Parkinson's disease: Boosting dopamine promotes movement

By Catharine Paddock PhD  --  February 5, 2018

New research with implications for the treatment of Parkinson's disease suggests that when we want to move, all our brain needs is a quick burst of dopamine.

The results, by scientists at the Champalimaud Center for the Unknown in Portugal as well as Columbia University in New York City, NY, question the idea that the brain needs a constant level of dopamine for normal movement.

A report on the study, published in the journal Nature, describes how immediately before they initiated movements, the associated neurons, or nerve cells, showed peaks in dopamine activity.

"Our most important result," says first study author Dr. Joaquim Alves da Silva, a psychiatrist and neuroscientist from the Champalimaud Center and the Nova University of Lisbon in Portugal, "is that we showed, for the first time, that the change in neural activity is necessary to promote movement."

"And, also for the first time," he continues, "we showed that the dopamine peak that precedes movement initiation does not only regulate initiation, but also regulates movement vigor."

Death of dopamine cells leads to Parkinson's

Parkinson's disease is a progressive disorder that develops when dopamine-producing cells in the substantia nigra, which is an area of the brain that controls movement, die.

Dopamine is a neurotransmitter, or a chemical messenger that carries signals between neurons. It is linked to a number of brain functions, including the control of movement and behavior that is associated with reward and pleasure.

The main symptoms of Parkinson's disease include tremor, stiffness, slowness of movement, and impaired coordination and balance. As the symptoms progress, they make it harder to talk, walk, carry out everyday tasks, and live independently.

Although the disease mostly affects people over the age of 60, around 4 percent of Parkinson's cases are diagnosed in those under the age of 50.

Worldwide, there are more than 10 million individuals living with Parkinson's disease. In the United States — where approximately 60,000 people are diagnosed with Parkinson's every year — the total cost of the disease is estimated to be $25 billion per year.

There is currently no cure for Parkinson's disease. However, there are drugs that can substantially relieve symptoms for many people by helping to replenish and maintain the brain's diminishing supply of dopamine.

Difficulty is movement initiation, slowness

The new study is particularly significant because it suggests that there might be a better way to correct dopamine shortage.

Dr. Alves da Silva explains that individuals with Parkinson's "do not have a global motor problem," but a specific one. Under the right circumstances, they can perform complex motor tasks. For example, if given a push at the right time, they can even ride a bicycle.

"The patients' problem," he adds, "is in the difficulty to initiate movement and in the slowness of movement." It was this observation that spurred the team to investigate further.

For the new study, the researchers used a technique called optogenetics, which employs laser light to rapidly stimulate neuron activity in the brains of mice.

Optogenetics is a relatively new technology that is changing "the landscape of neuroscience" by improving our understanding of how particular brain circuits work in health and disease.

Dr. Alves da Silva says that they used it to ensure that they only recorded activity in the dopamine-producing neurons of the mice's substantia nigras.

Burst of dopamine neuron activity

The scientists recorded what happened in the mice's brains as they moved freely in an open space. Using motion sensors, they could detect when the animals started moving and pinpoint the activity of the dopamine-producing cells in the period leading up to their moves.

The results showed that the activity of the dopamine-producing neurons peaked just before the mice started a given movement.

Then, in another experiment, they allowed the mice to roam freely, except that they manipulated the activity of their dopamine-producing neurons by using the laser to switch them on and off.

Again, with the help of the motion sensors, they could link this to when the mice were moving and not moving.

Dr. Alves da Silva notes that activating the dopamine-producing neurons when the mice were not moving "for half a second was enough to promote movement — and with more vigor — than without these neurons' activity."

But, if they activated the neurons when the mice were already in motion, the animals continued as they were — there was not change in the movement or its vigor, which they defined from changes in acceleration.

Results may also explain link to motivation

The researchers found same result when they switched off the dopamine-producing neurons in the middle of an ongoing movement — there was no change in the movement or its vigor.

"These results," explains senior author Rui Costa, a professor of neuroscience and neurology who works at Columbia University, "show that the activity of dopamine neurons can act as a gate to permit or not the initiation of movements."

"They explain why dopamine is so important in motivation, and also why lack of dopamine in Parkinson's disease leads to the symptoms that it does," he adds.

One of the drugs that is currently used to treat Parkinson's disease is levodopa, which raises the body's level of dopamine.

"But levodopa elevates dopamine all the time, not just when we want to move," says Prof. Costa, adding that long-term use of the drug also leads to dyskinesia, a condition characterized by involuntary and erratic movements.

"

Our study suggests that strategies that would boost dopamine when there is a desire to move would work better."

Prof. Rui Costa

 https://www.medicalnewstoday.com/articles/320826.php 

Mechanism behind common Parkinson's mutation discovered

 February 5, 2018 by Will Doss, Northwestern University

Lipid reduction using an FDA-approved glucosylceramide synthase inhibitor (GCSi) reduces pathological alpha-synuclein in cell bodies (top) and neurites (bottom) of Parkinson’s patient neurons. Yellow staining indicates pathological alpha-synuclein. Credit: Northwestern University

Northwestern Medicine investigators have discovered how a gene mutation results in buildup of a toxic compound known to cause Parkinson's disease symptoms, defining for the first time the mechanism underlying that aspect of the disease.

The study, published in Neuron, points to a potential novel therapeutic pathway using drugs originally intended to treat another condition, Gaucher's disease, according to senior author Joseph Mazzulli, Ph.D., assistant professor in The Ken & Ruth Davee Department of Neurology, Division of Movement Disorders.

In Parkinson's, a protein called alpha-synuclein is converted to insoluble, toxic clusters in the central nervous system—but the exact mechanism of conversion was unknown until now.

One of the strongest risk factors for developing these clusters is a mutation in the gene GBA1, which normally degrades a lipid called glucosylceramide. Patients with one mutation in the gene suffer an increased level of glucosylceramide and have been shown to have a five-fold increased risk for Parkinson's; patients with two mutant forms of the gene, one inherited from each parent, can develop Gaucher's disease, a lysosomal storage disorder.

Mazzulli and his colleagues used this genetic connection to elucidate the mechanism of GBA1-influenced Parkinson's disease. Using stem cell models of neurons, they used a pharmacological inhibitor to increase levels of glucosylceramide without a mutated GBA1 gene. Even without the mutation, this resulted in a dramatic build-up of toxic alpha-synuclein in neurons.

"This suggested to us that the critical factor in converting alpha-synuclein from its normal form to its pathogenic form was not necessarily the presence of the mutated GBA1 protein, but more importantly the decreased activity and accumulation of glucosylceramide," Mazzulli said.

With that realization in mind, the investigators took a closer look at the conversion process, finding the healthy form of alpha-synuclein actually existed in two different forms, a simple molecule and a more complex molecule. While it was assumed previously that only the simple molecule was converted into the toxic variety, Mazzulli and his colleagues unexpectedly found the complex molecule was directly converted by glucosylceramide into toxic alpha-synuclein.

"We were surprised to find that toxic aggregation occurred by direct conversion of the large alpha-synuclein complex," Mazzulli said. "We thought the complex would have to first disassemble before forming toxic aggregates, but that's not what our data indicated."

These discoveries suggest that future therapies targeting this pathway might utilize drugs originally intended for treating Gaucher's disease, Mazzulli said. While the pharmaceutical industry has been interested in the use of those lipid-reducing agents for some time, this study defines the molecular process behind those efforts and demonstrates how it might work.

"Some companies have been using synthase inhibitors to reduce the synthesis of the lipid, and we used a similar compound on patient-derived neurons in our study," Mazzulli said. "We were able to show it reduced toxic alpha-synuclein aggregation directly within neurons derived from Parkinson's patients."

In addition, the study gives future drug trials an important metric to measure success, Mazzulli said.

"Our ultimate goal is to reduce alpha-synuclein levels in patients, however measuring the levels of alpha synuclein from the central nervous system of a living patient is complicated," Mazzulli said. "It's far easier to measure the effects of therapeutics that alter glucosylceramide in patients, since the lipid can be directly measured from easily accessible fluids, such as blood or cerebral spinal fluid."

The next step towards a functional treatment will be to graduate from stem cell-derived neurons to animal models, according to Mazzulli.

"We're trying to determine if this occurs in a living animal and if we can reverse it using similar compounds to what's being tested in these clinical trials," Mazzulli said. "If we can intervene before any insoluble amyloid protein develops, maybe we can reverse it to its normal state."

Journal reference: Neuron

Provided by: Northwestern University 

https://medicalxpress.com/news/2018-02-mechanism-common-parkinson-mutation.html

New options for Parkinson's patients

 February 5, 2018 by Laura Wright, University of Kentucky

Parkinson's disease is a degenerative neurologic condition that affects more than one million people in the United States and 10 million people worldwide. Parkinson's attacks the nerves in the brain, causing tremors, rigid muscles, and other problems so that people gradually lose their ability to move fluidly. There is no cure, but drugs can help reduce the severity of some symptoms.

These drugs, however, can have significant side effects, and after long-term use, these side effects can be almost as bad as the disease itself. When those drugs are no longer effective, some patients turn to Deep Brain Stimulation (DBS), a device that functions as a sort of pacemaker for the brain to regulate the signals that control movement.

DBS implantation requires two surgeries. During the first surgery, a physician will place one or two insulated wires called "leads" in the brain. These leads are strategically placed based on detailed pre-surgical testing in the exact locations that control specific symptoms you're experiencing. 

A week or two after the leads are placed, you will undergo a second procedure to implant a "stimulator" – a device about the size of a stopwatch that powers the leads. It is typically implanted under the skin in the chest, much like a pacemaker for the heart. The stimulator will be turned on after the second surgery, producing mild electrical impulses to stimulate a specific region of the brain and help "override" tremors and other movement problems.

But DBS also has drawbacks: the batteries in the neurostimulator must be replaced every three to five years, which presents an ever-increasing risk for serious – even life-threatening – infections.

Now, however, there is a new option that uses a rechargable battery with a 15-year lifespan. This new technology could save patients a minimum of three additional surgeries.

Even better: the new device can be attached to the existing system, which means that people who already have DBS can switch without replacing the entire system.

Doctors at the Kentucky Neuroscience Institute were the first in the U.S. to switch a patient from the old device to the new.

DBS is also approved for treatment of dystonia and obsessive-compulsive disorder and is also being studied as a treatment for chronic pain, PTSD, and other affective disorders.

While DBS is not a cure, it may help improve day-to-day life for patients with Parkinson's disease. If you are considering DBS for the first time, or if you already have DBS, consult your doctor about this new option.

Provided by: University of Kentucky

https://medicalxpress.com/news/2018-02-options-parkinson-patients.html

New kind of homing beacon targets cancerous cells and other diseases

February 5, 2018 by ​Andrew Myerse, Stanford University

The CD19 molecule on a leukemia cell is like a tiny radio broadcasting to the world, “I’m leukemia. Come and get me.” Credit: Kevin Craft

Leukemia is a deadly cancer in which rogue white blood cells roam the bloodstream, slowly killing the body that gave them life.

But this insidious killer has an Achilles' heel. Many leukemia cells are betrayed by a molecule on their exterior surfaces known as CD19.

When activated, CD19 will kill the cancer cell to which it is attached. To cancer biochemists, CD19 is like a tiny radio signal broadcasting to the world, "I'm leukemia. Come and get me." But when a body is without the immune cells equipped to hear CD19's siren song, the leukemia is free to carry on its lethal business undeterred. So, researchers created leukemia-specific human immune cells that track down and kill any leukemia cell exhibiting the CD19 signal.

Developing better hunter-killer cells to target cancers is part of what goes on in the lab of Stanley Qi, assistant professor of bioengineering and of chemical systems biology. In a recent article in Nature Communications, Qi and his team explained how they used the CRISPR gene-editing technique to equip certain immune cells with a homing beacon to target leukemia.

Though this is still basic research, Qi's approach could one day lead to new ways to treat the roughly 170,000 Americans who were diagnosed leukemia and other blood-related cancers last year.

But leukemia is just the beginning. Cancers of the blood system account for a mere fraction of all cancers, most of which are solid tumors—clumps of cells that grow inappropriately in breasts, ovaries, lungs and prostate, for example. Solid tumors take refuge within a complex microenvironment of molecules, hormones and growth factors that help these unwanted cells spread and suppress the immune system agents that seek to kill the tumor.

Qi hopes to prove that his technique could work on all cancers because it targets a beacon found not just on leukemia, but on almost every type of cell in the body, including solid cancers. That is why Qi's team is so excited. By using CRISPR to hack ever more precisely into the genome, Qi believes it may one day be possible to bioengineer therapeutic agents to dial in on not just cancers, but other diseases that use the same radio-like signaling that has already used to attack leukemia.

Hacking biochemical communications

Qi's team describes used the CRISPR gene-editing technique to modify cellular receivers known as G protein-coupled receptors—GPCRs for short.

One of the largest and most important families of chemical receptors in human physiology, GPCRs are like cellular antennae, constantly searching for biochemical signals that allow cells to communicate and to function together as tissues. When antennae molecules recognize a particular signal—a molecule like CD19, for instance—they initiate a cascade of cellular communications with the nucleus that triggers a broad array of genetic outcomes ranging from immune responses to chemical generation to cell reproduction.

When GPCRs detect opiates, for instance, they instruct cells to flood the body with pleasure-enhancing, painkilling dopamine. As such, GPCRs are the gateways—the input/output devices—by which various important hormones, proteins, fatty acids and drugs communicate on a cellular level.

GPCRs are found on the surface of almost every cell type in the body. Of the 20,000 or so genes that make up the human genome, 800 alone are dedicated to distinct GPCR variations. "That's a huge proportion of our genetic code," Qi says, noting that some 40 percent of all drugs already on the market today target GPCRs.

Therein lies the excitement in this research. By developing a technique that can turn the plethora of GCPRs into tattle tales for different illnesses and dysfunctions, Qi's team has developed a platform for hacking into the body's biochemical communications network to battle disease. In the cancer example described above, the team has been able to recalibrate the GPCR antennae to home in on key molecules present in the tumor microenvironment.

Doing the ChaCha

Qi has dubbed their variation of the CRISPR technique "ChaCha" for the way it involves a dance of two molecules to modify the genetic code of GPCRs. "With ChaCha we can now create GPCR antenna devices that recognize virtually any molecule imaginable, including hormones, cellular growth factors and synthetic drugs," he says.

While there are existing CRISPR techniques that target GPCRs, ChaCha has two key advantages. First, ChaCha is dose dependent. A GPCR trained to recognize a specific hormone, for instance, would be able to modulate its response based on the relative presence of that hormone—more hormone would mean a greater response, and vice versa. "This is a programmable logic by which cells can figure out what their charge is and when they have completed an assigned task," he notes. "We're trying to design smarter cells."

The second advantage is that ChaCha is reversible. A cell modified for a specific task could be returned to its normal state once its duty was complete.

Early clinical trials have been promising and are already leading to new leukemia therapies. What has been most revolutionary, however, is a growing ability to use living cells as therapies, opening a world beyond traditional chemotherapies.

Qi and collaborators are excited by the broader prospect of adapting their genetic approach to an array of diseases ranging from solid tumors to neurological disorders such as Parkinson's disease and autoimmune disorders like lupus.

Asked about next steps for ChaCha, Qi says he plans to continue to test the bounds of his technique to make it easier to create cells to attack disease or to conjure desirable chemicals in the body. There has already been commercial interest in the approach. "We are just at the beginning of a very exciting period in predictably designing living cells for medical uses," Qi says. "Now we're moving quickly and in the right direction."

Provided by Stanford University 

https://medicalxpress.com/news/2018-02-kind-homing-beacon-cancerous-cells.html

Exit driving

By Jose Pujalte Jr.  February 4, 2018

Jose Pujalte Jr.

“I don’t worry about getting old. I’m old already.” — George Burns (1896-1996), US entertainer

For many people, independence is symbolized by the freedom and ability to drive his or her own car. Some people who can afford chauffeuring may still want to drive by themselves occasionally. But for those aging and yet forced to drive to and from work, to drive to market, or bring the last teenage daughter to a party, there may be a few serious reasons for giving up getting in front of the wheel altogether.

Vision Problems. Aging affects vision and hearing, two main requirements for fast reaction time in driving. Night vision deteriorates. A driver with vision problems can hit objects and may be unable to avoid people darting out of nowhere. In particular, the driver can have:

• Cataracts – or clouding of the lens of the eye. Obviously, this can cause cloudy or hazy vision and the sensitivity to light that comes with the condition makes night driving an ordeal.
• Glaucoma – or high pressure within the eyeball will cause problems with peripheral vision, another necessary component for normal driving.
• Macular degeneration – will affect central vision as retinal tissue deteriorates. This affects reaction to traffic lights and to pedestrians crossing in front of the driver.

Medical Problems. The chronic problems of aging such as arthritis, diabetes, or Parkinson’s disease can make driving impossible and dangerous. Elderly people who insist on driving may not be fully aware of possible consequences. We’ve all heard of or read stories of cars suddenly plowing into sidewalks full of people. If the driver isn’t a drunk or stoned teenager, he or she is usually a senior citizen who had a heart attack, a stroke, or an adverse reaction to medication followed by the obvious inability to drive.

• Degenerative Arthritis – causes painful joints of the hands, the neck, the shoulders, hips and knees, usually. Driving-wise, decreased joint motion means slower movements in looking at the rear view mirror, looking from side-to-side to assess traffic both vehicular and pedestrian, and slower pumping of foot pedals for gas, clutch, and brakes.
• Diabetes – as a chronic disease, the hands and feet may become numb leading to poor control of the steering wheel and foot pedals; any unforeseen drop in blood sugar on the road can lead to catastrophic dizziness or even loss of consciousness.
• Parkinson’s Disease – causes involuntary shaking of the extremities which is disastrous in driving where steady hands and feet are a given.

Signs to Hand Over the Car Keys. Before maiming or even killing innocent pedestrians or other drivers, there are signs to watch out for in finally deciding to give up driving.

• Slow reaction time to traffic lights, whether “stop” or “go.”
• Erratic and uncontrolled movements.
• Failing vision.
• Driving too slowly in the highway.
• Becoming nervous in a traffic jam.
• Losing attention most of the time.
• Falling asleep at the wheel.

Protective Driving. In general, driving can be made safer by:

• Wearing a seat belt.
• Avoiding alcohol if you are the designated driver.
• Bringing along a younger relative or friend who knows how to drive.
• Resting before driving.

Sooner or later, old people will have to give up driving. It should be a good idea to hire a driver or at least get someone to drive for important appointments. Leave the stress of driving to other people.

E-mail: jspujalte@yahoo.com

https://news.mb.com.ph/2018/02/04/exit-driving/

Banned from the game?

 February 4, 2018 Home By Bill Baker

Roundup and its main ingredient, glyphosate now have yet another strike against them. You would think this stuff would be out of the game by now, but Roundup is still the most used product of its kind in America and in the world.

The newest strike? Roundup can severely impair your immune system, brain function and digestion according to a new French study.

Doctors, scientists, and environmentalist already know that Roundup has been linked to prostrate, breast and lung cancers; kidney failure; severe birth defects; heart disease including heart failure; attention deficit disorder; brain cancer; autism; depression; Alzheimer’s disease; colitis; Lou Gehrig’s Disease (ALS); Parkinson’s Disease;  multiple sclerosis (MLS); liver disease; chronic respiratory disease; non-Hodgkin’s lymphoma; pregnancy problems including infertility, miscarriages, stillbirths; and extreme inflammatory bowel disease.

Doesn’t it make you wonder why Roundup and its main ingredient glyphosate hasn’t been sent to the showers and banned from the game years ago?

Doctors also knew that Roundup and its main ingredient glyphosate caused problems with peoples’ gut bacteria but recent studies have shown that this could be even more severe than previously thought.

Gut bacteria helps us digest food and helps keep dangerous bacteria from affecting us. This gut bacterium is what doctors say is part of the human microbiome that helps us digest what we eat, protects our immune systems and helps our brains function.

Now these microorganisms have been proven to be severely impaired by Roundup and its main ingredient, glyphosate.

Roundup is pricey and a host of other products available at your local hardware or garden center work just as well and are much safer.

Why put you, your family and friends in danger by using anything with glyphosate like Roundup?

Is using this stuff worth the risk?

http://bbaker.bangordailynews.com/2018/02/04/home/banned-from-the-game/

These Dogs Are Trained to Detect the Smell of Parkinson’s Just by Sniffing a Tee Shirt

 Feb 4, 2018

https://youtu.be/iNp-9IwSAIU

Parkinson’s disease is a debilitating neurodegenerative disorder that currently has no objectively approved screening method. Doctors are only able to make a diagnosis by interviewing the patient and examining their medical history – and this leaves plenty of room for error and inaccuracies.

A team of dogs on San Juan Island in Washington, however, could identify hundreds of Parkinson’s patients simply by using their noses.

The Parkinson’s Canine Detection Project is an initiative that trains 20 different pups to sniff out the disease on peoples’ shirts. The shirts – or “samples”, as they’re called – are sent to the initiative’s training center where the dogs are allowed to sniff the samples and determine whether they belong to a patient who is at risk for Parkinson’s.

The project’s volunteers found that by exposing the samples to multiple trained dogs for a consensus, the results were accurate—at the end of 2017 alone, the hounds sniffed out results that had a 90% accuracy of diagnosis.

The project was first started in 2016 when Joy Milne, a Scottish woman whose husband passed away from Parkinson’s six years ago, found that she was able to smell the disease on her husband before he was ever officially diagnosed.

Once Milne’s story was broadcasted by news outlets around the world, Lisa Holt, the program director of Parkinson’s Alert Dogs (PADS), got the idea to train canines to develop the same kind of ability.

“All dogs have the ability, but successful dogs usually display high drive for the work,” Holt told Good News Network. “There is one other program for training dogs to detect Parkinson’s Disease in the U.K. We are the only program in the United States.”

In a scientific study of Milne’s astonishing abilities, researchers found that she was best able to smell the disease’s “oily” odor around the neck and back regions of a tee shirt. She was also better at detecting the scent when the patient had been wearing a shirt made out of 100% cotton.

By replicating the methods used by Milne, Holt found that the PADs experienced similar results.

Being able to diagnose Parkinson’s disease in its early stages has a multitude of benefits. According to Holt, “a growing body of evidence from medical literature describes numerous advantages that may be associated with early therapeutic intervention”, such as reduced symptoms, delay of medication side effects, slowed disease progression, and decreased chance of developing a tolerance for the treatment.

While Holt and the PADS team continues to hone the accuracy and technique of the pups, they hope that the project’s development will result in an innovative new way of screening Parkinson’s patients – and eventually saving lives.

https://www.goodnewsnetwork.org/dogs-trained-detect-smell-parkinsons-just-sniffing-tee-shirt/

‘Next step’ for medical marijuana

By Diane Wagner, Staff Writer
February 3, 2018

Rep. Katie Dempsey, R- Rome

A coalition of Republican state representatives wants to let voters settle the stalemate on medical marijuana in Georgia.

Possession of low THC oil with a prescription has been legal since 2015, but it can’t be manufactured or bought in the state and it’s against federal law to bring it across state lines.

House Resolution 36 — sponsored by Rep. Alan Peake, R-Macon, and four other GOP leaders — would set up a statewide vote on regulating the production and sale of medical cannabis. Because it would be a constitutional amendment, it requires a two-thirds vote in each chamber of the Georgia General Assembly to make it on the ballot.

The measure is awaiting a hearing in the House Judiciary Non-Civil Committee.

Meanwhile, Peake, who chairs the Medical Cannabis Working Group, is also trying to move his House Bill 645, submitted at the close of last year’s session.

The measure would allow the Georgia Department of Public Health to license up to 10 medical marijuana dispensaries and two facilities to produce the low-THC oil.

‘Time is passing’

Rep. Katie Dempsey, R-Rome, is a member of Peake’s working group, which voted last month to support HB  645, but she wasn’t optimistic about its chances Friday.

“It’s got a ways to go,” she said.

Dempsey said the best solution for Georgia, and the 30 other states where medical marijuana is legal, is for Congress to step in and allow transportation across state lines. That would preclude the need for multiple regulated dispensaries and growing operations, and encourage more clinical trials, she said.

“I think there will be a great deal of discussion about it, but time is passing so fast,” Dempsey said. “We’re already halfway to Crossover Day … and some things just get caught in the crosshairs.”

Crossover Day, which is Feb. 28 this year, is the deadline for legislation to pass from one chamber to the other.

Rep. Eddie Lumsden, R-Armuchee, is a deputy whip — one of a cadre of representatives charged with rounding up votes for key legislation. He also said a change to federal law would be the best-case scenario but noted that there’s no sign on the horizon.

“This (HB 645) is the next step if we’re going to provide a way for those with a legitimate need to have access,” he said. “It’s the only solution I’ve heard that would accomplish that.”

Lumsden said Friday that he’s unaware of a concentrated push to pass either of Peake’s proposals, but he’s not counting them out.

“I don’t know what would happen in the Senate, but in the House we have been supportive of getting the oil to people with a legitimate need,” he said.

Floyd County businessman Harley Gambrell — whose autistic son is prescribed low THC oil but cannot legally acquire it — has called Georgia’s medical marijuana law “an empty promise” so far.

The General Assembly approved use of the oil in 2015 to treat eight conditions and, last year, added another six plus patients in hospice care. The oil does not get people high.

A state registry tracking prescriptions showed more than half went to patients controlling seizures or dealing with end-stage cancer, according to testimony in December by Donna Moore, director of the Georgia Public Health Vital Records Department that oversees the program.

Other conditions authorized for treatment under state law are severe or end-stage multiple sclerosis, peripheral neuropathy, Crohn’s disease, amyotrophic lateral sclerosis, mitochondrial disease, Parkinson’s disease, sickle cell disease, Tourette’s syndrome, autism, epidermolysis bullosa, Alzheimer’s disease and AIDS.

For a link to a previous story, click below:

Legalizing medical marijuana: An empty promise

http://www.northwestgeorgianews.com/rome/news/local/next-step-for-medical-marijuana/article_764fb13c-0931-11e8-9ce3-63af5b62209f.html

Israeli researcher discusses Alzheimer’s crisis at Palm Beach event

LIFESTYLE By John Nelander - Special to the Daily News
February 3, 2018

Itamar Kahn at The Chesterfield in Palm Beach. Photo by John Nelander

A researcher from an Israeli university offered fresh insight this week into medical conditions that threaten to overwhelm the health care industry over the next 30 years.

Itamar Kahn, an assistant professor at the Technion-Israel Institute of Technology, told a crowd of supporters Wednesday at The Chesterfield in Palm Beach that progress was being made in the search for a cure for brain disorders such as Alzheimer’s disease and Parkinson’s disease.

But he warned that predictions of a breakthrough in Alzheimer’s have proven premature.

“I remember an announcement that in 10 years Alzheimer’s would be gone,” said Kahn, director of the Brain Systems Organization in Health and Disease Lab at the Faculty of Medicine at Technion. “That was in 2002 – and it’s still here.”

New findings were reported in the journal JAMA Neurology earlier this week, linking disrupted sleep patterns and amyloid-beta protein in the brain to Alzheimer’s.

But a major hurdle, Kahn said, is that Alzheimer’s disease is likely not caused by just one thing. Although symptoms may be similar, there could be multiple triggers. Treatment that helps one person may not help another.

Projections are not encouraging. About 47 million people worldwide suffer from Alzheimer’s disease, and that’s expected to grow to 75 million by 2030 and 131.5 million in 2050, according to the Alzheimer’s Disease’s International’s World Alzheimer Report. The reason for the stunning growth rate is a rise in world population along with the fact that people are living longer.

“This is something that as a society we have to deal with,” Kahn said.

“When we look at people with symptoms, we want to find out if it’s all the same type or maybe something different,” he said in an interview. “It’s possible that some of the earlier clinical trials failed because we had a heterogenous population” – patients with similar symptoms caused by different problems.

“So, we have to improve the selection methods for clinical trials, and develop methods that will allow us to distinguish between the different sub-populations. It’s called precision medicine. We’re going to be more precise in our treatments.”

Technion was founded in Israel in 1912, long before the state was established. It originally focused on engineering, but in the 1960s they started doing medical research. Kahn’s expertise is in technology, and he uses new kinds of technology to study the brain.

For example, Technion helped develop and refine new MRI equipment that can analyze the functionality of a mouse’s brain. It shows ebbs and flows of oxygen levels, the key to communication within the brain.

“Our ability to look at the brains of mice with the same tools we have available for humans allows us to develop very sensitive diagnostic tests,” he said. “Then we can try therapies on these mice and use the results to leverage funding for clinical trials in people.”

The American Technion Society (ATS) has chapters throughout the United States that have helped support the Israeli facility with more than $2 billion in donations since 1940. Palm Beach chapter Co-President Sharon Pikus said she became involved because she was impressed with Technion’s level of research after a family member was diagnosed with a brain tumor.

“There’s nothing like it,” said Pikus, who lives in Palm Beach Gardens. The Technion facility in Haifa, Israel, is subject to bombing raids “and yet, they keep on trucking,” she added. “They’re so resilient.”

Some came to the evening program armed with specific medical questions, while others were interested in learning about Technion in general.

Resident Madeleine Singer said she shows up every time she hears about a Technion event.

“I think the people at Technion are some of the best innovators in the world,” she said. “The speakers are always fascinating.”

http://www.palmbeachdailynews.com/lifestyles/health/israeli-researcher-discusses-alzheimer-crisis-palm-beach-event/RSBZokGsyP1NsvqDETw98K/

Parkinson's disease symptoms improve with singing, study finds

By Lexy Hamilton-Smith
February 4, 2018

They say laughter is the best medicine, but singing is just as good, according to a group of people with Parkinson's disease who took part in an Australian first trial.

More than 70 patients from Queensland participated in the ground-breaking Griffith University study that looked at how song could help battle the disease.

Parkinson's disease is a neurological condition that affects speech and movement, and there is no cure.

Queensland Conservatorium Research Centre's Professor Don Stewart said it did not matter if they could hold a note or not, they just had to commit to "trying" to sing for an hour once a week for six months.

Professor Don Stewart found all participants experienced a better quality of life during the trial.

"But in particular one that stands out is stigma or perceived stigma for example where people felt they had to conceal their Parkinson's from others or avoid situations which involve eating or drinking in public," he said.

"They felt less worried about people's reaction to them. Felt less embarrassed," he said.

"We also got significant improvements in terms of mobility."

The group held their first Australian concert at the weekend at the Queensland Conservatorium.

Choir received encore for performance

As part of the performance, the group honoured Neil Diamond, who has just cancelled his 50th anniversary Australian shows in March and April due to a diagnosis of Parkinson's disease.

The choir got an encore and are planning to perform in public again.

Adrienne Lynch, 77, who lives in Toowoomba, was diagnosed three years ago.

While she admits to not being able to sing in tune, it has not stopped her trying," she said.

PHOTO: Participants in the study said singing helps take their minds off the condition and has improved their wellbeing.

It is also helping my voice be a bit stronger. And I have a really good feeling of well being."

First clinic trial of UK developed program 

In each session participants not only sang, but did vocal warm ups, breathing exercises and got to take part in social activities afterwards.

The study was based on a UK program called 'Sing to Beat Parkinson's' that had never been clinically tested.

"We set out using the Sing to Beat Parkinson's project to see if we could enhance the quality of life of people with Parkinson's as well as their carers," he said.

"To help reduce their emotional burden, depression, anxiety and stress."

The disease affects about 3 per cent of the Australian population, which is about 700,000 people.

It also strikes more men than women and more frequently presents in people over 50.

Researchers said the next step is to extend the program through Queensland, then the nation.

"It now has a platform to spread globally," said Professor Stewart.

UK Professor Grenville Hancox, who set up the first "Sing to Beat Parkinsons" group 10 years ago in England, has been involved in the Australian study.

He said the results were ground-breaking because they confirmed all the "anecdotal evidence" he collected, but had never been able to put under the scientific microscope.

Singing helped with depression, tremors: participants

Madonna Brady said it helped her battle depression associated with the disease.

"Feeling happy and having something to do. And the songs we have sung are pretty joyful and fun," she said.

Lilian Olszewski said the trial helped her focus on fun things rather than her Parkinson's, which she has battled for 10 years.

"It has also been good to share our stories about Parkinson's because there is no text book Parkinson's case," she said.

Ms Olszewski said the breathing exercises helped control her tremors as well.

While Tom Dawson, who was diagnosed in 2009, maintains the singing has made him feel less anxious. 

He also runs a support group through the choir.

"They are out there mixing with people now, where as before they would lock themselves away," he said.

Researchers from the US, Europe and Asia attended an international symposium in Brisbane where the results of the study were released.

http://www.abc.net.au/news/2018-02-04/parkinsons-singers-trial-australian-first/9394346