Welcome to Our Parkinson's Place

I copy news articles pertaining to research, news and information for Parkinson's disease, Dementia, the Brain, Depression and Parkinson's with Dystonia. I also post about Fundraising for Parkinson's disease and events. I try to be up-to-date as possible. I have Parkinson's
diseases as well and thought it would be nice to have a place where
updated news is in one place. That is why I began this blog.
I am not responsible for it's contents, I am just a copier of information searched on the computer. Please understand the copies are just that, copies and at times, I am unable to enlarge the wording or keep it uniformed as I wish. This is for you to read and to always keep an open mind.
Please discuss this with your doctor, should you have any questions, or concerns. Never do anything without talking to your doctor. I do not make any money from this website. I volunteer my time to help all of us to be informed. Please No advertisers, and No Information about Herbal treatments. Please no advertisements.
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Thank you.

Saturday, February 20, 2016

How EVOO Exerts Neuroprotective Activity Against Alzheimer’s and Parkinson’s Disease

Phenols in extra virgin olive oil exert antioxidant and anti-inflammatory effects on the brain that scavenge pesticide induced free radicals that contribute to neurological disorders such as Alzheimer’s and Parkinson’s.

By JEDHA DENING on February 20, 2016
Filed in Health
One of the major contributing factors to neurological disorders such as Alzheimer’s and Parkinson’s is oxidative stress.
A recent study on rats, published in Journal of Food Science and Technology, (Jan. 5, 2016), suggests that high amounts of polyunsaturated fats (PUFA) in the body create substrates that are easily oxidized, increasing the rate of reactive oxygen species (ROS). This, combined with low levels of antioxidant enzymes and high oxygen use in the central nervous system, leads to more oxidative damage that is thought to play a key role in such diseases.
Since the 1940s an herbicide known as 2,4-Dichlorophenoxyacetic acid (2,4-D), has been widely used in agriculture and forestry industries, which humans and animals are frequently exposed to through “contaminated air, drinking water, soil and foodstuff or during production of the herbicide.” 2,4-D has been shown to have neurotoxic effects due to the generation of free radicals.
The study suggests that the biological actions of phenols in extra virgin olive oil (EVOO) exert antioxidant and anti-inflammatory effects on the brain, with the ability to scavenge ROS. These phenols have been shown in various studies to have neuroprotective effects against, not only Alzheimer’s and Parkinson’s, but cerebral ischemia, spinal cord injury, Huntington’s disease and peripheral neuropathy.
The aim of this rat study in particular, was to establish if EVOO had effects on 2,4-D induced oxidative stress. Using rat brain slices, the researchers had three different groups, extra virgin olive oil (EVOO), olive oil extracting the hydrophilic fractions (OOHF) and olive oil extracting the lipophilic fractions (OOLF). They tested lipid peroxidation and antioxidant defence systems with a particular focus on brain lipid profile and fatty acid composition.
After 4 weeks of exposure to 2,4-D treatment, the brain weight of the rats decreased along with AChE activities – an indicator of cell membrane damage. The brains also displayed a decrease in membrane PUFA contents. Both the EVOO and OOLF groups presented with the same fatty acid composition, 17 percent saturated fatty acids, 65 percent monounsaturated, 15 percent PUFA. The changes induced to the brain via pesticide exposure were all counteracted with the addition of EVOO or it’s fractions, restoring brain weight and stimulating AChE activity.
In addition, supplementing with the EVOO also restored antioxidant enzyme activities and lipid peroxidation to normal levels. The PUFA levels were also restored to normal, especially DHA levels, providing an observable neuroprotective effect of EVOO. ROS reduced in the brain also.
The study suggests that the beneficial effects of EVOO are due to its high antioxidant substances and monounsaturated fatty acids.
Though this is only a study in rats, early data suggests that EVOO could be a natural protective agent against acute 2,4-D neurotoxicity exposure. And while more research is needed, the authors suggest EVOO could be a therapeutic strategy to protect against, not only 2,4-D exposure, but other types of pesticide exposure that contribute to neurological disorders such as Alzheimer’s and Parkinson’s and increased oxidative stress.

EXCLUSIVE: New statin danger revealed: 150,000 at risk of developing Parkinson’s disease, Term life

Friday, February 19, 2016

Study Shows How Waste Product of Physical Exercise Protects Neurons From Trauma Damage

Feb. 19, 2016

Lausanne, Switzerland (Scicasts) — Researchers led by EPFL have found how lactate, a waste product of glucose metabolism can protect neurons from damage following acute trauma such as stroke or spinal cord injury. 
Stroke or spinal cord injury can cause nerve cells to receive excessive stimulation, which ultimately damages and even kills them. This process is known as excitotoxicity, and it is one of the reasons why time following such trauma is critical, while it also implicated in progressive neurodegenerative diseases, e.g. Alzheimer's disease.
A team of scientists led by EPFL has now discovered that lactate, which is produced in the brain and even muscles after intense exercise, can be used to protect neurons against excitotoxicity. The study is published in the Nature journal Scientific Reports.

Step-by-step description of how lactate protects neurons against excitotoxicity: (1) Excessive glutamate activity triggers a strong influx of calcium (Ca2+) into the neuron through NMDA receptors, which leads to cell death. (2) Lactate is transported into the neuron and (3) converted to pyruvate by the enzyme lactate dehydrogenase (LDH). (4) Pyruvate is then transported into mitochondria by the mitochondrial pyruvate carrier (MPC) where it generates ATP. (5) ATP is then released through pannexins and activates the receptor P2Y, which (6) activates the PI3K pathway. (7) This triggers the opening of potassium channels (K+), which causes the neuron to hyperpolarize, decreasing the neuron's excitability, and thus protecting it from excitotoxic damage. Image: Pascal Jourdain (EPFL)
Following acute trauma such as a stroke or spinal cord injury, a certain type of receptors go into overdrive and overwhelm the target neuron with a barrage of electrical signals. This causes a build-up of calcium ions inside the neuron, which triggers toxic biochemical pathways that ultimately damage or kill it.
The receptors that cause this are called NMDA receptors, and interact with the neurotransmitter glutamate. NMDA receptors are a major target in research and medicine, as they are implicated in a number of disorders, including epilepsy, schizophrenia, Parkinson's and even Alzheimer's.
A team of researchers led by Pierre Magistretti from EPFL and the King Abdullah University of Science and Technology, investigated the effects of glutamate on cultured neurons from the brains of mice. The scientists used a new, non-invasive imaging technique called Digital Holographic Microscopy that can visualize cells structure and dynamics with nanometer-level resolution.
Previous studies have suggested that, lactate could protect neurons against excitotoxicity. Lactate is produced in the brain and in muscles after intense exercise as a waste product of glucose metabolism. Nonetheless, how lactate protects neurons has eluded scientists until now.
The researchers tested the effects of glutamate on the mouse neurons with and without lactate. The results were revealing: glutamate killed 65% of the neurons, but when with lactate, that number dropped to 32%.
The researchers then aimed to determine how lactate protects neurons. By using different receptor blockers on the mouse neurons, they determined that lactate triggers the production of ATP, the cell's energy molecule. In turn, the produced ATP binds and activates another type of receptor in the neuron, which turns on a complex cascade of defense mechanisms. As a result, the neuron can withstand the onslaught of signals from the NMDA receptor.
The breakthrough can advance our understanding of neuroprotection, which could lead to improved pharmacological ways to ameliorate the irreparable damage caused by stroke, spinal cord injury, and other trauma.
Article adapted from a École Polytechnique Fédérale de Lausanne news release.
Publication: L-Lactate protects neurons against excitotoxicity: implication of an ATP-mediated signaling cascade. Jourdain, P et al. Scientific Reports (19 February, 2016).

"Marvel molecule" could enable new treatments for a range of inflammatory diseases

 FEBRUARY 18, 2015

The newly identified molecule could hold the key to improved treatments for a variety of inflammatory diseases (Shutterstock)
A team of researchers at Trinity College Dublin has unearthed what they are calling a "marvel molecule." Said to be capable of suppressing a key activator of various inflammatory diseases, it is hoped the molecule will lead to more effective treatments for conditions ranging from Alzheimer’s disease, to rheumatoid arthritis and motor neuron disease.
The massive potential of the molecule lies in its ability to block a key activator of inflammatory diseases known as the NLRP3 inflammasome. Inflammasomes, protein clusters responsible for triggering a range of inflammatory processes, have long been considered potential therapeutic targets for treating a range of conditions.
Through the study, the researchers found the molecule, dubbed MCC950, to be very promising in warding off multiple sclerosis. But what really pleased the researchers was the fact that the target, the NLRP3 inflammasome, also plays a strong role in the onset of other inflammatory diseases including Alzheimer’s, atherosclerosis, gout and Parkinson's disease.
"MCC950 is blocking what was suspected to be a key process in inflammation," says Dr Rebecca Coll, lead author of the paper. "There is huge interest in NLRP3 both among medical researchers and pharmaceutical companies and we feel our work makes a significant contribution to the efforts to find new medicines to limit it."
The findings are said to confirm that while different inflammatory conditions may cause different parts of the body to become inflamed, the diseases all share a common process. This has the potential to spawn new kinds of cheaper, non-invasive treatments for inflammatory diseases.
"MCC950 is able to be given orally and will be cheaper to produce than current protein-based treatments, which are given daily, weekly, or monthly by injection," says Professor Matt Cooper from the University of Queensland, a co-senior author of the study. "Importantly, it will also have a shorter duration in the body, allowing clinicians to stop the anti-inflammatory action of the drug if the patient ever needed to switch their immune response back to 100 percent in order to clear an infection.”
The researchers say that the molecule may also benefit sufferers of Muckle-Wells disease, a rare genetic disorder that can cause rashes, joint pain and other inflammations. Treating blood samples of patients with Muckle-Wells disease, the molecule was shown to block the rogue gene that triggers these recurring inflammatory processes.
"We are really excited about MCC950," says Professor of Biochemistry at Trinity College Dublin and joint senior scientist behind the discovery. "We believe this has real potential to benefit patients suffering from several highly debilitating diseases, where there is currently a dire need for new medicines."
The research was published in the journal Nature.

TSRI and JCVI scientists find popular stem cell techniques safe

February 19, 2016

A new study led by scientists at The Scripps Research Institute (TSRI) and the J. Craig Venter Institute (JCVI) shows that the act of creating pluripotent stem cells for clinical use is unlikely to pass on cancer-causing mutations to patients.
The research, published in the journal Nature Communications, is an important step in assessing patient safety in the rapidly developing field of stem cell therapies.
The new study focused on the safety of using induced pluripotent stem cells (iPSCs) in human patients. Because iPSCs can differentiate into any kind of cell in the body, they hold potential for repairing damage from injuries or diseases such as Parkinson's and multiple sclerosis.
"We wanted to know whether reprogramming cells would make the cells prone to mutations," said Jeanne Loring, professor of developmental neurobiology at TSRI and co-leader of the new study with Nicholas J. Schork, professor and director of human biology at JCVI. "The answer is 'no.'"
"The safety of patients comes first, and our study is one of the first to address the safety concerns about iPSC-based cell replacement strategies and hopefully will spark further interest," added Schork.
To make an iPSC, scientists must reprogram an adult cell, such as a skin cell, to express a different set of genes, which can be accomplished using viruses as delivery vehicles or with molecules called messenger RNAs (mRNAs).
The researchers looked at three popular methods of iPSC production (integrating retroviral vectors, non-integrating Sendai virus and synthetic mRNAs), assessing each for the potential to trigger cancer-causing mutations. While the researchers noted some minor alterations in the iPSCs, none of the methods led to significant mutations. The researchers repeated the experiments two more times and again found no significant risk.
"The methods we're using to make pluripotent stem cells are safe," said Loring.
The scientists do warn that even though iPSCs don't gain cancer-causing mutations during reprogramming, potentially harmful mutations can accumulate later on as iPSCs multiply in lab cultures. Loring said scientists must analyze their cells for these mutations before using them in therapies.
"We need to move on to developing these cells for clinical applications," said Loring. "The quality control we're recommending is to use genomic methods to thoroughly characterize the cells before you put them into people."

Local Doctor Leads Study Of Gene Therapy Treatment For Parkinson’s Patients

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February 18, 2016 By Dr. Maria Simbra

PITTSBURGH (KDKA) – When part of the brain is no longer working properly, would it be possible to put something in to boost function?
Neurosurgeon Dr. Mark Richardson is trying to find out.
“What we’re trying to do with this study is to replace an enzyme that’s lost as cells degenerate in Parkinson’s disease,” Dr. Richardson said. “The enzyme helps the brain make dopamine.”
The brain chemical dopamine is important to keeping movements smooth. The problem in Parkinson’s disease is the lack of dopamine because of worn out brain cells, and you end up with shaking, stiffness, and slowness of movement.
People can take medicine for Parkinson’s disease, but there can be symptom fluctuations and at higher doses, side effects.
“Typically in Parkinson’s disease, these symptoms kind of go up and down like this, and they can be masked very well by medication, but unfortunately what tends to happen for all of these patients is progression to more of a roller coaster ride of ups and downs during the day,” Dr. Richardson said.

Dr. Richardson is leading part of a study, first funded by the Michael J. Fox Foundation and now by a biotherapy company, to see whether inserting a gene into a specific part of the brain will be the on switch for more dopamine production.
“The idea of brain surgery for a chronic disease is very different than continuing to take medication,” Dr. Richardson said.
The gene is delivered into the brain through the skull by a thin tube and carried by a virus
“The idea of a virus probably sounds very scary to some people. But, this virus cannot reproduce,” Dr. Richardson said. “It can insert itself into a cell, and it can only do one thing there. It can release the gene to allow this enzyme to be made.”
Dr. Richardson and the lead investigator in San Francisco are looking for 20 patients to participate. They will be followed for three years, and their need for medication will be evaluated and compared before and after.
To qualify you have to be between 40 and 70 and on certain medicines for Parkinson’s disease for at least three years with increasing fluctuations in movement.
Dr. Richardson hopes gene therapy leads to smoother days and fewer symptoms.
“If we can show this is a small group of patients, the trial will be expanded,” Dr. Richardson said. “With a little bit of luck, within the next decade, we will see a gene therapy accepted as a proven and viable treatment option.

Is leg pain a symptom of Parkinson’s?

admin February 19, 2016

Leg pain can be significant and have many causes; some related to Parkinson’s disease, some that increase in frequency with age and others that are more common in both conditions. Here are just a few:

     Pain associated with Parkinson’s 

    Off related pain – diffuse aching and/or throbbing pain that increases at end of dopaminergic medicine dosing or when medication levels are low. Unlike joint pain, this pain is often located in the muscle such as the thigh or calf but not the knee of ankle. PD medications can often improve this pain.
    Restless leg syndrome – uncomfortable sensations most commonly felt in legs that is worse at night and while resting and relieved with movement. See related post on restless leg syndrome for more information.
   Dystonia-involuntary contraction of muscle. This can be common as a symptom of PD, an off related symptom or as a form of dyskinesia from medication. An example is early morning foot dystonia described as painful cramping of the toes and feet. Botulinum toxin (Botox, Myobloc) therapy can help
      Arthritis of the knee, hip or ankle typically causes pain in the join and not muscle. Although this is unrelated to PD, arthritic pain can worsen when the natural biomechanics of the joint is altered with PD rigidity, loss of strength and loss of flexible. Physical therapy and anti-inflammatory agents are an important treatment for this and the condition described next.
     Achilles tendonitis is pain located at the ankle and plantar faciitis is pain located under the sole of the foot. Both conditions can flare with a change in exercise routine, with improper stretching and secondary to the tightness of the ankle and foot often found in PD.
      Peripheral neuropathy is caused by nerve damage that begins in the feet. Associated symptoms are pain, burning, numbness and tingling. The most common causes are aging, diabetes, vitamin B12, deficiency, thyroid deficiency and blood protein disorders. this condition not only causes pain but also can worsen balance. Blood tests can help identify the cause of this problem.
      Radiculopathy or sciatic nerve compression can cause pain in the thigh, calf in foot depending on the nerves affected. Causes could include arthritis and disk disease of the spin and compression of the sciatic nerve in the buttock region due to muscle tightness,
    Spinal stenosis is a problem of narrowing of the spinal canal. Often          associated with back pain and pain in both legs. this type of pain often improves when a person is bent forward.

General Pain
Leg swelling can occur with PD, medications and other medical conditions. Abrupt change in leg swelling associated with pain could be a sign of a blood clot requiring immediate medical attention. Lack of movement and dehydration can increase this risk in PD.

This information does not represent all types of pain that can occur. As always, be sure to talk with your healthcare provider if you are experiencing pain in your legs.

Monique L. Giroux, MD
Guest Blogger, Former Medical Director of NWPF