I Ask This Of You!

I have Parkinson's diseases and thought it would be nice to have a place where the contents of updated news is found in one place. That is why I began this blog.

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 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. I will not accept any information about Herbal treatments curing Parkinson's, dementia and etc. It will go into Spam.

This is a free site for all with no advertisements.

Thank you for visiting!

Saturday, November 21, 2015

Electronic “Noise” Machine May Help Parkinson’s Patients

Nov. 21, 2015
 electronic device that delivers “noise” to a part of the brain appears to help people with Parkinson’s disease keep their balance. The device delivers a tiny electrical signal to the centers of balance in the brain through patches that are placed just behind the patient’s ears.This device does not require surgical implantation of a nerve stimulator into the brain, as is done with deep brain stimulation, which is a treatment for severe Parkinson’s. The patches deliver a small electrical charge through the skin to the vestibular system of the brain, the part that controls balance, which can be an issue with people who have Parkinson’s disease. In practice, the device is similar to the device used in transcutaneous electrical nerve stimulation therapy, which is used for pain relief.
Researchers at the University of Gothenburg in Sweden tested the device on ten patients with Parkinson’s disease in a double-blind study. Patients were treated with either vestibular stimulation or a sham treatment where no stimulation was delivered on alternate days and were given balance tests. The treatment was tested when the patients were using levodopa, the most commonly used drug for Parkinson’s disease, and without it.
The tests showed that the electric stimulation improved patients’ balance and other symptoms. The stimulation helped patients correct their balance in tests and decreased the amount that they swayed when their eyes were closed. The combination of levodopa and stimulation worked best at helping with balance.
Patients could not tell when the stimulation was being delivered to the patches and when it was not, outside of improving their balance.
One of the problems with Parkinson’s is that levodopa stops working for patients as their disease progresses. Worse, the drug starts causing involuntary movements called dyskinesia.
The study was published in the journal Brain Stimulation.

Smartphones to detect early stages of Parkinson’s disease

Nov. 20, 2015

A novel new way to diagnose Parkinson’s disease may involve nothing more complicated than carrying a smartphone in your pocket.
Researchers at Aston University have developed a phone app that can spot signs of the disease with more than 90 per cent accuracy.
The phone provides a range of checks including a voice analysis, monitoring of the person’s gait and also dexterity tests using features already provided on most smart phones, said Dr Max Little of Aston’s Nonlinearity and Complexity Research Group.Early diagnosis is very difficult, he said. “They don’t know how to detect the disease before it is too late when symptoms arise.”
His app is grounded in work he began back in 2006, when given a block of voice recordings provided by Intel.
Minor “voice impairments” represented a possible means of early diagnosis and by finding a way to detect these he managed to reach 86 per cent accuracy in diagnosis.Things have progressed much further however with the appearance of smart phones.
These can provide high definition voice recordings for analysis but they also feature built-in “accelerometers”, used to keep the the screen display upright.
However, when the phone is used as a diagnostic tool, the person is asked to pronounce a sound for the phone recorder, walk 20 paces so the accelerometers can record movements and then the person completes simple finger dexterity tests on the touch screen.
Results so far are “promising”, he said. “The tool is extremely accurate.”
The phone app is able to give objective data for doctors that can be used to support decision making on treatment options in the clinic, Dr Little said.
He is involved with Oxford University on a joint study of 2,500 subjects and five years into the project he recently received funding for a further five years.

Muhammad Ali on Parkinson’s disease: “I’m a prisoner in my own body”

Nov. 21, 2015

Manager Gene Kilroy says Ali can “just about walk and his speech is slurred”
After more than three decades of living with Parkinson’s disease, Muhammad Ali – widely regarded as the greatest boxer to have ever lived – is still bravely fighting the condition, according to his manager Gene Kilroy.
Ali confided to Kilroy that he felt like “a prisoner in his own body,” but that his “mind is good”.
Kilroy, who is in regular contact with the 73-year-old Ali, told the Daily Mirror: “It’s hard seeing him as he is today. He can just about walk and his speech is slurred. It takes huge effort for him to make the simplest communication now, but when he does, every word is worthwhile.”

Ali was diagnosed with Parkinson’s in 1984, three years after his retirement from boxing, a glorious career in which he won 56 of his 61 fights.
Kilroy added: “But even now he has no fear. He says, ‘I’ll stay here as long as God wants me to. When my time comes I’ll have no regrets. I have achieved a lot’.”

In December last year, he was rushed to hospital after contracting what was believed to be pneumonia. He was readmitted a few weeks later, after doctors determined he was actually suffering from a urinary tract infection.
Speaking to The Telegraph, Kilroy said: “When he got Parkinson’s and his voice wasn’t as strong as it used to be, he said, ‘Well, maybe God is punishing me for some of the things I didn’t do right. I believe that when you die and go to heaven God won’t ask you what you’ve done but what you could’ve done. Maybe I’m getting punished. He said I’m lucky, I have no pain with this Parkinson’s. I’m a prisoner in my own body but I don’t have any pain. My mind is good. My speech maybe slurred but my mind is good’.”
by Geoffrey Chang

Friday, November 20, 2015

Brainstem 'stop neurons' make us halt when we walk

Friday 20 November 2015 
A population of 'stop cells' in the brainstem is essential for the ability of mice to stop their locomotion, according to a new study by scientists at Karolinska Institutet in Sweden. In an article published in the journal Cell, they report a brainstem pathway specifically dedicated to enforce locomotor arrest; its selective activation stops locomotion, while its silencing favors it. The study thus identifies a novel descending modality essential for gating the episodic nature of locomotor behavior.
Locomotion is an essential motor behaviour needed for survival in both humans and animals. It has an episodic nature: we move when we want or need and, equally well, we can terminate ongoing movements. This episodic control has generally been attributed to descending excitatory signals in the brainstem that contact and activate neuronal circuits in the spinal cord. But is the stop of locomotion only due to a lack of activating signals from the brainstem or is there a dedicated stop signal?
In the present study, the researchers Julien Bouvier and Vittorio Caggiano together with Professor Ole Kiehn and colleagues studied how the complex brainstem neuronal circuits control locomotion in mice. They used advanced methods, including optogenetics, which makes it possible to selectively activate specific groups of neurons with light, as well as genetic silencing to selectively block neuronal activity.
Somewhat unexpectedly, they found a population of excitatory neurons that turned out to be essential for the ability of mice to stop. When those 'stop cells' are activated, mice immediately halt their locomotion. Conversely, when those neurons are silenced, mice had difficulties when trying to stop walking.
"We found that the stop cells depress the neuronal networks involved in generating the locomotor rhythm, the clock in the network, and not the motor neurons that directly contract muscles", says Ole Kiehn, who leads the laboratory behind the study at Karolinska Institutet's Department of Neuroscience. "In this way activity in the stop cells allows the animal to make a gracious stop without losing its muscle tone, just as we experience ourselves when we voluntarily stop for example in front of an obstacle."
Although the study addresses the normal brain function the findings may provide insights to how locomotion is affected in the diseased brain.
"For example, in Parkinson's disease, a pronounced motor symptom is a gait disturbance with freezing of the gait", says Ole Kiehn. "t is possible that the stop cells have an abnormally increased activity in Parkinson's disease, contributing to the gait disturbances."
Adapted by MNT from original media release

Thursday, November 19, 2015

Molecular Mechanism at Root of Chain Leading Parkinson’s Identified

Study reveals mechanism behind apoA-I mutations that cause amyloid disease


Boston University School of Medicine and Northeastern University researchers have proposed a molecular mechanism by which only certain mutations in human apoA-1 protein cause familial amyloidosis while others do not. The research paper, entitled “Structural Stability and Local Dynamics in Disease-Causing Mutants of Human Apolipoprotein A-I: What Makes the Protein Amyloidogenic?”, was published in the Journal of Molecular Biology

Alzheimer’s and Parkinson’s disease are included in the amyloidosis family of diseases, characterized by the abnormal deposit of insoluble protein aggregates, forming amyloid fibrils that damage organs and tissues. More than 26 proteins are currently known to potentially form amyloid aggregates.
One of the proteins forming amyloid fibrils is the apolipoprotein A-I (apoA-I), the major protein of plasma high-density lipoprotein (HDL), also known as the “good cholesterol” that removes cellular cholesterol and prevents atherosclerosis. In its normal form, the protein is essential to protect against cardiovascular disease. However, mutations or misfolding in the protein can cause familial amyloidosis, a potentially fatal condition where the protein forms aggregates in vital organs.
To understand the mechanism behind protein misfolding and why some mutations cause amyloidosis while others don’t, researchers analyzed the structure and stability of the human apoA-I and several natural occurring mutant forms. Results, from diverse molecular and structural techniques, revealed that a major amyloid vulnerable “hot spot,” thought to cause disease, does not always lead to amyloidoisis. Furthermore, mutations at one end of the protein were found to have a structural and functional effect in other parts of the protein. Certain mutations led to clearance of protein clumps instead of amyloid disease in humans.
According to a press release, the researchers suggest this finding is not limited to apoA-I but possibly applies to other amyloid-forming proteins, and may have important implications for potential treatments. Dr. Olga Gursky, professor of Physiology and Biophysics at BUSM and corresponding author of the study, commented, “If one could predict what makes any given protein to form amyloid, one could begin to design tools to decelerate or even block this pathogenic process before it starts.”

New technique negotiates neuron jungle to target source of Parkinson’s disease

Nov. 20, 2015

Researchers from Imperial College London and Newcastle University believe they have found a potential new way to target cells of the brain affected by Parkinson’s disease.
The new technique is relatively non-invasive and has worked to improve symptoms of the disease in rats.
Parkinson’s disease causes progressive problems with movement, posture and balance. It is currently treated with drugs, but these have severe side-effects and can become ineffective after around five years. The only treatment subsequently available to patients is deep brain stimulation, a surgical technique where an electrical current is used to stimulate nerve cells in the brain.
As well as being an invasive treatment, it has mixed results — some patients benefit while others experience no improvement or even deteriorate. Researchers believe this is because the treatment is imprecise, stimulating all types of nerve cells, not just the intended target.

The new study, published in the journal Molecular Neurodegeneration, examined a less invasive and more precise alternative, designed to target and stimulate a particular type of nerve cell called cholinergic neurons. These are found within a part of the brain called the pedunculopontine nucleus, or PPN.
“If you were to peer inside the PPN, it is like a jungle with a massive variety of nerve cells that behave differently and have different jobs to do,” said Dr Ilse Pienaar, Honorary Lecturer in Neuroscience at Imperial College London.

Scientists already suspect that cholinergic neuron cells are involved in Parkinson’s disease. This is because in post mortem studies of patients’ brains, about half of these cells have perished, for reasons that are currently unknown.

The researchers worked with rats that had been treated to recreate the symptoms of Parkinson’s disease. They used a harmless virus to deliver a specially-designed genetic ‘switch’ to the cholinergic neurons. The rats were then given a drug that was designed to activate the ‘switch’ and stimulate the target neurons.
Following the treatment the rats made an almost complete recovery and were able to move normally.
Dr Pienaar adds: “This study confirms that cholinergic neurons are key to the gait problems and postural instability experienced by advanced Parkinson’s disease patients. It also suggests that it’s possible to target those cells that remain to compensate for those that are no longer functioning effectively, possibly due to weak communication between nerve cells. If we can transfer this technique into people, we believe this could help patients regain mobility.”
“At the moment, neurosurgeons are attempting to target specific areas with deep brain stimulation, but it is a blunt tool with correspondingly mixed results. We think we have found a way to target only the cholinergic neurons within an area such as the PPN.”
Dr Joanna Elson at the Institute of Genetic Medicine at Newcastle University added: “The structure we studied is complex, very complex. Despite this complexity and the intricacy of the techniques and the brain region analysed, the results are exciting because of the potential to advance patient treatment.
“This paper will help us understand how deep-brain stimulation works, but more importantly it is a step towards offering less invasive treatment options to patients with Parkinson’s and other neurodegenerative disorders.”
The researchers believe the technique could transfer into people in the next five to ten years. They also think their technique could have wider potential. Dr Pienaar said: “Parkinson’s disease patients experience a complex set of symptoms and we hope to use the same method to understand how different cells within the brain contribute to the disease.”

Secrets of dark proteome

Nov. 19, 2015

Proteins are often referred to as the building blocks of life, and make up about 15 per cent of the mass of the average person, performing a wide variety of essential functions in the body.
Scientists have long speculated about the nature of the dark proteome, the area of proteins that are completely unknown, but a recent study by CSIRO has mapped the boundaries of these dark regions, bringing us one step closer to discovering the complete structure and function of all proteins.
The work, led by Dr Sean O'Donoghue, a data visualisation scientist with CSIRO and the Garvan Institute, has been published today in the prestigious Proceedings of the National Academy of Sciences journal.
As knowledge of three-dimensional protein structures continues to expand, we can identify regions within each protein that are different to any region where structure has been determined experimentally, coined the 'dark proteome'.
"These dark regions are unlike any known structure, so they cannot be predicted," Dr O'Donoghue said.
"Identifying these areas is very exciting as we now have a map to focus our research efforts."
"Our map defines the boundaries right at the edge of protein knowledge."
The research has yielded some surprising results, including that nearly half of the proteome in eukaryotes is dark and has unexpected features, including an association with secretory tissues, disulfide bonding, low evolutionary conservation, and very few known interactions with other proteins.
This work will help future research shed light on the remaining dark proteome, revealing molecular processes of life that are currently unknown.
It may also provide insight into protein based illnesses like cancertype 2 diabetes, and many neurodegenerative diseases, such as Parkinson's disease and Alzheimer's.
Protein molecules compose many of the major elements of our body, and dark proteins -- those with completely unknown structure -- are abundant in skin and hair, and glands that make saliva, semen, and milk.
"The dark proteome undoubtedly plays a key role in human health, as well as many other areas of life science," Dr O'Donoghue said.
"We believe that studying the dark proteome will clarify future research directions, as studies of dark matter have done in physics."
The discovery was made using Aquaria, CSIRO's free web based tool that uses data from the Protein Data Bank to create 3D structural models for 546,000 protein sequences.

End Stage Parkinson’s Disease Symptoms

Nov.19, 2015


Parkinson’s disease is not fatal and does not shorten the average life expectancy of the patient, according to the National Institute of Neurological Disorders and Stroke. As the disease progresses, however, secondary complications may lead to death. Neurologists measure progression of the disease by using the Unified Parkinson’s Disease Rating Scale, which describes various symptoms, all of which may not be present to the same degree. A patient who receives the highest score on the scale will be someone who is completely disabled and helpless. Some patients live for 15 years following diagnosis and never reach this point, say Dr. William Weiner and colleagues in their book “Parkinson’s Disease: A Complete Guide for Patients and Families.”

Movement and Balance Difficulties

The National Institute of Neurological Disorders and Stroke lists the four primary symptoms of Parkinson’s disease: tremor, rigidity, slowness of movement and impaired balance. These symptoms worsen until the person has a complete absence of facial expression, cannot speak and cannot stand or walk. According to Dr. Weiner and colleagues, movement problems include extreme loss of balance and freezing while walking, which result in the patient falling frequently.

Cognitive and Behavioral Problems

The patient may experience any of a variety of mental issues such as confusion, memory loss, hallucinations, delusions, depression and anxiety. According to Dr. Weiner and colleagues, confusion and memory problems, known as dementia, develop in one out of every four to five Parkinson’s patients at a level severe enough to interfere with daily activities.

Nervous System Impairments

The autonomic nervous system controls unconscious functions such as breathing, blood pressure, digestion and urination. In the end stage of Parkinson’s disease a patient becomes incontinent, constipated and subject to a drop in blood pressure when going from a seated position to standing, which may result in fainting, according to Dr. Weiner and colleagues.

Drooling and Difficulty Swallowing

In Parkinson’s disease the swallowing reflex deteriorates, which can lead to choking when eating or drinking. The patient will not swallow saliva frequently. As saliva pools in the mouth, the patient may drool and choke. Caregivers may need to feed some end stage Parkinson’s patients through a tube inserted in the stomach through the abdomen.

Medication Problems and Drug-Induced Symptoms

According to the National Institute of Neurological Disorders and Stroke, as Parkinson’s disease progresses the response of the patient to medication becomes less predictable. The medication may wear off faster and no longer control symptoms adequately. The patient may need more frequent doses. As the drug dose increases so do the side effects, including dyskinesia, an uncontrollable, involuntary writhing movement, which may disable the patient as much as the original Parkinson’s symptoms do.
By Ruth Warre

The effect of a longer period of exercise in people with Parkinsons disease

Nov. 18, 2015

Short-term exercise interventions have been shown to benefit health and wellbeing and reduce motor and non motor symptoms in the short term in people with Parkinson’s disease (PD). Exercise over a longer period of time may reduce the impact of disability for people with PD but the effect of longer-term exercise has not been established. People with PD tend to have low activity levels and reduce their physical activity over time. To achieve an ongoing active lifestyle people with PD will need to be able to use community facilities. However, people with PD report feeling deterred from using community exercise schemes. As such it is unsurprising that people with PD are observed to have low levels of physical activity and participation in exercise despite expressing a desire to be active. With the help of fitness professionals, people with PD and NHS clinicians we have developed a community exercise programme for people with PD.

We propose to study: People with Parkinson’s disease who are able to walk 100m    How we would undertake the investigation: Participants will be recruited from neurology services in Oxfordshire and Reading. We will randomly assign participants into one of two groups –a community exercise programme group or to a comparison control group who will perform a hand writing programme. The exercise programme will be supported from current PD NHS services and delivered in community fitness centres and gyms by a fitness professional supported by a physiotherapist and patient information materials.    How we would evaluate the study: Recruited patients will be monitored at entry to the study and at three, six, and twelve months. We will evaluate the effect of the exercise programme on PD motor and non motorsymptoms, fitness, health and wellbeing. We will ask participants their views on the process and service.    Expected outcome: We will determine the effect of exercising for a longer period of time and if further investigations are needed.

New Strategy Reduces Side Effects in Parkinson’s Treatment

Nov.19, 2015

In an  study, Northwestern Medicine scientists and colleagues have identified a novel strategy for reducing the side effects of uncontrolled movement caused by the drug levodopa, commonly used to treat the stiffness, tremors and poor muscle control of Parkinson’s disease.
These unwanted movements caused by levodopa significantly diminish the quality of life for Parkinson’s disease patients.A team lead by D. James Surmeier found neurons in the brain responsible for the side effects have a distinctive surface receptor that normally helps balance the effects of levodopa treatment. When mouse or primate models of Parkinson’s disease were given a compound that boosts functioning of this receptor, the uncontrolled motor side effects of levodopa treatment were dramatically reduced. is the Nathan Smith Davis Professor and chair of physiology at Northwestern University Feinberg School of Medicine.
The study was published Nov. 18 in the journal Neuron.
Although this new compound — an M4 muscarinic receptor positive allosteric modulator — is not currently approved for human use, it is in development with the goal of clinical trials, a Phase I trial possibly starting by 2017.
“There has been an international effort to find a drug that can be combined with levodopa to reduce the uncontrolled movement,” Surmeier said. “If clinical trials confirm our preliminary findings, the eventual drug developed could make a significant improvement in the quality of life for people with Parkinson’s disease.”Parkinson’s is the second most common neurodegenerative disease in the U.S., affecting more than a million people, a number expected to double by 2030. In its early stages, the primary symptom of the disease — difficulty moving — can be effectively treated by levodopa.
But as the disease progresses, the dose of levodopa required to alleviate symptoms rises and side effects begin to appear. The most prominent of these is uncontrolled movement or dyskinesia. There are no treatment strategies that can help other than neurosurgery.
Surmeier’s effort was built upon previous work of his lab and other research exploring the striatum, a part of the brain circuitry targeted by levodopa and thought to drive dyskinesia. At doses of levodopa treatment that produce dyskinesia, part of the striatal network becomes abnormally re-wired.
Surmeier’s team found a protein in one type of these striatal neurons that could counter-balance the effects of levodopa without diminishing its positive effect on movement. By using a novel class of drug — one that augments the normal function of the receptor — scientists could boost function of this ‘balancing’ M4 muscarinic receptor. This novel compound or drug lead was developed by the group of Jeffrey Conn at Vanderbilt University in Nashville, Tennessee.
While all of the studies in Surmeier’s lab and that of his collaborator Dr. Angela Cenci Nilsson of Lund University in Sweden, were conducted in mice, scientists wanted to make sure they were relevant to humans. To test the effects in non-human primates, Dr. Erwan Bezard’s group in Bordeaux, France, gave a variant of the compound tested in mice to Parkinsonian primates. As in the mice, the novel compound significantly reduced dyskinesia induced by levodopa treatment without compromising its symptomatic benefit.
Other authors of the study are Dr. Paul Greengard, a Nobel laureate at The Rockefeller University, Dr. Richard Neubig of Michigan State University and Jurgen Wess of the National Institutes of Health. Other Northwestern co-authors include Weixing Shen, Joshua L. Plotkin and Zhong Xie.
The article is titled: “M4 muscarinic receptor signaling ameliorates striatal plasticity deficits in models of L-DOPA-induced dyskinesia.”
by Marla Paul