Hurricane

September 9, 2017

I am sorry but Hurricane Irma is going to hit all of Florida.

More than likely I will not be able to post the news for Parkinson's for a while.

I pray that everyone stays safe.

God Bless everyone

Brain chemical lost in Parkinson’s may contribute to its own demise

BY  LAURA SANDERS  SEPTEMBER 7, 2017

In a hopeful note, treating dopamine-producing nerve cells with antioxidants lessened damage

DOPAMINE DAMAGE  In Parkinson's disease, a dangerous form of the chemical messenger dopamine may help destroy the nerve cells that produce it, a new study suggests.

The brain chemical missing in Parkinson’s disease may have a hand in its own death. 

Dopamine, the neurotransmitter that helps keep body movements fluid, can kick off a toxic

 chain reaction that ultimately kills the nerve cells that make it, a new study suggests.

By studying lab dishes of human nerve cells, or neurons, derived from Parkinson’s patients,

 researchers found that a harmful form of dopamine can inflict damage on cells in multiple

 ways. The result, published online September 7 in Science, “brings multiple pieces of the 

puzzle together,” says neuroscientist Teresa Hastings of the University of Pittsburgh School 

of Medicine.

The finding also hints at a potential treatment for the estimated 10 million people worldwide 

with Parkinson’s: Less cellular damage occurred when some of the neurons were treated 

early on with antioxidants, molecules that can scoop up harmful chemicals inside cells.

Study coauthor Dimitri Krainc, a neurologist and neuroscientist at Northwestern University 

Feinberg School of Medicine in Chicago, and colleagues took skin biopsies from healthy 

people and people with one of two types of Parkinson’s disease, inherited or spontaneously 

arising. The researchers then coaxed these skin cells into becoming dopamine-producing 

neurons. These cells were similar to those found in the substantia nigra, the movement-

related region of the brain that degenerates in Parkinson’s.  

DARK MARK  Dark spots of neuromelanin (arrow) appear inside 90-day-old cells derived from a person carrying a Parkinson’s-related mutation. These deposits, visualized by electron microscopy, contain a damaging form of dopamine.

After neurons carrying a mutation that causes the inherited form of Parkinson’s had grown

in a dish for 70 days, the researchers noticed some worrisome changes in the cells’

mitochondria. Levels of a harmful form of dopamine known as oxidized dopamine began

rising in these energy-producing organelles, reaching high levels by day 150. Neurons

derived from people with the more common, sporadic form of Parkinson’s showed a

similar increase but later, beginning at day 150. Cells derived from healthy people didn’t

accumulate oxidized dopamine.

This dangerous form of dopamine seemed to kick off other types of cellular trouble.

Defects in the cells’ lysosomes, cellular cleanup machines, soon followed. So did the

accumulation of a protein called alpha-synuclein, which is known to play a big role in

Parkinson’s disease.

Those findings are “direct experimental evidence from human cells that the very chemical

lost in Parkinson’s disease contributes to its own demise,” says analytical neurochemist

Dominic Hare, of the University of Technology Sydney. Because these cells churn out

dopamine, they are more susceptible to dopamine’s potential destructive forces, he says.

When researchers treated neurons carrying a mutation that causes inherited Parkinson’s

with several different types of antioxidants, the damage was lessened. To work in people,

 antioxidants would need to cross the blood-brain barrier, a difficult task, and reach the

mitochondria in the brain. And this would need to happen early, probably even before

symptoms appear, Krainc says.

“Without this human model, we would not have been able to untangle the pathway,” Krainc

says. In dishes of mouse neurons with Parkinson’s-related mutations, dopamine didn’t kick

off the same toxic cascade, a difference that might be due to human neurons containing

more dopamine than mice neurons. Dopamine-producing neurons in mice and people

“have some very fundamental differences,” Krainc says. And those differences might help

explain why discoveries in mice haven’t translated to treatments for people with

Parkinson’s, he says.

Over the past few decades, scientists have been accumulating evidence that oxidized

 dopamine can contribute to Parkinson’s disease, Hastings says. Given that knowledge,

the new results are expected, she says, but still welcome confirmation of the idea.

These toxic cellular events occurred in lab dishes, not actual brains. “Cell cultures aren’t

the perfect re-creation of what’s going on in the human brain,” Hare cautions. But these

types of experiments are “the next best thing for monitoring the chemical changes” in

these neurons, he says.

https://www.sciencenews.org/article/brain-chemical-lost-parkinsons-may-contribute-its-own-demise

Parkinson’s disease: New drugs and treatments, but where are the doctors?

September 7, 2017

Parkinson’s disease responds well to a range of treatments, but more specialists are needed to know how to best tailor treatment for patients.

For many, hearing the word “Parkinson’s” conjures an image of tremors. But Parkinson’s disease, brought about by loss of nerve and other brain cells, is actually an incredibly complex movement disorder that can cause symptoms as wide-ranging as smell loss, thinking issues, depression and swallowing problems. More than 1.5 million people in the U.S. have the illness, and millions more loved ones and caregivers are affected by it, too.

Thanks to medical advances and better treatments, both patients and physicians understand that Parkinson’s is a livable disease, and that people with this condition can be happy, healthy and successful. 

And yet, there is a critical shortage of doctors trained specifically in how to treat Parkinson’s disease. Only 40 to 50 new Parkinson’s specialists – neurologists with fellowship training in the disease – go into practice each year across this country. And according to national doctor fellowship match data, this number has been relatively flat for the last five years. This shortage could worsen as the 70 million baby boomers age, as Parkinson’s typically afflicts older people; the average age of diagnosis is in the early 60’s. 

Recently I wrote an article which provides an update on current treatments of Parkinson’s disease for the Journal of the American Medical Association. A key takeaway of my new article is that there are many treatments for Parkinson’s, and some patients are going to live for 10, 20, 30, even 40 years with the disease.

Also, as national medical director of the National Parkinson Foundation, I have come to realize that there is a gap between how physicians manage Parkinson’s in clinics nationwide and what we actually know from evidence and from experience in treating this disease for many years. In particular, many generalists remain unaware of treatments beyond the standard use of medications that have been used since the 1970s, and there is a lack of appreciation for the importance of the timing of medication dosages. 

Updating approaches to Parkinson’s

We know from the scientific literature that patients who see even a general neurologist have lower rates of morbidity, mortality and nursing home placement. But given that the majority of Parkinson’s patients are under the care of general practitioners, internists and family medicine doctors, how do we help all of those who are affected by Parkinson’s?

Based on studies that show that people are living longer with Parkinson’s, one of the first messages we need to impart is that life is most certainly not over.

A second important message is that new medications can and do make a difference.

These findings underscore the necessity of having doctors trained in Parkinson’s.

Surgeons are vitally important, but doctors who specialize in Parkinson’s are becoming crucial as well. lenetstan/Shutterstock.com

For example, there is a myth that when you diagnose Parkinson’s, you prescribe a medicine called carbidopa-levodopa (also called Sinemet) three times a day, and that’s all.

But Parkinson’s is an incredibly complex disease with more than 20 motor and nonmotor features. The idea that dopamine, the main active ingredient in carbidopa-levodopa, is the only drug and the only treatment and there’s nothing more you can do – that’s a myth. This is something we must make sure to emphasize and educate doctors in training and those seeing these patients in practice.

Timing may not be everything, but it is important

In my JAMA article, I tried to lay a framework for the different phases a Parkinson’s patient may go through and the many types of treatments that are available today. We now know, for example, that in the early phase of Parkinson’s, specific exercises can be just as important, if not more important in some patients, than medications. Understanding the options and windows of opportunity can be the difference between success and failure.

Some medications for Parkinson’s disease need to be given at specific times each day. Billion Photos/Shutterstock.com

We also now know that the timing of medications is critical and in many cases needs to be exactly aligned to particular hours of the day. In addition, some patients see benefits by changing drug dose, adjusting medication intervals and possibly the addition of one of many other drugs. 

There are windows of opportunity for some patients where great benefit may result from surgical therapy. These include deep brain stimulation or the use of an externally worn pump that infuses a gel formation of a dopamine medication directly into the small intestine, which is a newer therapy approved by the FDA two years ago. But the physician must be aware of what those windows are, and who are the patients likely to experience benefit.

In other words, we must tailor the treatment to the patient.

What’s more, in Parkinson’s disease there is the possibility of an array of nonmovement-related symptoms, such as speech problems, hallucinations and depression. These nonmotor symptoms are commonly more disabling than the motor symptoms such as tremor or stiffness. Today, experts are involving social workers and counselors and also commonly using antidepressant and cognitive enhancers in their care.

As a field, we need to better understand that Parkinson’s patients have many choices of therapies and this is a compelling reason why special Parkinsons’ doctors are needed. When treated appropriately, we really can make this a livable condition. We need to educate more general practitioners and general neurologists on the basics of tailoring care for Parkinson’s disease, and we need to dedicate more money to training more Parkinson-specific neurologists.

There is more reason for hope for patients of Parkinson’s and their loved ones, and every Parkinson’s patient should have a tailored plan which will ensure success and a happy life. We need to make sure we have enough doctors specifically trained to meet the needs of a growing patient population.

Author- Michael Okun, Professor of Neurology, University of Florida

1. https://theconversation.com/parkinsons-disease-new-drugs-and-treatments-but-where-are-the-doctors-83334

Science Says: How repeated head blows affect the brain

September 7, 2017   by Lindsey Tanner

This combination of photos provided by Boston University shows sections from a normal brain, top, and from the brain of former University of Texas football player Greg Ploetz, bottom, in stage IV of chronic traumatic encephalopathy. According to a report released on Tuesday, July 25, 2017 by the Journal of the American Medical Association, research on 202 former football players found evidence of a brain disease linked to repeated head blows in nearly all of them, from athletes in the National Football League, college and even high school. (Dr. Ann McKee/BU via AP)

Researchers are tackling fresh questions about a degenerative brain disease now that it has been detected in the brains of nearly 200 football players after death. The suspected cause is repeated head blows, an almost unavoidable part of contact sports.

As a new NFL season gets underway, here's a look at what's known—and what still needs to be learned—about the condition:

WHAT'S NEW?

The largest report to date on chronic traumatic encephalopathy included 202 brains from football players at the youth, college and professional level, all donated post-mortem to a Boston brainbank. CTE was detected in all but one of the 111 NFL players studied, 90 percent of the college players and 20 percent of the high school players. It was absent in two younger players' brains.

A previous report had described the disease in an 18-year-old football player, but finding additional cases at the high school level raises new questions about the game's safety for young players.

HOW COMMON IS CTE?

The high occurrence of CTE in donated brains surprised researchers at Boston University and the VA Boston Healthcare System, whose brain bank is billed as the world's largest focusing on traumatic brain injury and CTE.

But whether CTE is truly common in sports or the general population isn't known. Most brains studied for CTE have been donated by family members because of concerns about mental symptoms that might be related to the disease—they don't come from a random population of people. Some experts think it isn't common since many athletes get repeated head blows and never develop symptoms.

WHAT CAUSES CTE?

Repeated knocks to the head are the most likely cause of CTE. Scientists believe genes probably play a role and may explain why some people with repeated head blows never develop the disease. Lifestyle habits including diet, alcohol and drugs may also somehow contribute.

HOW DO HEAD BLOWS AFFECT THE BRAIN?

Though the brain is jello-like in texture and cushioned in cerebrospinal fluid, a powerful hit—from a hard tackle, a fist or bomb shock wave—can cause a concussion, forcing the brain to ricochet back and forth inside the skull. Besides bruising and swelling, researchers believe that force can cause the brain to elongate, stretching nerve cells and their axons—fiber-like parts that transmit messages between cells. With a mild blow, these cells may return to normal, but a forceful hit may cause them to die.

Common symptoms after a concussion include dizziness, confusion, headaches, nausea and sometimes temporary loss of consciousness.

CTE has been linked with repeated concussions and some scientists believe it may occur after repeated head blows that don't cause any obvious symptoms. But they still don't know how many head hits is too many.

WHAT HAPPENS IN CTE?

The disease involves progressive brain damage, particularly in the frontal region, which controls many functions including judgment, emotion, impulse control, social behavior and memory. A signature feature is abnormal deposits of tau protein that accumulate around small blood vessels in brain crevices. Tau occurs normally in brain cells, helping them maintain their shape and function.

But researchers believe that multiple head blows may dislodge tau protein from the cell structure and cause it to form clumps inside nerve cells. These tau clumps can damage and ultimately kill nerve cells, and can spread as the disease progresses. At advanced stages, brain shrinkage may occur.

Abnormal tau deposits in different shapes, patterns and locations have been implicated in other brain diseases, including Alzheimer's Parkinson's disease and amyotrophic lateral sclerosis or ALS.

WHAT ARE THE SYMPTOMS?

Research suggests early stages of CTE may cause no obvious symptoms. Many players whose autopsies showed more advanced disease had experienced personality changes, aggressive behavior, paranoia, poor memory, attention problems, dementia and depression. Some died by suicide. Whether the tau changes associated with CTE cause those symptoms is unclear.

IS IT JUST A FOOTBALL DISEASE?

What's now called CTE was once thought to mainly affect boxers; the earliest known reference in the medical literature was a 1928 report by a New Jersey pathologist who referred to a "punch-drunk" syndrome.

The first published finding about CTE in a retired NFL player was a 2005 report on Pittsburgh Steelers Hall of Famer Mike Webster.

CTE also has been found in other contact sports including soccer, baseball and ice hockey; in soldiers exposed to bomb blast waves; domestic violence victims; and in psychiatric patients who engaged in repeated head-banging.

WHAT'S FOOTBALL'S RESPONSE?

Thousands of former players are due to get damage awards from a $1 billion settlement stemming from lawsuits claiming the league hid what it knew about a link between concussions and CTE.

Earlier this year the NFL hired a Vanderbilt University sports concussion expert, neurosurgeon Dr. Allen Sills, as its first full-time chief medical officer.

Injury risks are part of football, but the league is trying to make the game safer, Sills said.

New "no-go" criteria this season for when to keep injured players out of the game list confusion, amnesia and loss of consciousness after an on-field injury. Injured players will be evaluated in new portable sideline exam tents, for privacy and to reduce distractions for those with suspected concussions.

There also will be a ban on "leaper" block attempts, where a defender leaping over the offense to block a kick is tackled midair.

WHAT'S NEXT?

Researchers are seeking to refine brain scan techniques to identify CTE tau deposits in living brains. They're also looking for clues in blood or cerebrospinal fluid that would allow them to diagnose CTE before death. If such markers exist, they could be targets for drug treatment.

Symptoms associated with CTE can sometimes be managed with drugs or other treatment, but there's no cure and the only way to prevent it is to avoid head blows.

Studies are underway to identify if specific genes make certain athletes more vulnerable to brain damage from head blows, and researchers hope to pin down how many head blows it takes to develop CTE.

https://medicalxpress.com/news/2017-09-science-affect-brain.html

Treating with antioxidants early in Parkinson's disease process may halt degeneration and improve neuronal function

September 7, 2017

Northwestern Medicine scientists have identified a toxic cascade that leads to neuronal degeneration in patients with Parkinson's disease (PD) and figured out how to interrupt it, reports a study to be published September 7 in the journal Science.

Intervening with an antioxidant early in the disease process may break the degenerative cycle and improve neuron function in PD, the study showed.

The scientists also discovered that mouse models of PD didn't have the same abnormalities they found in human PD neurons, revealing the importance of studying human neurons to develop new therapies.

Dr. Dimitri Krainc, the Aaron Montgomery Ward Professor and chair of neurology at Northwestern University Feinberg School of Medicine, is the study senior author. Lena Burbulla, a postdoctoral fellow in Krainc's laboratory, is first author.

The research was started about six years ago in Krainc's lab at Massachusetts General Hospital and Harvard Medical School and was completed in the last four years at Feinberg.

PD is the second most common neurodegenerative disorder, primarily caused by the death of dopamine-containing neurons in the substantia nigra, a region of the brain involved in motor control. While people naturally lose dopamine neurons as they age, patients with PD lose a much larger number of these neurons and the remaining cells are no longer able to compensate.

Understanding how and why these neurons die is an important step in identifying treatments, Krainc said. While previous research indicated that the cellular mechanism behind the cell death involved the mitochondria and lysosomes, how these two pathways converge in dopamine neurons to cause cell death remained unknown up until now.

Using human neurons from Parkinson's patients, Krainc and colleagues identified a toxic cascade of mitochondrial and lysosomal dysfunction initiated by an accumulation of oxidized dopamine and a protein called alpha-synuclein. Specifically, the current study demonstrated that an accumulation of oxidized dopamine depressed the activity of lysosomal glucocerebrosidase (GCase), an enzyme implicated in PD. That depression in turn weakened overall lysosomal function and contributed to degeneration of neurons.

The accretion of oxidized dopamine didn't just interfere with lysosomes, however. Krainc and his colleagues discovered that the dopamine also damaged the neurons' mitochondria by increasing mitochondrial oxidant stress. These dysfunctional mitochondria led to increased oxidized dopamine levels, creating a vicious cycle.

"The mitochondrial and lysosomal pathways are two critical pathways in disease development," said Krainc, who also is the director of the Center for Rare Neurological Diseases and a professor of neurological surgery and of physiology. "Combined with the alpha-synuclein accumulation, this study links the major pathological features of PD."

Once they had catalogued this toxic cascade, Krainc and his colleagues began looking for ways to interrupt it.

"One of the key strategies that worked in our experiments is to treat dopamine neurons early in the toxic cascade with specific antioxidants that improve mitochondrial oxidant stress and lower oxidized dopamine," Krainc said. "With this approach, we found that we can attenuate or prevent the downstream toxic effects in human dopaminergic neurons."

This approach to interrupting the toxic cascade of oxidized dopamine may provide a target for the development of future therapies. However, identifying patients or subjects with early-stage neurodegeneration can be difficult, because damage has often occurred far before any symptoms are apparent, according to Krainc.

Consequently, genetic testing will be central to future diagnostic efforts. Causative genes are prime candidates for screening, while risk genes such as GBA1 are less conclusive but still important markers, Krainc said. Early detection will also rely on brain imaging and other clinical signifiers.

Interestingly, when compared to human cellular models, mouse models of PD did not demonstrate the same toxic cascade, according to the study. Krainc and his colleagues showed this is due to differences in metabolism of dopamine between species, and underscored the importance of studying human neurons to discover new targets for drug development.

More information: L.F. Burbulla el al., "Dopamine oxidation mediates mitochondrial and lysosomal dysfunction in Parkinson's disease," Science(2017). science.sciencemag.org/lookup/ … 1126/science.aam9080 

Journal reference: Science

Provided by: Northwestern University 

https://medicalxpress.com/news/2017-09-antioxidants-early-parkinson-disease-halt.html

Intermittent electrical brain stimulation improves memory

September 7, 2017

Intermittent electrical stimulation of an area deep inside the brain that degenerates in Alzheimer's appears to improve working memory, scientists report.Conversely, continuous deep brain stimulation, like the type used for Parkinson's and currently under study in humans with Alzheimer's, impairs memory, according to study results in adult non-human primates reported in the journal Current Biology. Credit: Phil Jones, Senior Photographer, Augusta University

Intermittent electrical stimulation of an area deep inside the brain that degenerates in Alzheimer's appears to improve working memory, scientists report.

Conversely, continuous deep brain stimulation, like the type used for Parkinson's and currently under study in humans with Alzheimer's, impairs memory, according to study results in adult non-human primates reported in the journal Current Biology.

With intermittent stimulation - currently not used in any application in the brain in patients - the monkeys were able to remember things up to five times longer in a standard test of working memory.

"That takes a monkey from being sort of a middle-of-the-pack performer to the top of the class," says Dr. David T. Blake, neuroscientist in the Department of Neurology at the Medical College of Georgia at Augusta University. "A monkey who is a poor performer becomes a middle-of-the-pack performer after two to three months of this stimulation."

In the new studies, scientists used the technique of placing hair-thin electrodes into the brain to deliver electricity and increase the activity of the nucleus basalis of Meynert, a small area in the forebrain that is inexplicably degenerated in both Parkinson's and Alzheimer's.

"The natural response of many brain systems to continuous input is to start to ignore the input," says Blake. In fact, constant stimulation in other areas like the globus pallidus garners desired clinical benefit like tremor reduction in Parkinson's disease.

"In the case of Parkinson's, deep brain stimulation is effectively downregulating that part of the brain," says Blake, the study's corresponding author. "What we wanted to do instead was to upregulate an area."

Their goals included making more of the chemical messenger acetylcholine available in the region. The nucleus basalis has a large concentration of neurons that are connected to brain areas critical for memory and cognition, and under healthy conditions have a ready supply of acetylcholine that enables the important communication between them.

As we age, acetylcholine levels in the brain naturally decrease, but Alzheimer's causes a dramatic multiplier effect that takes us from being forgetful to a different level, says Dr. Alvin V. Terry, chair of the MCG Department of Pharmacology and Toxicology and a study coauthor.

They started with continuous stimulation, like the clinical approaches, and saw an unexpected decline in performance. Equally surprising, they found intermittent stimulation resulted in more available acetylcholine in the region and better performance.

In fact, use of the cholinesterase inhibitor donepezil restored memory performance in animals that received constant stimulation but had no impact on those whose memory was already enhanced by intermittent stimulation.

"Normally neurons don't fire nonstop," Terry notes. "They are pulsing if you will."

Sixty pulses per second for 20 seconds followed by a 40-second interval without stimulation provided optimal benefit in the study.

The scientists suspect the benefit resulted from the impact of increased levels of acetylcholine directly on neurons and their supportive cells in that region. However it may also result from a slight increase in blood flow to the brain region, they write. Cholinesterase inhibitors, drugs used to treat Alzheimer's, are known to increase blood flow to the brain about 10-15 percent in humans. Blood flow is typically reduced in Alzheimer's.

The MCG team has submitted a grant proposal to start a clinical trial in early Alzheimer's using their new evidence of the benefits of intermittent pulsing. They note that a variety of brain regions and stimulation patterns are currently under study in clinical trials in the United States and Europe.

The adult but not aged monkeys in the current study were already part of an investigation to determine whether stimulation could improve the sense of touch, which also decreases with age. The scientists realized that with stimulation the monkeys were able to detect finger taps essentially 100 percent of the time versus about 60 percent of the time without it.

So they also used a classic working memory task in which a colored square cue shows up, then disappears, followed by a delay and then a choice between a cue-colored square and a distractor square. The monkeys get a food reward for making the cue match.

"There was every reason to think that we would find what we found if we could actually boost acetylcholine, and switching from continuous to intermittent stimulation was the step that was necessary to do that," Blake says.

In fact, after months of intermittent stimulation, the monkeys got more adept at the memory test even without the stimulation.

While that seems like more good news, the reason for the enduring effect is not 100 percent clear: it could be the brain cells make more connections, it could be more acetylcholine keeps getting released, it could be both, the scientists note.

"There are two main classes of effects that acetylcholine has in the central nervous system," Blake says. "It changes the way neurons talk to each other. It causes some neurons to become more active, some to become less active. The second class of effects is that it improves blood flow," he says. More blood means more of the energy source glucose and vital oxygen get to the brain, so it's not surprising that the brain becomes healthier over time with these increased assets, Blake says. "The idea is that it's going to have a longer-term effect," Terry adds.

Deep brain stimulation, which is comparable to a pacemaker for the heart, also is more selective than drugs, appearing to only stimulate acetylcholine in the targeted brain site. We have acetylcholine receptors all over our body and cholinesterase inhibitors make more of the chemical available bodywide, increasing the risk of side effects like nausea, loss of appetite, joint pain and muscle cramping.

In fact, responses to intermittent stimulation in the study were as strong as those experienced by patients taking high doses of cholinesterase inhibitors, the scientists report.

"The primary drugs that are used to treat Alzheimer's enhance this cholinergic function but they are nonspecific so they are causing all these peripheral side effects," Terry says. "This is a much more selective way of enhancing that region."

Deep brain stimulation basically supplements the normal brain processes that enable the release of acetylcholine, Blake says. The brain operates on a combined biochemical and electrical system that has electrical spikes running the length of an axon - long arms that reach from one neuron to another neuron or other cell type. Where two cells connect is called a synapse and the electrical spike results in the release of acetylcholine at the synapse, which impacts the cell it touches possibly activating it electrically or changing how it functions some other way. Electrical activation of a single neuron actually also activates other neurons in close proximity.

The success of implanted defibrillators/pacemakers and deep brain stimulation for Parkinson's has led to the exploration of its potential for problems like Alzheimer's. The Food and Drug Administration approved deep brain stimulation for Parkinson's and essential tremor in 1997.

Aging baby boomers, who began turning 65 in 2011, are drivers behind dramatic increases in those at risk for Alzheimer's and other age-related dementia. By 2050, the population age 65 and over is projected to reach 83.7 million, almost double the estimated population of 43.1 million in 2012, according to the U.S. Census Bureau.

Journal reference: Current Biology 

Provided by: Medical College of Georgia at Augusta University

https://medicalxpress.com/news/2017-09-intermittent-electrical-brain-memory.html

FWP's poisoning pristine streams is a bureaucratic betrayal of trust

• JACK D. JONES

Montana residents should be concerned with the tangent of Montana Fish, Wildlife and Parks to destroy more diversified wild fisheries in our streams, lakes and rivers to replace that producing resource with a hybrid hatchery-reared low survival sub-species they identify as the west-slope.

It was all originally spawned from the “experiment” in 2003 and 2004 to poison pristine Cherry Lake producing large Yellowstone cutthroat trout inside the Lee Metcalf Wilderness area and 77 miles of pristine diversified fishery in pristine waters of upper Cherry Creek, which flows into the Madison River. I fished both areas as a youngster and it was a fabulous wild fishery then. What has that early “boondoggle” produced after millions of fisheries dollars spent with contributions of Ted Turner -- there’s nothing there now and perhaps the brook trout returned hopefully?

As of today we still do not have a sustainable hybrid west-slope population available for sport fishing in any stream, lake or river where the same boondoggles have occurred; it is an ongoing fisheries failure producing no sport fishing now or for the future. This single hybrid subspecies, a hatchery-reared subspecies, will not survive in the diversified environments of Montana waters. Low survival and reintroduced in the same water over and over with little success. FWP is bent on a single subspecies, a mono-culture in a diversified environment. I have asked FWP to send the list of streams where this has been successful. No reply. Twin Lakes near Wisdom was a great brook trout fishery. What happened there, FWP?

During the Cherry Lake–Cherry Creek boondoggle, the U.S. Fish and Wildlife Service stated the west-slope does not qualify for threatened or endangered under the Endangered Species Act, true to this day. In the meantime Montana has lost diversified wild trout fisheries and many sport fishing opportunities especially for youngsters. Still available on YouTube is “Dead Wrong.” Please view it now! FWP is “dead wrong” to this day. FWP wants free reign to place rotenone and other toxic pesticides in pristine water classified in Montana as “outstanding resource water” and associated pristine habitat. These poisons are retained in wetlands for years.

In Montana the Yellowstone cutthroat, Montana’s state fish, is still classified as an S2 species and a higher rating than S3 for the hybrid west-slope. Rotenone is extremely toxic pesticide especially in flowing water and the Nature Neuroscience journal reported Parkinson’s disease results from toxins in the environment from the use of this pesticide. FWP states little concern -- they will use it anyway for the “experiment.” FWP will not mention the impacts to avian species, mammals, invertebrate as the sculpin and, of course, the human risk which they have no data on for the area before poisoning. “Poison and see what happens.” Is that science?

FWP has lost its way today. What was once a fisheries management and game management agency no longer exists, with its all “environmental experiments” and nonsense. However, FWP receives most all its funding -- 75 percent -- from those who buy fishing and hunting licenses and equipment under the Pittman-Robertson Wildlife Restoration and Dingell-Johnson Sport Fish Restoration acts. Sportsmen are funding FWP to destroy the very resource that provides sport fishing now and for the future.

What is so evil about managing our Montana fishery resource in place and working? Perhaps FWP personnel should be working for some environmental organization. No Endangered Species Act dollars available since the hybrid west-slope doesn’t qualify under the ESA for federal money, but FWP using sportsmen dollars today is a “betrayal of the trust.’’ FWP wants the sportsmen money used for more “experiments,’’ studies and personnel which overrides the existing resource.

When you buy a fishing license and fishing equipment, you could be paying for poisoning and introducing a hybrid sub-species that will never survive or provide fishing opportunity -- a bureaucratic betrayal of the public trust. FWP is due for a complete overhaul.

-- Jack D. Jones, Butte, worked as a wildlife biologist in Montana for 36 years with the Bureau of Land Management.

http://mtstandard.com/opinion/editorial/fwp-s-poisoning-pristine-streams-is-a-bureaucratic-betrayal-of/article_256b7aa2-8583-5dc4-b79e-7edb147c3c16.html

Elton John, Steven Tyler among stars performing at 2017 Celebrity Fight Night in Italy charity events

September 7, 2017

ABC/Randy Holmes; Zack WhitfordElton John, Aerosmith's Steven Tyler and The Eagles' Joe Walsh are among the many stars who will perform during the fourth annual Celebrity Fight Night in Italy, a seven-day vacation experience and charity fundraiser in Rome that got underway Tuesday.

The seven-day event, which will raise money for the Andrea Bocelli Foundation and the Muhammad Ali Parkinson Center, features star-studded concerts, along with gourmet dinners, parties and other activities.

John and Tyler will perform at a concert Friday at Rome's historic Colosseum. The show's lineup also includes Andrea Bocelli, pop composer David Foster, pop-jazz trumpet player Chris Botti [BOE-tee], 2Cellos and others.

Walsh will participate in a show that's part of the finale of this year's Celebrity Fight Night in Italy: an all-white gala taking place on Sunday at the Cinecittà [chee-nay-chee-TAH] film studio. The venue will be transformed to make attendees feel like they are in ancient Rome.

That concert also will feature performances by Bocelli, Foster, Motown legend Smokey Robinson, R&B singer Brian McKnight, Broadway and screen star Kristen Chenowith and country acts Reba McEntire, Brooks & Dunn and The Band Perry, among others.

The Muhammad Ali Parkinson Center in Phoenix, AZ, provides medicine and treatment for people stricken with Parkinson's disease.  The Andrea Bocelli Foundation supports Italian-based national and international programs that aid people in need because of illness, poverty and other issues.

Visit CelebrityFightNight.org/Italy for more information.

http://www.wjbdradio.com/music-news/2017/09/06/elton-john-steven-tyler-among-stars-performing-at-2017-celebrity-fight-night-in-italy-charity-events