight in Healthy Living, we have the details of Duopa, which recently received FDA approval.

James has been on Duopa for four years now.

Dr. Truong says, "The drug is effective over a 16 hour period every day the patient uses the therapy."

But it is unknown how long it'll be effective; there's just not enough information yet.

He also says Duopa is for advanced Parkinson’s cases and patients need to exhaust conventional treatment first

http://health.einnews.com/article/306236184/b5qPmOP8q7fnCIEn

Scientists reveal 4 foods which could stop you getting cancer, Alzheimer’s and Parkinson’s disease

January 13, 2016  Lussy williams

A natural compound found in each of the four foods could make a person’s body less prone to age-related diseases, according to experts

Four foods with anti-ageing properties could help stave off cancer, Alzheimer’s and Parkinson’s diseases.

That’s the view of scientists behind a significant new study into cell matabolism.

According to the experts, peas, blue cheese, corn and soybeans contain a natural compound called spermidine, which reverses the body’s circadian rhythm.

Peas

Corn

This makes the body ‘younger’ and less prone to age-related diseases.

Dr Gad Asher, of the Weizmann Institute of Science in Israel, said: “This discovery demonstrates the tight intertwining between circadian clocks and metabolism and opens new possibilities for nutritional interventions that modulate the clock’s function.

“Impaired circadian rhythmicity has been linked to a wide variety of age-related diseases, including cancer, Alzheimer’s disease, Parkinson’s disease, and inflammation.”

The study published in Cell Metabolism said polyamines, of which spermidine is an example, are essential molecules present in all living organisms that are derived from dietary sources and synthesised by our own cells.

They regulate a variety of key cellular processes such as cell growth and proliferation.

Dr Asher suspected that polyamines might also play a role in circadian biology because they are known to influence the clock’s function.

When young mice were treated with a drug that inhibits polyamine synthesis, their circadian clock slowed down by about 11 minutes per day compared to untreated young mice.

On the other hand, adult mice that received extra spermidine in their drinking water had clocks that ran about eight minutes faster than untreated adult mice.

The effects of polyamines on the circadian clock were less pronounced in mice than in cells due to the tight regulation of these critical compounds in their natural physiological context.

Healthy: Soybeans were also listed among the four disease-beating foods

However, even subtle clock deviations have been associated with a wide variety of metabolic and age-related diseases.

The crosstalk between circadian rhythms and metabolism may serve to fine-tune and reinforce the function of the clock, he added.

He said: “Our findings basically rely on experiments with mice and if they hold true in humans, they will have broad clinical implications.

“The ability to repair the clock simply through nutritional intervention, namely polyamine supplementation, is exciting and obviously of great clinical potential.”

Surprise: Blue cheese isn’t an obvious health food, but it could stave off disease

But Asher warned: “I would not recommend that old people rush out for anything, especially not to buy polyamines, until this is tested and proven in humans.

“Even if one consumes high amounts of polyamines, similar to many vitamins, an excess of them will simply not be absorbed or will be secreted in the urine unless the body is in need of them.

“But I do envision testing polyamines in clinical trials as a tool against a wide variety of age-related diseases in humans.

“There is evidence in flies and mice that polyamines extend lifespan, and future studies might also support the use of polyamines in humans.”

http://personalhealthrecords.in/index.php/2016/01/13/scientists-reveal-4-foods-which-could-stop-you-getting-cancer-alzheimers-and-parkinsons-disease-2/

Many Parkinson’s Disease Programs in Development, GBI Research Reports

Analysts count 365 PD programs in all stages of development, including 94 first-in-class products 

 JANUARY 13, 2016

BY CAROLINA HENRIQUES

An analysis from business intelligence provider GBI Research titled “Frontier Pharma: Parkinson’s Disease — Identifying and Commercializing First-in-Class Innovation,” claims the current Parkinson’s disease (PD) treatment market relies on neuromodulators, and even though symptoms might be soothed, no neuromodulator has demonstrated neuroprotective properties to prevent or even slow down neuronal cell death.

However, the pipeline for PD is highly active, with 365 programs in all development stages and with diverse ranges of molecular targets.

“The Parkinson’s disease treatment pipeline is characterized by a high level of innovation compared to the central nervous system segment and the industry as a whole, with 43 percent of all pipeline programs with disclosed molecular targets being first-in-class,” analyst Angel Wong said in a press release.“While neuromodulators remain dominant in the pipeline, there are a number of targets which address different pathogenic mechanisms underlying neurodegeneration in Parkinson’s disease. This demonstrates a shift from traditional symptomatic treatments to disease-modifying therapies.”

Wong said potentially disease-modifying treatments are still in their early stages of development but are expected to fulfill significant unmet needs in the PD market in the long run. The report continues by stating there are 94 first-in-class products available for strategic consolidations, which means a wide range of investment opportunities are open for licensing or co-development deals in the field of PD.

“There is substantial focus on early-stage collaboration in Parkinson’s disease, especially for first-in-class products,” Wong said. “This is predominantly driven by growing unmet needs, the current lack of disease-modifying therapies and a desire for risk-sharing. Several first-in-class products have demonstrated promising pre-clinical evidence, and have significant potential to become game-changing products, representing high-reward investments.”

PD is a chronic and progressive disorder with an unknown cause and no present cure, despite treatment options such as medication and surgery. PD involves the malfunction of vital neurons, which, when dying, produce dopamine — a chemical that interferes with the part of the brain that controls movement and coordination.

As PD progresses, there is less dopamine in the brain, leading to the patient’s inability to control movement. Main symptoms include bradykinesia (slow movements), tremor, postural instability or rigidity (stiffness of the limbs). It is estimated that nearly 1 million people live with PD in the U.S.

http://parkinsonsnewstoday.com/2016/01/13/parkinsons-disease-treatment-pipeline-is-likely-to-meet-many-unmet-needs-says-gbi-research/

Rapid eye movement sleep without atonia may help diagnose Lewy body...

Rapid eye movement sleep without atonia may help diagnose Lewy body disease in middle-aged and older patients with somatic symptom disorder.

by: Takayuki Munechika, Hiroshige Fujishiro, Masato Okuda, Kunihiro Iwamoto, Youta Torii, Shuji Iritani, Norio Ozaki

January 13, 2016

Lewy body disease (LBD), including Parkinson's disease (PD) and dementia with Lewy bodies (DLB), is defined pathologically as degeneration in the central and peripheral nervous system associated with Lewy bodies. Somatic symptom disorder often predates the clinical diagnosis of PD and DLB. It is crucial to make an initial diagnosis of LBD in patients with psychiatric symptoms because administering psychotropic drugs often causes or exacerbates extrapyramidal signs. Given the close association between rapid eye movement (REM) sleep behaviour disorder and LBD, REM sleep without atonia on polysomnography may help to diagnose LBD in middle-aged and older patients with somatic symptom disorder. We reviewed the clinical profiles of five patients with an initial diagnosis of somatic symptom disorder who exhibited REM sleep without atonia on polysomnography. 

There were three men and two women, with a mean age of 68.4 years (range: 55.0-78.0 years). The mean Mini-Mental State Examination score was 26 (range: 22-30). Only two patients had a clinical history of dream-enacting behaviour and fulfilled the clinical criteria for REM sleep behaviour disorder, but clinical conditions in the other three patients corresponded to subclinical REM sleep behaviour disorder. Final clinical diagnoses were made as probable DLB in three patients; two patients did not meet the clinical criteria for PD or DLB. Neurological examinations revealed mild extrapyramidal signs in these two patients, and their scores on the motor component of the Unified Parkinson's Disease Rating Scale were 8 and 5 points, and their Mini-Mental State Examination scores were 30 points. 

Neither patient exhibited dream-enacting behaviour, but both had constipation. Cardiac (123) I-metaiodobenzylguanidine scintigraphy revealed mild increased washout rates. REM sleep without atonia may provide an opportunity to identify LBD in patients with somatic symptom disorder, even before they fulfil the clinical criteria for PD or DLB. Continued follow-up will be needed to determine whether these psychiatric patients are in the prodromal stage of PD or DLB.

 © 2016 The Authors. Psychogeriatrics © 2016 Japanese Psychogeriatric Society.

http://www.topix.com/health/parkinsons-disease/2016/01/rapid-eye-movement-sleep-without-atonia-may-help-diagnose-lewy-body

Can a cholesterol-lowering drug help to treat Parkinson's?

R. SIVA KUMAR

January 13, 2016

Amazingly, it seems to show some promise. Through a clinical trial as part of The Cure Parkinson's Trust's (CPT's)  Linked Clinical Trials Programme, the potential of the cholesterol-lowering drug, Simvastatin, was probed. It shows the ability to treat the "progressive neurological condition" afflicting about 10 to 20 million people around the world. This number is thought to double by 2030.

Being a "double-blinded placebo study", the experiment will involve 198 patients in 21 centers across the United Kingdom, including Plymouth. The Plymouth University researchers are searching for patients of Parkinson's who are not in the station.

The Cure Parkinson's Trust contacts Parkinson's experts globally every year, to check out a number of pre-selected compounds showing the potential to be brought to clinical trials. The compounds are thought to be safe and some are even used in other applications.

" It is encouraging to see new compounds that are already approved as being safe for use in the man being trialed for use in Parkinson's," said Camille Carroll, who will help conduct the trial, in a press release. "There have been few innovations in the treatment of Parkinson's for over 40 years and for the more than 127,000 people living with the condition in the U.K., the results of this trials programme could lead to new and highly effective treatments in the armoury of medications to tackle Parkinson's."

"We want to make a difference to those of us living with this condition within five years," added Tom Isaacs, co-founder of CPT. "The results of a recent trial in multiple sclerosis with simvastatin, and the pre-clinical work investigating its effect on alpha-synuclein clumping (which is a common feature of Parkinson's) indicate that it could be an effective treatment to slow down the progression of Parkinson's."

http://health.einnews.com/article/306179927/dIgJR8zvH-Xc-TTp

New type of antidepressant found to act quickly in mice

Jan. 13, 2016

The compound CGP3466B, already proven nontoxic for people, may effectively and rapidly treat depression, according to results of a study in mice.

The Johns Hopkins Medicine neuroscientists who conducted the research say that the compound -- previously shown to block cocaine craving in the brains of rodents -- delivers antidepressant effects to mice within hours instead of weeks or months, like currently available antidepressants. The results of the study will be summarized online in the journal Molecular Psychiatry.

"One of the promising things about CGP3466B is that it targets a new network of proteins," says Solomon Snyder, M.D., professor of neuroscience at the Johns Hopkins University School of Medicine. "That means it may work in patients who are unresponsive to other types of drugs and it lays the foundation for the development of a new class of fast-acting antidepressants that target the same network."

The team's discovery came out of investigations into the workings of a different drug, ketamine, long used primarily at high doses to induce anesthesia during surgery but known, at lower doses, to be a fast-acting antidepressant. Unfortunately, Snyder says, ketamine is addictive and can produce schizophrenialike symptoms, making it unsuitable for prolonged use, but his team hoped it could shed light on how to make a better fast-acting antidepressant.

Maged Harraz, Ph.D., a research associate and the first author of the newly published research paper, says the researchers already knew that ketamine interacts with excitatory NMDA receptors on nerve cells in the brain to block their activity.

Using biochemical tests on mouse nerve cells, Harraz and the team worked out the steps of the molecular chain reaction responsible for ketamine's NMDA-blocking antidepressant effects. They found the drug stimulates the creation of proteins that help build certain connections between nerve cells.

Specifically, they found the proteins GAPDH and Rheb in the middle of the chain reaction. Previous work from Snyder's group had shown that the compound CGP3466B prevents the addition of nitric oxide to GAPDH; this turned out to also block GAPDH from interacting with Rheb and continuing the chain reaction's signaling.

"CGP3466B works on the same network of proteins as ketamine, but since it works later in the chain reaction, it has fewer side effects," says Harraz.

To see if CGP3466B, like ketamine, has antidepressant effects in mammals, the researchers used two standard behavioral tests on mice. The first tested how quickly mice give up trying to escape from a pool of water. Compared to normal mice given no treatment, mice given CGP3466B spent an average of an extra half a minute working the problem. In the second test, treated mice were twice as fast to brave an unsheltered new environment to get a piece of food. Both behaviors in mice are considered surrogates for nondepressed behavior.

"In the second test, the drug worked in only half an hour," Harraz says. "Other antidepressants tested in mice, like fluoxetine, can take three weeks to show similar results on the same test."

The team is optimistic about CGP3466B because it has already been shown to be nontoxic and nonaddictive in phase I clinical trials that explored its use for Lou Gehrig's and Parkinson's diseases -- though it did not prove effective in treating those conditions.

But the researchers caution that it will take several more years to get the compound into phase II clinical trials to test its potential as an effective and safe antidepressant for people.

http://www.medicalnewstoday.com/releases/305019.php?tw

Hacking Your Brain: Neurotech Startups Aim To Treat Depression, Alzheimer’s And Parkinson’s Through Headsets

BY DAVID GILBERT @DAITHAIGILBERT ON 01/13/16 

A boy addicted to the internet has his brain scanned for research purposes at Daxing Internet Addiction Treatment Center in Beijing, Feb. 22, 2014.

Startups are looking to disrupt the treatment of brain disorders by merging technology and neuroscience. They claim that advancements in brain imaging, coupled with the use of tiny electrical currents, have allowed them to create headsets that can change the way parts of the brain communicate. These startups also claim their products could help treat a range of diseases, including depression, Alzheimer’s and Parkinson’s.

One such company, Cerestim, is leveraging advancements in how brain activity can be monitored and altered to bring discoveries out of the laboratory and into the real world. Cerestim is developing a headset to treat depression and other disorders using a technique called transcranial brain stimulation, which addresses a huge gap in the current treatment methodology.

Brain disorders’ share of the total global burden of disability and mortality is projected to rise from 11 percent in 1990 to 15 percent in 2020, which would outpace even the anticipated increase in heart disease during that time. The biggest problem facing caregivers is that up to 30 percent of the afflicted cannot be treated with traditional pharmaceutical therapies, according to the World Health Organization — and this is where companies like Cerestim come in.

“Having a nonpharmacological treatment for such patients is absolutely essential, and I am optimistic that we can get some success in that area and offer some symptomatic relief to those individuals where the drugs don’t work whatsoever,” Alan Palmer, director of Cerestim, told International Business Times.

The company is developing a headset that can be used by patients in their homes and remotely monitored by physicians, who will be able to control how often the device is used. Cerestim also says that thanks to the headset's ability to read a patient's brain waves, it will be able to adapt treatment to each individual user — something current electrical treatments such as electroconvulsive therapy (ECT) simply cannot do.

Depression is a medical condition with a possible  biological basis. Although the exact causes are still being identified, companies developing headsets like Cerestim believe the problem lies in the miscommunication between certain areas in the brain due to misfiring cells or neurons.

Cerestim's headset aims to read a patient's brain waves to identify where this "dysfunctional communication" is happening and, using specially designed electrodes tailored for each individual, repeatedly deliver small alternating electric currents to a particular area of the brain to reset the firing mechanism.

The pervasive image of using electrical currents to alter brain function is of machines like this ECT machine from the St. Audry's Hospital asylum in Suffolk, England, which closed in 1993, but new companies are looking to change that view.

One of the challenges facing Cerestim and other companies developing products in this field is having to overcome the negative connotations of ECT. “Applying an electric current to your head is scary,” Palmer admits.

But whereas the smallest current an ECT machine can apply is 750 milliamps, Cerestim's headset will use an alternating current of just 2 milliamps. Additionally, where ECT purposely attempts to bring on convulsions, Cerestim’s solution will be painless. "It takes time for such technologies to be accepted, but I think the process has started,” Palmer said.

Cerestim, which is based in the U.K., was founded in 2014 by Dr. Nir Grossman, who is researching transcranial electrical stimulation at MIT Media Lab at the Massachusetts Institute of Technology. The company says that proof of concept has been demonstrated, and it is close to signing a clinical research organization to put its technology into a clinical trial of patients with depression to establish efficacy.

Alzheimer’s Treatment

While the application of this technology to treat depression is likely to be the initial focus of testing, the method behind it can also be applied to a range of other disorders, including insomnia, migraines and potentially even Alzheimer’s disease.

Scientists know the physiological progression of Alzheimer's and that it follows a distinct pathway within the brain, beginning in the entorhinal cortex. “You could envisage the stimulation of the entorhinal cortex region of people with very early forms of Alzheimer’s,” Palmer said. “You could see some benefit in applying an electrical stimulation there to get the neurons in that vulnerable area more active.”

There are already a couple of companies with devices on the market that offer similar benefits to transcranial brain stimulation, using a different technique. This technology, called transcranial magnetic stimulation, also uses a tiny electrical current to alter patients' brain waves, but it requires a large magnet, necessitating a visit to a clinic for treatment, and each machine can cost in excess of $100,000.

Cerestim’s headset, on the other hand, will cost around $50, according to Palmer, when it comes to market in three to five years, pending regulatory approvals. And it will be fully portable — allowing patients to be treated in their own homes.

Relaxation Therapy

That said, this is still very much a medical device and will be controlled by doctors rather than the patients themselves. However, there is another set of companies that are looking to develop consumer-focused headsets that also take advantage of advancements in the ability to read brain waves and brain functions.

The Melomind headset from MyBrain Technologies aims to teach people to relax using an accompanying smartphone app.

Dr. Rohan Attal and Dr. Thibaud Dumas co-founded MyBrain Technologies after meeting at the Brain and Spine Institute in Paris, one of the most renowned centers for neuroscience research in the world. The pair’s first product is called Melomind, a headset that works in collaboration with an app on a smartphone to read brain waves and craft unique “audio journeys” to help the user learn to relax.

The company’s goal, according to Attal, is to “take the latest discoveries in neuroscience from the laboratories to the global market and provide a solution to provide better health and well-being.”

Attal and Dumas demonstrated their app on the sidelines of the Consumer Electronics Show in Las Vegas last week, seeking to set themselves apart from the flood of wearable and health-focused technology, which was one of the big trends of the show — but MyBrain is not interested in becoming the Fitbit for your brain.

“We didn’t want just a quantified-self product; we wanted something that can help people in a proactive way, improve their own brain function through the concept of brain training,” Dumas told IBT. Helping people relax and addressing stress may not sound like treating depression, but as Attal points out, a lot of physical disorders such as insomnia and migraines are related to stress.

http://health.einnews.com/article/306154064/3ZmqSfnjrnhL3aME