First Clinical Data of Therapeutic Parkinson's Disease Vaccine Encourages Continued Development

NEW YORK and VIENNA, July 31, 2014 /PRNewswire/ --

AFFiRiS AG announced today at a press conference in New York results of AFF008, a Phase I clinical trial of PD01A, a vaccine against Parkinson's disease. PD01A is the first therapy against the protein alpha-synuclein, a promising Parkinson's drug target, to enter clinical testing.

The Michael J. Fox Foundation for Parkinson's Research (MJFF) supported the study with a $ 1.5 million grant, and presented at the press conference on the impact a disease-modifying therapy would have for patients. The Foundation will support a follow-up study testing a boost vaccination, the next step toward a Phase II trial.

"A treatment that could slow or stop Parkinson's progression would be a game changer for the five million worldwide living with this disease and the many more who will become at risk as our population ages", said MJFF CEO Todd Sherer, PhD. "The AFF008 trial is one of the most promising efforts toward that goal, and we're proud to support this work of AFFiRiS AG."  

In this study, two different doses of PD01A were safe and well tolerated, meeting the primary endpoint of the trial. Secondary endpoints of the study included the induction of an alpha-synuclein-specific antibody response. A hallmark pathology of Parkinson's disease is aggregates of protein - chiefly alpha-synuclein - called Lewy bodies that accummulate in brain cells, leading to cell degeneration and cell death. Researchers hypothesize that reducing alpha-synuclein accumulation will be neuroprotective; AFFiRiS is using active immunotherapy to test that theory and develop a disease-modifying treatment.

PD01A was applied at two different doses (15 µg and 75 µg) to 12 patients per group. All received four vaccinations in monthly intervals, and all completed the study. Eight patients on best medical care, including standard symptomatic medication, served as a control group. Each patient was regularly seen and evaluated during a 12-month period.

Fifty percent of the vaccinated patients generated alpha-synuclein-specific antibodies as measured in serum samples. Additionally, vaccine-induced antibodies were detectable in cerebrospinal fluid. This induction of antibodies against alpha-synuclein is strong preliminary evidence in support of the principle of AFFiRiS' proprietary therapeutic vaccine.

Furthermore, analysis of clinical endpoints revealed a trend, consistent over all parameters, towards functional stabilization of the vaccinated groups as compared to non-vaccinated control patients. The pharmacodynamic profile of PD01A and its clinical effects will be the basis of later phase studies, should development continue.

"The safety and tolerability observed in this study, especially in a protein such as alpha-synuclein where we do not yet know its normal function, are encouraging," said Walter Schmidt, PhD, Co-founder and CEO of AFFiRiS AG. "We are grateful for the continued support of The Michael J. Fox Foundation as we progress in clinical development."

The next study will take place in Vienna, Austria and focus on assessing the immunological and clinical effects of a boost vaccination. Recruitment is expected to begin September.

A recording of the press conference will be made available at http://totalwebcasting.com/view/?id=affiris

Photographs from the press conference are available for download immediately after the event at http://imgur.com/a/EwZUK

Further pictures are available at http://www.affiris.com/html/de/presse_medien/bildmaterial_logos.php

Disclaimer:

This press release contains forward-looking statements and should not be used for investment decisions.

About AFFiRiS AG (By: May 2014) 

Based on its proprietary IP positions AFFiRiS develops tailor-made drugs mainly as Peptide-based vaccines. Target diseases include Alzheimer, Parkinson, Diabetes and other indications with attractive markets and unmet medical need. Alzheimer is the lead indication. Current investors are: MIG-Fonds and Athos Service GmbH, both Munich, Germany. AFFiRiS is located at the campus of the Vienna Biocenter, Vienna Austria and employs 95 highly qualified employees. http://www.affiris.com

About The Michael J. Fox Foundation for Parkinson's Research 

As the world's largest nonprofit funder of Parkinson's research, The Michael J. Fox Foundation is dedicated to accelerating a cure for Parkinson's disease and improved therapies for those living with the condition today. The Foundation pursues its goals through an aggressively funded, highly targeted research program coupled with active global engagement of scientists, Parkinson's patients, business leaders, clinical trial participants, donors and volunteers. In addition to funding more than $ 450 million in research to date, the Foundation has fundamentally altered the trajectory of progress toward a cure. Operating at the hub of worldwide Parkinson's research, the Foundation forges groundbreaking collaborations with industry leaders, academic scientists and government research funders; increases the flow of participants into Parkinson's disease clinical trials with its online tool, Fox Trial Finder; promotes Parkinson's awareness through high-profile advocacy, events and outreach; and coordinates the grassroots involvement of thousands of Team Fox members around the world.

http://www.michaeljfox.org

Contact AFFiRiS AG:
Mag. Julia Bock
Karl-Farkas-Gasse 22
1030 Vienna, Austria
T +43/(0)1/798-15-75-303
E julia.bock@affiris.com
W http://www.affiris.com

Distribution:
PR&D - Public Relations for Research & Education
Mariannengasse 8
1090 Vienna, Austria
T +43/(0)1/505-70-44
E contact@prd.at
W http://www.prd.at

SOURCE AFFiRiS AG

Scripps Florida Scientists Make Diseased Cells Synthesize Their Own Drug

JUPITER, FL, September 2, 2014 – In a new study that could ultimately lead to many new medicines, scientists from the Florida campus of The Scripps Research Institute (TSRI) have adapted a chemical approach to turn diseased cells into unique manufacturing sites for molecules that can treat a form of muscular dystrophy.

“We’re using a cell as a reaction vessel and a disease-causing defect as a catalyst to synthesize a treatment in a diseased cell,” said TSRI Professor Matthew Disney.  “Because the treatment is synthesized only in diseased cells, the compounds could provide highly specific therapeutics that only act when a disease is present. This means we can potentially treat a host of conditions in a very selective and precise manner in totally unprecedented ways.”

The promising research was published recently in the international chemistry journal Angewandte Chemie.

Targeting RNA Repeats

In general, small, low molecular weight compounds can pass the blood-brain barrier, while larger, higher weight compounds tend to be more potent. In the new study, however, small molecules became powerful inhibitors when they bound to targets in cells expressing an RNA defect, such as those found in myotonic dystrophy.

Myotonic dystrophy type 2, a relatively mild and uncommon form of the progressive muscle weakening disease, is caused by a type of RNA defect known as a “tetranucleotide repeat,” in which a series of four nucleotides is repeated more times than normal in an individual’s genetic code. In this case, a cytosine-cytosine-uracil-guanine (CCUG) repeat binds to the protein MBNL1, rendering it inactive and resulting in RNA splicing abnormalities that, in turn, results in the disease.

In the study, a pair of small molecule “modules” the scientists developed binds to adjacent parts of the defect in a living cell, bringing these groups close together. Under these conditions, the adjacent parts reach out to one another and, as Disney describes it, permanently hold hands. Once that connection is made, the small molecule binds tightly to the defect, potently reversing disease defects on a molecular level.

“When these compounds assemble in the cell, they are 1,000 times more potent than the small molecule itself and 100 times more potent than our most active lead compound,” said Research Associate Suzanne Rzuczek, the first author of the study. “This is the first time this has been validated in live cells.”

Click Chemistry Construction

The basic process used by Disney and his colleagues is known as “click chemistry”—a process invented by Nobel laureate K. Barry Sharpless, a chemist at TSRI, to quickly produce substances by attaching small units or modules together in much the same way this occurs naturally.

“In my opinion, this is one unique and a nearly ideal application of the process Sharpless and his colleagues first developed,” Disney said.

Given the predictability of the process and the nearly endless combinations, translating such an approach to cellular systems could be enormously productive, Disney said. RNAs make ideal targets because they are modular, just like the compounds for which they provide a molecular template.

Not only that, he added, but many similar RNAs cause a host of incurable diseases such as ALS (Lou Gehrig’s Disease), Huntington’s disease and more than 20 others for which there are no known cures, making this approach a potential route to develop lead therapeutics to this large class of debilitating diseases.

In addition to Rzuczek and Disney, the other author of the study, “A Toxic RNA Catalyzes the In Cellulo Synthesis of Its Own Inhibitor,” is HaJeung Park of TSRI. For more information on the study, seehttp://onlinelibrary.wiley.com/doi/10.1002/anie.201406465/abstract

The work was supported by the Muscular Dystrophy Foundation, the Myotonic Dystrophy Foundation and the State of Florida.

About The Scripps Research Institute

The Scripps Research Institute (TSRI) is one of the world's largest independent, not-for-profit organizations focusing on research in the biomedical sciences. TSRI is internationally recognized for its contributions to science and health, including its role in laying the foundation for new treatments for cancer, rheumatoid arthritis, hemophilia, and other diseases. An institution that evolved from the Scripps Metabolic Clinic founded by philanthropist Ellen Browning Scripps in 1924, the institute now employs about 3,000 people on its campuses in La Jolla, CA, and Jupiter, FL, where its renowned scientists—including three Nobel laureates—work toward their next discoveries. The institute's graduate program, which awards PhD degrees in biology and chemistry, ranks among the top ten of its kind in the nation. For more information, see www.scripps.edu.

So What's the Between ALS and Parkinson's Disease?

 

Clockwise from top left: Robin Williams had been diagnosed with Parkinson’s before his death; Stephen Hawking has been living with ALS for 50 years; Lou Gehrig brought ALS, now also know as Lou Gehrig’s disease, to the public’s attention; and Michael J. Fox received his Parkinson’s diagnosis in 1992. (Photos: Getty Images)

News that Robin Williams had been grappling with a diagnosis of Parkinson’s disease before ending his life has sparked increased interest in the disorder this week. And that’s coincided with a fast-rising awareness of a similar disease — amyotrophic lateral sclerosis, or ALS — due to the Ice Bucket Challenge, a fundraising campaign that’s swept social media recently, prompting everyone from Ethel Kennedy to Justin Timberlake to dump freezing water over their heads in the name of research. (And it’s worked, raising millions for the cause.) So how closely linked to Parkinson’s is ALS? Both are progressive neurodegenerative diseases, and neither has a cure. But beyond that, the differences are vast.

“Both occur because some cells in the brain degenerate, and both are diseases of the motor system, meaning they affect how someone moves,” Dr. U. Shivraj Sohur, a movement disorder specialist with the MassGeneral Institute for Neurodegenerative Disease, told Yahoo Health. “From there, the separation happens quickly, both from a neurology point of view and from a patient’s experience.”

Related: Robin Williams: Is Parkinson’s Disease Linked to Suicide?

While ALS is currently getting perhaps its biggest publicity boost since baseball player Lou Gehrig’s suffering made it part of the public lexicon in 1939, Parkinson’s has consistently been in the sphere of public knowledge. And much of that, Sohur said, is due to “sheer numbers.” Currently, an estimated 30,000 Americans are living with ALS and about 5,600 are diagnosed each year. Meanwhile, the number of those living with Parkinson’s is closer to 1 million, which translates to about 60,000 diagnoses a year. Funding for each disease tends to reflect those numbers — according to the National Institutes of Health, ALS public funding in 2013 totaled $39 million, while public funds for Parkinson’s hit $135 million.

Related: #IceBucketChallenge Goes Big on Social Media

“Awareness is an important thing,” Jim Beck, PhD, vice president of scientific affairs for the Parkinson’s Disease Foundation, told Yahoo Health, “as is scientific research.” He stressed that breakthroughs for either could very well inform the other, as well as myriad other neurological disorders, and added, “You never know where it could lead.” To that end, we’ve broken down the details on both diseases:

ALS (Lou Gehrig’s disease)

What it is: The progressive disease results from a degeneration of motor neurons until those neurons die off, Sohur explained. “Two groups are affected — a group of cells on top of the brain, on the cortex,” he said, “and those within the spinal cord.” Amyotrophic comes from Greek, the ALS Association explains on its website, with “A” meaning no or negative, “myo” referring to muscle, and “trophic” meaning nourishment, so “No muscle nourishment.” When a muscle has no nourishment, it atrophies, or wastes away.

Who gets it: ALS can strike anyone between the ages of 40 and 70. It’s 20 percent more common in men than in women, and, though typically not genetic, can be hereditary in about 10 percent of cases.

History: ALS was first discovered in 1869 by the French neurologist Jean-Martin Charcot, but Lou Gehrig, through his own diagnosis, first brought national and international attention to the disease (as well as an alternative name) in 1939.

Symptoms: Early clues can include increasing muscle weakness, particularly in one’s limbs, that can also affect speech, swallowing or breathing. “It’s initially difficult to recognize,” noted Sohur. “Usually muscles will jump and there will be weakness in one muscle at a time, all while a person is in generally good health.” Because the disease progresses quickly, though, diagnosis gets easier, he said. As muscles stop functioning, they begin to atrophy, and patients in the later stages of the disease may become completely paralyzed, while affected muscle regions harden — the aspect known as “sclerosis.”

Treatments: While nothing can stop or reverse the effects of ALS, there is a single FDA-approved drug, Riluzole, that slightly slows its progression; several other drugs in clinical trials are promising, according to the ALS Foundation.

Prognosis: “An ALS diagnosis is a death sentence,” said Beck. The average life expectancy from time of diagnosis is just two to five years. However, he added, “It’s a complicated disease, meaning the way it presents itself is always different.” More than half of all patients live more than three years after diagnosis, while ten percent will live for more than 10 years and 5 percent more than 20. Physicist Stephen Hawking, who has lived with the disease for nearly 50 years now, represents an exceptionally rare case.  

Parkinson’s disease

What it is: Parkinson’s is caused by the malfunction and death of neurons in an area of the brain called the basal ganglia and, within that, the “substantia nigra,” Sohur said. Some of the dying neurons produce dopamine, a chemical that sends messages to the part of the brain that controls movement and coordination.

Who gets it: The average age of onset is 60. Still, while incidence of the disease increases with age, an estimated 4 percent of people with Parkinson’s are diagnosed before the age of 50. Men are one and a half times more susceptible than women.

History: While the condition has been known about since ancient times, London doctor James Parkinson was the first to formally describe it in a detailed medical essay, in 1817.

Symptoms: While very early signs can include sleep disorders and the loss of one’s sense of smell, the most common collection of primary symptoms is something Sohur refers to with the acronym TRAP: tremor (involuntary trembling of a limb or limbs); rigidity (muscle stiffness); akinesia (slowness or difficulty when moving); and postural instability (trouble with balance or walking). Other signs may include shrinking handwriting and a masklike expression.

Treatments: There are many medications available to treat Parkinson’s symptoms, though none reverse the disease. Some people respond to an option called deep brain stimulation surgery, which involves electrodes being inserted into the brain, while a device called an impulse generator (similar to a pacemaker) is implanted under the collarbone to provide an electrical impulse to the brain’s motor function region. 

Prognosis: “People don’t die of Parkinson’s; they die of complications from Parkinson’s disease,” said Sohur. And, like ALS, its presentation and progression vary from person to person. “I always say, if you’ve met one person with Parkinson’s, you’ve met one person with Parkinson’s,” Beck said. “Their journey is often as unique as their own lives.”

Beth GreenfieldSenior WriterAugust 15, 2014

PARKINSON’S DISEASE – NOT ONE, BUT MANY

A pair of clinical researchers from the Department of Clinical Neurosciences and Mental Health, Faculty of Medicine at the University of Porto, in Porto, Portugal have written a scholarly article that refines and defines how the varying symptoms presented by people with PARKINSON’S DISEASE can be assessed and understood.  They make a convincing argument that a “leap in concepts and a shift in research” is needed to enable therapeutic advances toward early treatment with specific neuroprotective agents for each unique presentation of symptoms.

In the past, PARKINSON’S DISEASE was thought to be caused by a loss of dopaminergic neurons in the substantia nigra.  Positive diagnosis was delayed until motor symptoms were obvious and depended on the patient’s response to the ‘gold standard’, that is if the patient’s symptoms responded to levodopa.  Positive response meant a diagnosis of PARKINSON’S, no response meant PARKINSONISM.  Although patients had positive motor improvement responses to dopamine replacement, the results were only temporarily palliative; progression of the disease and the development of non-motor symptoms could not be halted.  Many non-motor symptoms such as Rapid Eye Movement Sleep Disorder, loss of sense of smell, cognitive changes and mood problems may be present years before the motor symptoms present, and they involve neurological systems other than the dopamine system of the substantia nigra.  These non-motor symptoms may well be precursors to the disease process, and appropriate treatments for them could delay or even halt the development of the motor symptoms.

Studies of the genetics of PARKINSON’S DISEASE have found only a few examples of heritable forms of the disease.  But studies of those same genes have yielded further information of the specific roles each of those genes play in modifying or affecting various cellular processes that occur in the development of the disease.  The alpha-synuclein gene (SNCA) when mutated, causes aggregations of alpha-synuclein but also has interactions with the PARK genes, with the LRRK2 or the GBA genes. The results of those various and individual interactions contribute significant differences in their presentation in the clinical and neuropathological features of the disease.

Post mortem examinations have shown that patients whose motor symptoms presented early and who had a good response to levodopa but then had a more rapid decline, including dementias, had mutations in the SNCA genes.  Patients who had a slower progression of motor symptoms but had more dystonia or tremors usually carried LRRK2 mutations. GBA mutations were found in brains of patients who had early onset with both sides of the body equally affected and also more pronounced neuropsychiatric issues, such as symptoms often being found in Alzheimer’s disease patients. Another unique mutation in the VPS35 gene causes motor complications that get a significant benefit from dopamine replacement and no diminishment of cognitive function.  PARK2 carriers had a slower progression of symptoms and responded well to dopamine replacement, but frequently were prone to develop dyskinesias. Dementia was rare in these cases and synucleinopathy was not found in post mortem examinations; however, much deterioration of the substantia nigra was seen.

The above descriptions show that many share multiple symptoms with PARKINSON’S DISEASE, but also demonstrate many differences in clinical presentation, imaging and other neuropathological features.  While they may share a common response to dopamine replacement, they may, indeed, be manifestations of other similar but different diseases.  There currently are no reliable biomarkers that can accurately predict the onset of the disease or distinguish one form from another, or even monitor its progression.  Given the differing symptom presentations, genetics and pathological findings, it is likely that PARKINSON’S DISEASE is not a single disease, but an umbrella that covers multiple, but similar diseases.

Monteiro, A., Massano, J. Parkinson’s disease cluster:  the wind of change; Open Access Publication http://ijcnhmh.arc-publishing.org ; 24 March 2014

Researchers find roving detection system for treating cancer, Parkinson's disease and ALS

Published on August 26, 2014 at 5:52 AM · 

Duke University researchers have found a "roving detection system" on the surface of cells that may point to new ways of treating diseases like cancer, Parkinson's disease and amyotrophic lateral sclerosis (ALS).

The cells, which were studied in nematode worms, are able to break through normal tissue boundaries and burrow into other tissues and organs -- a crucial step in many normal developmental processes, ranging from embryonic development and wound-healing to the formation of new blood vessels.
But sometimes the process goes awry. Such is the case with metastatic cancer, in which cancer cells spread unchecked from where they originated and form tumors in other parts of the body.
"Cell invasion is one of the most clinically relevant yet least understood aspects of cancer progression," said David Sherwood, an associate professor of biology at Duke.
Sherwood is leading a team that is investigating the molecular mechanisms that control cell invasion in both normal development and cancer, using a one-millimeter worm known as C. elegans.
At one point in C. elegans development, a specialized cell called the anchor cell breaches the dense, sheet-like membrane that separate the worm's uterus from its vulva, opening up the worm's reproductive tract.
Anchor cells can't see, so they need some kind of signal to tell them where to break through. In a 2009 study, Sherwood and colleagues discovered that an extracellular cue called netrin orients the anchor cell so that it invades in the right direction.
In a new study appearing Aug. 25 in the Journal of Cell Biology, the team shows how receptors on the invasive cells essentially rove around the cell membrane "hunting" for the missing netrin signal that will guide the cell to the correct location.
The researchers used a video camera attached to a powerful microscope to take time-lapse movies of the slow movement of the C. elegans anchor cell during its invasion.
Their time-lapse analyses reveal that when netrin production is blocked, netrin receptors on the surface of the anchor cell periodically cluster, disperse and reassemble in a different region of the cell membrane. The receptors cluster alongside patches of actin filaments -- thin flexible fibers that help cells change shape and form invasive protrusions -- that pop up in each new spot.

Rather than the whole cell having to move around, its receptors move around on the outside of the cell until they get a signal. Once the receptors locate the netrin signal, they stabilize in the region of the cell membrane that is closest to the source of the signal."It's kind of like a missile detection system," Sherwood said.
The findings redefine decades-old ideas about how the cell's navigation system works. "Cells don't just passively respond to the netrin signal -- they're actively searching for it," Sherwood said.
Given that netrin has been found to promote cell invasion in some of the most lethal cancers, the findings could lead to new treatment strategies. Disrupting the cell's netrin detection system, for example, could prevent cancer cells from finding their way to the bloodstream or the lymphatic system and stop them from metastasizing, or becoming invasive and spreading throughout the body.
"One of the things we're gearing up to do next are drug screens with our collaborators to see if we can block this detection system during invasion," Sherwood said.
Scientists have also known for years that netrin plays a key role in wiring the brain and nervous system by guiding developing nerve cells as they grow and form connections.
This means the results could also point to new ways of treating neurological disorders like Parkinson's and ALS and recovering from spinal cord injuries.
Tinkering with the cell's netrin detection machinery, for example, may make it possible to encourage damaged cells in the central nervous system -- which normally have limited ability to regenerate -- to regrow.

Partners in Parkinson's

When asked to be an ambassador for a new health initiative co-sponsored by the Michael J. Fox Foundation (MJFF) and Abbvie — I jumped at the opportunity to be part of this groundbreaking effort, which promises to provide new educational tools and resources to help ensure optimal care for patients at every stage in PD progression.

Success is dependent on patients making greater use of Movement Disorders Specialists (MDS) — neurologists with advanced training in PD and up to date knowledge of cutting edge PD treatments and clinical trials. Currently, less than one-third of those diagnosed with PD see a MDS, meaning the majority likely are not receiving the best care available to them.

Explore the new “Partners in Parkinson’s” web site (http://www.partnersinparkinsons.org) to find new tools to help you locate a MDS near your home and empower you in the overall treatment process. Register to receive ongoing updates, information on events (including clinical trials) in your area, and access to new tools and resources as they become available.

Those who have long advocated for patients to have a seat and a voice at the table where decisions are made about our healthcare needs, should appreciate that this initiative is patient-centered, designed with patient input to benefit patients. Grab a seat before the music stops.

Once again, MJFF has stepped up to the plate and shown its willingness and ability to lead in research and beyond. As patients and care partners we must publicly recognize this and continue to urge all the national orgs to combine into one community working towards one common set of goals.

Small but mighty, the Parkinson’s community is bound together by a common thread — a progressive, incurable “designer disease” that affects no two of us the exact same way. Sidelined way too young, and feeling marginalized, many of us seek opportunities that will allow us to apply our experience, skills, and knowledge to leave the Parkinson’s community a better place than we found it.Partners in Parkinson’s may just be our best opportunity yet.

15 Mental Tricks That Fight Pain

What Is Pain?

Pain is a characteristically complex issue, involving both the emotional centers of the brain and the nociceptors of the body. When the body undergoes trauma, an external stimulus is relayed from the nociceptors (or pain receptors), to the nervous system. The brain’s limbic system then adds an additional component to the pain, making it emotional in nature-this is why pain is so bothersome. It is interesting to note that when certain emotional brain structures are removed surgically, chronic pain patients report feeling the pain, but are no longer perturbed by it at an emotional level.

Pain is a multidimensional issue that can impair one’s mood, psychological state, decision making, relationships and productivity. It is projected that millions of Americans suffer from chronic pain, and rely extensively on anti-inflammatory medications in order to mitigate these symptoms.  However, the human body can develop a considerable tolerance for pain meds over time, and consistent ingestion of heavy pain med doses can exact a toll on the liver functions of the body.

Mental Tricks

In recent years, the masses have become more acquainted with the mind’s infinite capabilities and its ability to govern the body. People who suffer from temporary or chronic pain can utilize mental techniques to mollify some of their agonizing symptoms. In scientific studies, patients who suffered from severe injuries mentally envisioned increased blood flow to the site of injury, and ended up expediting the healing process. This is a prime example of what the human body is truly capable of.

Using the following metal tricks, you can experience temporary relief from your pain.

#1 Did you know that fantasizing about food can stimulate the production of pain fighting chemicals in the body? In a University of Wisconsin study, students were instructed to place their hands in a bowl of icy water. Then, they were advised to envision delectable foods, such as brownies or ice cream. This vivid mental imagery actually  reduced their pain levels and detracted from the discomfort associated with the freezing water temperatures.

#2 Meditation is among the most potently effective pain mitigation techniques available.Meditation calms the body, and reorganizes the brain, providing it with a more positive, rational outlook. Mindfulness meditation, for instance, is a technique that utilizes breathing control. In a study, this form of meditation was believed to lower the intensity of pain from 11% to 70%, and eliminate the emotional aspect of pain by 20%-93%.

#3 Deep breathing exercises can elicit a parasympathetic response, which counters the response induced by a pain stimulus. Deep breaths centered in the diaphragm can have a calming effect on the body’s pain processing, offering one a temporary relief.

#4 Pain has a variety of useful survival functions, and contributes to our general safety and well being. But when pain is both unremitting and unbearable, a good distraction may serve you well. Consider allocating your attention to something else when your pain arises. For example, you may choose to direct your attention to other body parts, or to simply engage in your favorite activity. The more positive a distraction is, the better you will feel. However, a negative emotional distraction will merely exacerbate your pain.

#5 Mantras have an intrinsically powerful effect on the human body. They have the capacity to stimulate the production of your own organically produced morphine and pain fighting chemicals. A mantra refers to a repetitive word, phrase, or prayer that you repeat. This practice can dilute the intensity of your pain.

#6 Positive visualization is one of the powerful mechanisms of the human mind. Did you know that the brain contains a topographic map of the entire body? This means that your brain is intimately tied to every facet of your anatomical being. One simple technique entails imagining peaceful images, such as that of a sunset or a waterfall. You may also consider envisioning the site of your pain as fully functioning and pain free. For example, imagine that there is a clam, warming sensation hovering over the body part that is in pain.

#7 The body consists of many interlinking nerves and energy fields. Various pressure points correspond to particular regions of the body, and exerting pressure on them can activate a sizable pain numbing response. Some have concluded that massages increase circulation and counteract pain responses to a certain degree. While the basis of pressure points remains unexplained, it certainly works.

#8 Many people who suffer from sudden or chronic pain report  repetitive, negative thoughts that simply increase the intensity of the pain. Therefore, a positive outlook is key to combating main when it arises in the body.

#9 Music has the capacity to remove us from our negative chain of thoughts, and place on into a blissful state of existence. For this reason, it is naturally attuned to combating our pain messages.

#10 According to many studies, people who record their feelings on paper reduce their pain levels and increase their immune function.

#11 Activating your creative faculties can provide you with a temporary distraction from your pain.

#12 Laughter is a wonderful medicine that increases immune function and releases pain fighting endorphins, a natural analgesic.

#13 Affection releases serotonin, or happiness chemicals, in the brain-thereby increasing positivity and fighting pain.

#14 Affirming a healthy and pleasant state of being can reduce your pain levels.

#15 Many people find that they are unable to sleep with their pain levels. If you do, however, fall asleep, you will feel refreshed and renewed upon waking up, as sleep has healing properties that even curb pain.  

http://www.chronicbodypain.net/15-mental-tricks-that-fight-pain/

Fall prevention: Simple tips to prevent falls

Falls put you at risk of serious injury. Prevent falls with these simple fall-prevention measures, from reviewing your medications to hazard-proofing your home.

By Mayo Clinic Staff

Fall prevention may not seem like a lively topic, but it's important. As you get older, physical changes and health conditions — and sometimes the medications used to treat those conditions — make falls more likely. In fact, falls are a leading cause of injury among older adults. Still, fear of falling doesn't need to rule your life. Instead, consider six simple fall-prevention strategies.

1. Make an appointment with your doctor

Begin your fall-prevention plan by making an appointment with your doctor. Be prepared to answer questions such as:

• What medications are you taking? Make a list of your prescription and over-the-counter medications and supplements, or bring them with you to the appointment. Your doctor can review your medications for side effects and interactions that may increase your risk of falling. To help with fall prevention, your doctor may consider weaning you off certain medications — such as sedatives and some types of antidepressants.
• Have you fallen before? Write down the details, including when, where and how you fell. Be prepared to discuss instances when you almost fell but were caught by someone or managed to grab hold of something just in time. Details such as these may help your doctor identify specific fall-prevention strategies.
• Could your health conditions cause a fall? Certain eye and ear disorders may increase your risk of falls. Be prepared to discuss your health conditions and how comfortable you are when you walk — for example, do you feel any dizziness, joint pain, numbness or shortness of breath when you walk? Your doctor may evaluate your muscle strength, balance and walking style (gait) as well.

2. Keep moving

Physical activity can go a long way toward fall prevention. With your doctor's OK, consider activities such as walking, water workouts or tai chi — a gentle exercise that involves slow and graceful dance-like movements. Such activities reduce the risk of falls by improving strength, balance, coordination and flexibility.

If you avoid physical activity because you're afraid it will make a fall more likely, tell your doctor. He or she may recommend carefully monitored exercise programs or refer you to a physical therapist. The physical therapist can create a custom exercise program aimed at improving your balance, flexibility, muscle strength and gait.

3. Wear sensible shoes

Consider changing your footwear as part of your fall-prevention plan. High heels, floppy slippers and shoes with slick soles can make you slip, stumble and fall. So can walking in your stocking feet. Instead wear properly fitting, sturdy shoes with nonskid soles.

4. Remove home hazards

Take a look around your home. Your living room, kitchen, bedroom, bathroom, hallways and stairways may be filled with hazards. To make your home safer:

• Remove boxes, newspapers, electrical cords and phone cords from walkways.
• Move coffee tables, magazine racks and plant stands from high-traffic areas.
• Secure loose rugs with double-faced tape, tacks or a slip-resistant backing — or remove loose rugs from your home.
• Repair loose, wooden floorboards and carpeting right away.
• Store clothing, dishes, food and other necessities within easy reach.
• Immediately clean spilled liquids, grease or food.
• Use nonslip mats in your bathtub or shower.

5. Light up your living space

Keep your home brightly lit to avoid tripping on objects that are hard to see. Also:

• Place night lights in your bedroom, bathroom and hallways.
• Place a lamp within reach of your bed for middle-of-the-night needs.
• Make clear paths to light switches that aren't near room entrances. Consider trading traditional switches for glow-in-the-dark or illuminated switches.
• Turn on the lights before going up or down stairs.
• Store flashlights in easy-to-find places in case of power outages.

6. Use assistive devices

Your doctor might recommend using a cane or walker to keep you steady. Other assistive devices can help, too. For example:

• Hand rails for both sides of stairways
• Nonslip treads for bare-wood steps
• A raised toilet seat or one with armrests
• Grab bars for the shower or tub
• A sturdy plastic seat for the shower or tub — plus a hand-held shower nozzle for bathing while sitting down

If necessary, ask your doctor for a referral to an occupational therapist. He or she can help you brainstorm other fall-prevention strategies. Some solutions are easily installed and relatively inexpensive. Others may require professional help or a larger investment. If you're concerned about the cost, remember that an investment in fall prevention is an investment in your independence.

Study Shows Pesticide Exposure Dramatically Increases Risk of Developing Parkinson’s Disease

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New research published in the journal Neurology further supports the causative link betweenpesticide exposure and Parkinson’s disease. Emanuel Cereda, M.D., Ph.D., of the IRCCS University Hospital San Matteo Foundation in Pavia, Italy, and coauthor Gianni Pezzoli, M.D., analyzed 104 studies published between 1975 and 2011 to determine the link between pesticides and solvents to Parkinson’s disease.

The researchers analyzed exposure using information on proximity to large farms likely to use pesticides, likelihood of well water consumption and occupations that cause greater exposure to pesticides and solvents used to kill weeds, insects, fungus and rodents. Overall, researchers found exposure to pesticides increased the risk of developing the disease by 33 percent to 80 percent. Some pesticides were considered to be of higher risk than others, with weed killers likeparaquat and fungicides maneb and mancozeb causing twice the risk for development of Parkinson’s disease. While risk increased the longer people were exposed to pesticides, researchers indicate there is still a need for further research on the chemical threshold for harm to the brain.

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The study builds on recent research that has linked Parkinson’s disease to pesticide exposure. In a 2011 article published in the journal Molecular Neurodegeneration, researchers at the University of Missouri School of Medicine invented a new antibody that allowed them to detect how oxidative stress affected proteins when exposed to a variety of environmental toxins, such as the pesticide rotenone. In another study, individuals with certain genetic factors who are exposed to organophosphates exhibited more than twice the risk of Parkinson’s disease compared to others without exposure. Another recent publication found that rural residents who drank contaminated well water had an increased risk—up to 90 percent—of developing Parkinson’s.

The research adds to the body of knowledge on the role of pesticide exposure in diseases like Parkinson’s. “I think the study is actually a big advance in our research knowledge of the relation between chemical exposures and the basic neurological injuries,” said Arch Carson, Ph.D., at the University of Texas School of Public Health in Houston, TX. “This report is the first to show that there is a positive relationship between not only insecticides and herbicides but also some other solvent chemicals to which many people are exposed and the development of Parkinson’s syndrome.”

The second most common neurodegenerative disease, Parkinson’s disease occurs when nerve cells in the substantia nigra region of the brain are damaged or destroyed and can no longer produce dopamine, a nerve-signaling molecule that helps control muscle movement. People with Parkinson’s have a variety of symptoms including loss of muscle control, trembling and lack of coordination. They may also experience anxiety, constipation, dementia, depression, urinary difficulties and sleep disturbances. Over time, symptoms intensify. At least 1 million Americans have Parkinson’s and about 50,000 new cases are diagnosed each year. With less than one percent of cases caused by genetics, researchers have been looking for the potential risk factors for developing Parkinson’s disease.