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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.

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Thank you for visiting!

Saturday, March 5, 2016

Holistic clinic used by the Royals is probed over 'dangerous' ads which claim its natural therapies can cure MS and Parkinson's

Hale Clinic in London boasts 'widest range of holistic treatments in Europe'

  • Its clients have included the late Princess Diana and the Duchess of Cornwall
  • Advertising Standards Authority looking at 'misleading' claims made by clinic
  • It claimed one type of massage 'can be of great assistance… after a stroke'
  • Also said 'the Hale Approach' has potential to cure people of multiple sclerosis and Parkinson's disease

A natural health clinic whose clients include members of the Royal Family has been slammed for making 'potentially dangerous' claims about its alternative therapies.

The Hale Clinic in West London was opened by Prince Charles in 1988 and boasts that it has 'the widest range of holistic treatments in Europe'.
Princess Diana and the Duchess of Cornwall have visited the clinic, while Kate Middleton was given a 'bee sting facial' by one of its beauty therapists, Deborah Mitchell, shortly before her marriage to Prince William.
But the Advertising Standards Authority is now taking a close look at what scientists say are 'misleading' claims by the clinic on its website that its treatments can help combat a variety of serious illnesses. 

However, many of those claims were removed after The Mail on Sunday contacted the clinic.

The Good Thinking Society, which aims to crack down on 'quack' medicine, has presented a dossier to the ASA about assertions made by the clinic, which has also treated celebrities such as Kylie Minogue and Simon Cowell.

The report accuses the clinic of claiming that 'the Hale Approach' has the potential to cure people of the savage neurodegenerative disease multiple sclerosis and Parkinson's disease sufferers should use 'complementary treatments' as they are 'far more likely to be beneficial than orthodox drugs'.

Read more:

Friday, March 4, 2016

Sheer willpower: 5 inspiring people defying Parkinson’s disease

Author: Parkinson's Life editorsPublished: 3 March 2016

Playing guitar while under the knife, winning body building competitions and making 90,000 glass beads for a massive mosaic mural – watch these five inspiring people living with Parkinson’s disease achieve amazing things.

The Bodybuilder
In 2011 Malcolm Nordaby, a 51-year-old body builder from Colorado, entered a ‘master’ bodybuilding show. When he entered the competition he’d been living with Parkinson’s disease for 23 years. He wrote: “I think that working out is a large reason that my disease has progressed so slow.”

Living with Parkinson’s disease doesn’t have to mean limitations on life; these five people have overcome the condition to fulfil their goals and have inspired others along the way

The Concert Pianist
Here’s a video of 82-year-old Lucien Leinfelder, a retired concert pianist, who in 2015 was still able to play great piano concerts due to unfaltering muscle memory in his fingers – despite advancing Parkinson’s disease. 
See him on You tube:

The Artist
US-based artist, Richard Herdegen, spent 18 months creating a 12-panel mosaic mural from 90,000 tiny pieces of glass, which he painstakingly handcrafted himself. Most of the time his Parkinson’s symptoms are mild enough for him to safely operate the welding equipment.
However, when his symptoms are more exaggerated due to fatigue, stress, or tension, it’s a different story. His right side shakes when his tremors begin, and managing the welding equipment and working with hot glass can get “wild”.
“It caused me to step on the gas,” Richard said. “You never know how much time you’ll have to work on your craft.”
See it on You Tube:

The Actor
Actor and musician Brad Carter plays his guitar while undergoing deep brain stimulation surgery. Brad was awake for the surgery in 2013 so that doctors could monitor his dexterity and pinpoint the ideal location to place the electrodes.
video: the clip 

The Athletic Champion

Ruth Wilson is a duathlete and paratriathlete for Team GB. Despite being diagnosed with Parkinson’s disease six years ago, she has competed on the international stage against able-bodied athletes.

Ruth, was crowned the national PT4 paratriathlon champion in 2015 and holds the course record at Mallory Park in the UK. All this from someone who couldn’t even swim or ride a bike before she took up the sport!

A treatment for Parkinson’s disease reveals a brain switch for sadness

The patient’s facial expressions revealed her roller-coast of emotions as an electrical pulse fired into her brain triggered symptoms of depression. When the electrical pulse was turned off, her despair subsided. (The New England Journal of Medicine ©1999)

Surgeons snaked the electrodes under the 65-year-old woman’s scalp. Thirty years of Parkinson’s disease had almost frozen her limbs. The wires, connected to a kind of pacemaker under the skin, were aimed at decreasing the woman’s rigidity and allowing for more fluid movement.
But five seconds after the first electrical pulse was fired into her brain, something else happened. Although awake and fully alert, she seemed to plunge into sadness, bowing her head and sobbing.
One of the doctors asked what was wrong.“I no longer wish to live, to see anything, to hear anything, feel anything,” she said.
Was she in some kind of pain? “No, I’m fed up with life. I’ve had enough,” she replied. “Everything is useless.”
The operating team turned off the current. Less than 90 seconds later, the woman was smiling and joking, even acting slightly manic. Another five minutes more, and her normal mood returned.
The patient had no history of depression. Yet in those few minutes after the electrical pulse was fired, the despair she expressed met nine of the 11 criteria for severe major depressive disorder in the Diagnostic and Statistical Manual of Mental Disorders.Fascinated by the anomaly, the French physicians wrote up the episode for the New England Journal of Medicine. The year was 1999, and hers was one of the first documented cases of an electrically induced, instantaneous, yet reversible depression. 
Additional testing was done, including a brain scan eight months later during which the same procedure was repeated. And again, when the pulse was on, the woman said she felt as though she was being sucked into a black hole.
The scan revealed a significant increase in blood flow in several brain areas, including the left frontal cortex. The precise contact area of the electrode could not be determined, but it was located in the mid-brain’s basal ganglia, which controls some limb movement and is connected to other structures implicated in unpleasant feelings.
The fact that doctors had inadvertently found a source of symptoms for one of the most pernicious of psychological maladies — and in a bit of gray matter no larger than the head of a pin — prompted a singularly bizarre question:
Why would depression, which is responsible for so much misery in the world, be hard-wired into the brain?
Two psychiatric researchers think they have an answer. Charles Raison at the University of Arizona and Andrew H. Miller at Emory University in Atlanta think depression once had an evolutionary, adaptive purpose for our primitive ancestors. 
For millennia, one of the world’s leading causes of death was infection. The body’s natural counter to infection includes a number of genetic mutations that rachet up the immune system. Researchers now know that one of those altered genes, known as NPY, is linked to major depression.
Why would the body need to leverage depression to fight off infection? In a 2012 study, Raison and Miller contended that symptoms of depression such as social withdrawal and apathy played to the advantage of ancient humans for two important reasons: Keeping still helped their bodies fight infection, and social isolation helped prevent the spread of contagious germs.
There is no direct evidence for this theory. There are, however, additional cases of Parkinson’s patients undergoing pallidotomy (the placement of electrodes in the mid-brain’s globus pallidus, which plays a role in movement and coordination) who have also experienced instantaneous depression. Likewise, stimulation of other areas of the basal ganglia have induced spontaneous laughter in others.
Perhaps the question the French doctors needed to consider wasn’t whether they had turned on depression in their patient, but whether they had turned off happiness.
Pulitzer Prize-winning reporter Amy Ellis Nutt covers health and science for The Washington Post.

'Embracing Elderhood' event to focus on effects of aging

 Thursday, 03 March
Written by Cliff Newell

Experts will offer tips for caregivers and people living with Parkinson's disease or  dementia


Lake Oswego’s Adult Community Center will shed new light on the aging process March 13 with a special program called “Embracing Elderhood.” 
The event, which is scheduled from 1-4 p.m., will feature two of the top experts in their fields: Tony Borcich of Parkinson’s Resources of Oregon will offer hope to caregivers of people living with Parkinson’s disease and other dementia-related illnesses, while Dr. Meagan Lawler of Marylhurst University will talk about how often the common wisdom about aging is simply wrong. 
“Contrary to popular belief, mental ability does not decline as you grow older,” Lawler says. “There is a great misconception about this. The brain changes, but it doesn’t decline until you reach your 80s. Your mind becomes richer, deeper and your judgment improves. Your speed lessens, but the other things improve.” 
That should come as great news to members of the rapidly aging baby boomer generation, many of whom struggle with the effects of getting older. 
“You should not worry so much about forgetting things,” Lawler says. “It’s because you have more information files to check. Instead of declining, you are becoming more of what you are.” 
Julie Ouellette, owner of NW Senior Resources of Lake Oswego, agrees. Her organization is co-sponsoring the March 13 event. 
“It’s easy to say I’m losing it, but you’re really not,” Ouellette says. “You may lose speed, but you gain wisdom.” 
Berta Dermann, the Adult Community Center’s programming director, says that’s one of the key messages of the “Embracing Elderhood” seminar — that “there are positive contributions that older people can make to society.” 
Lawler says she believes elderhood can actually be a healing force in society. 
“The impact, we hope, will be a less impatient, less reactionary society,” Lawler says. “Maybe we can become a more tolerant society.”

Borcich’s presentation will focus on the caregivers who help people living with Parkinson’s disease and dementia-related illnesses. These folks are often in danger of losing their own mental and physical health, but Borcich says it doesn’t have to be that way. 
“This program will be for everyone touched by this disease,” the veteran social worker says. “Stress on caregivers can be quite high as Parkinson’s disease progress. People who suffer from it become more physically challenged and have mental symptoms like dementia, anxiety and depression.” 
Because of this, Borcich says caregivers must pay attention to their own needs, and 
they should not feel guilty about it. 
“I’ll talk about mindfulness,” Borcich says. “Caregivers need it to alleviate their own depression. There can be a lot of guilt when we pursue a bit of our own lives.” 
Borcich has been talking about this topic for three years. “I’ve done previous programs with Nancy (Raske, former NW Senior Resources owner) and Julie,” he says. “I’ve had good attendance and have gotten a lot of good feedback.” 
Admission to “Embracing Elderhood” is free and refreshments will be served, but reservations are required. For more information, call 503 635-3758. The Adult Community Center located at 505 G Ave. in Lake Oswego. 

Contact Cliff Newell at 503-636-1281 ext. 105 or

Table tennis offers Parkinson’s patients physical, mental challenge

Pingpong night is part of growing menu of activities for Central Oregon Parkinson’s patients

By Kathleen McLaughlin / The Bulletin 
Published Mar 3, 2016 
Stiff-limbed from Parkinson’s disease, Jim Brougher gets help taking off his coat from his wife, Jan, as the couple prepare to play pingpong with fellow patients at the Boys & Girls Club of Bend gym. 
A former windsurfer, kayaker, swimmer and runner, the 83-year-old’s athletic nature still shows. He’s notorious in the Parkinson’s group for a quick, low-flying serve that’s difficult to return. While the Parkinson’s patients aren’t as nimble as the rest of the Bend Table Tennis Club players who fill out the gym on Monday nights, they say they benefit from the sport, which is popular because it requires physical and mental agility. 
When the Broughers joined the group last year, Jim needed to use the elevator to reach the second-floor gym. Now he’s taking the stairs. While the reversal of his physical ability is unusual, a growing body of research suggests exercise can at least help Parkinson’s patients manage the progressive physical and cognitive decline associated with the disease. 
“People are working very hard at keeping themselves as capable as they can for as long as they can,” said Margie Lussier, a Bend patient who started the twice-monthly pingpong night a year ago. “It seems to work.” 
Parkinson’s affects about 1 million Americans, and it’s the second-most common neurodegenerative disease, behind Alzheimer’s, according to the Parkinson Foundation. While patients and their advocates widely believe that exercise counters the physical and cognitive effects of the disease, whether it actually delays the progression remains unproven. Parkinson’s patients are sometimes ahead of the medical community in seeking out new ways to stimulate their bodies and minds, and that’s true in Central Oregon. Pingpong is one of several activities that Lussier and other patients have worked to make available over the last few years.The lineup of specially tailored classes now includes tai chi, dance and Pilates. Starting in March, a speech-language pathologist will offer a group communication skills class for people who want to keep up their speech therapy work. Parkinson’s affects the muscles of the throat, so patients often experience a softening of their voices and trouble swallowing. 
A personal trainer will offer high-intensity group exercise for patients who aren’t severely affected by the disease. Both of the new classes are sponsored by Parkinson’s Resources of Oregon in Portland, which has helped local instructors get certification. 
Lussier said starting pingpong was simply a matter of reaching out to table tennis club president Don Borne, who embraced the idea and reserves two tables every other Monday for the Parkinson’s group. 
Pingpong is one of the rare activities that patients and their families can do together, said Lussier’s husband, Jim Lussier. He and other spouses and relatives join in for rounds of doubles. 
The social element is important because depression is a common symptom of the disease, which causes a loss of dopamine-producing brain cells, Margie Lussier said. 
Jan Brougher said all physical activity seems to be helping her husband. The Broughers moved to Bend last year from California to be near their daughter, and they’re enjoying pingpong because it’s also a chance to socialize, Jan said. “Being new to the community and not knowing a whole lot of people, it’s wonderful to be with them,” she said. 
Recent research has tried to measure the benefits of specific activities, including tai chi, yoga, dance, resistance training and even boxing-style training. The idea behind all of it is to encourage neuroplasticity, which means the brain creates new connections between neurons to compensate for deficits elsewhere. 
It’s unclear whether the benefits of exercise are lasting or temporary. A literature review published in the journal Neurology in 2011 concluded that data published so far failed to “prove that exercise slows Parkinson’s disease progression, but a neuroprotective effect is certainly plausible if not compelling.” The study’s author, Mayo Clinic neurologist J. Eric Ahlskog, said doctors should encourage ongoing, vigorous exercise, defined as anything sufficient to raise heart rate and oxygen needs for 20 to 30 minutes at a time, and make sure it’s incorporated into physical therapy plans. He also urged doctors to use medication to maximize their patients’ capacity for exercise. 
Anecdotally, patients know they feel better if they stay active, said Holly Chaimov, executive director of Parkinson’s Resources of Oregon. It’s been difficult for doctors to recommend a specific course of activity because until about six years ago, scientific evidence was limited, she said. 
The American Academy of Neurology updated its guidelines on alternative therapy for Parkinson’s in 2013 to reaffirm that “no treatment has been shown to be neuroprotective,” and “exercise may be helpful in improving motor function.” 
The academy also said rigorous studies are needed in this area. 
In practice, Bend Memorial Clinic neurologist Steve Goins said he’s telling Parkinson’s patients they need to get 2½ hours of exercise a week on a regular, consistent basis. “We know that it improves balance, decreases falls and wards off depression,” he said. 
Medicine has taken a similar turn on Parkinson’s support groups, Chaimov said. Doctors used to think witnessing later stages of the disease would depress patients, but that’s no longer the case, she said. 
Central Oregon has seen the number of local support groups grow from one to three, including one just for Parkinson’s caregivers. As with the exercise classes, the growth in support groups is the result of advocacy by the Central Oregon Parkinson’s Council, Chaimov said. 
Parkinson’s Resources helped pay for local dance instructor Julie Carda to travel to New York City last year for training in Dance for PD, a program developed in collaboration with the Mark Morris Dance Group. The class uses various choreography styles and is adapted to accommodate people at any level of physical ability, from walking to wheelchair, she said. 
Carda said the class, held at First Presbyterian Church in Bend, has been a hit because it goes beyond exercise. There’s imagery, awareness of the body in time and space, rhythm and joy, Carda said. Those things help people forget about the fact they need to keep moving, which is hard enough when you’re not dealing with a loss of motor function, balance or tremors, she said. 
“We want them to show up for dance class because it’s exciting. Their brain is going to get stimulated, and their best friend is there, and they’re going to see them today.” 
Parkinson’s is a fairly recent diagnosis for George Lee, a retired police officer from Seattle. Hearing the news from a Bend neurologist last April, the 64-year-old was at first relieved to have an answer for the depression, anxiety, muscle soreness, tremor and memory problems that bothered him over the last two years. At the same time he’s facing a long-term progressively degenerative disease. Activities with other Parkinson’s patients have helped him come to terms with it. He goes to tai chi, and he dived into pingpong, which he played during his 24 years in the Army. “I thought I was good,” he said, but he found out, “I wasn’t as good as I thought I was.” 
Lee plays both with Parkinson’s patients and with the table tennis club members. He’s even taken some lessons from Borne, the club president. A friend of his is also in the table tennis club, so they play when they get together. 
“It’s really helped me to sort of get back into society,” Lee said. 
— Reporter:, 541-617-7860

Understanding Metabolic Changes in Parkinson’s Disease Could Lead to New Treatments

March 3, 2016
Alisa G. Woods, Ph.D., 

Novel research could advance the basic understanding of the genetic causes behind Parkinson’s disease (PD). Researchers have examined the defective DJ1 (PARK7) gene, which controls cellular metabolism and may play a role in Parkinson’s, and their report, Loss of DJ-1 impairs antioxidant response by altered glutamine and serine metabolism, appeared in the journal Neurobiology of Disease.
Parkinson’s disease is caused by a loss of dopamine-producing cells in the substantia nigra, a brain region that controls the start and stopping of movement. People with Parkinson’s develop problems with movement such as freezing, gait problems, tremors, and rigidity. Dopamine cell loss might be caused by a process known as oxidative stress during which cells produce harmful free radicals faster than the body can remove them. This can cause cell death in the nervous system.
Researchers have found that mutations in the DJ-1 gene, coding for a molecule that prevents oxidative stress, can increase the risk of developing Parkinson’s. The current study sought to further understand how DJ-1 can affect cells and possibly play a role in the development of this disease.
The research team, led by Dr. Johannes Meiser of Luxembourg Centre for Systems Biomedicine at the University of Luxembourg, grew mouse neurons in vitro (in the lab) that specifically lacked the DJ gene. They found that the cells could not make crucial amino acids that are necessary to prevent oxidative stress. The neurons did not take up the glutamine that is needed for the synthesis of both the neurotransmitter glutamate, as well as the amino acid serine. Disruptions in this pathway affected antioxidant production as well.
“Without DJ1, neurons cannot absorb enough glutamine and this affects serine production,” Meiser said in a news release. “Both amino acids are important for producing glutathione, which is used to neutralize free radicals. In the absence of DJ1, this defense mechanism does not work effectively and oxidative stress occurs. This prematurely ages the cells.”
According to the scientists, the microglia — the immune system cells of the brain — seemed to contribute to this oxidative stress. Taken together, all of these effects could explain how Parkinson’s-induced cell death occurs.
The investigators plan to further study how these findings might be used to develop treatments for Parkinson’s disease. Specifically, if the observed changes in glutamine and serine can be altered, it could provide a target for Parkinson’s medications. Also, targeting oxidative stress could be another avenue for potential therapies.
Image credit: University of Luxembourg

New deep brain stimulation improves symptoms in Tourette's patients

March 4, 2016

Specifically-targeted deep brain stimulation improves symptoms in patients with severe Tourette's, a study reports in the current issue of Biological Psychiatry.
Gilles de la Tourette syndrome, often just called Tourette's, is best known for the vocal and motor tics that are the most common symptoms of the disorder. Usually, these symptoms respond to a growing array of medications. However, some patients experience severe tics that do not respond to medications and may be disabling or even life-threatening. In these rare cases, deep brain stimulation may provide relief.
Deep brain stimulation is a neurosurgical technique that involves implanting a neurostimulator into the brain to deliver electrical signals. It is most commonly used to treat symptoms of Parkinson's disease and other movement disorders. It was first used an experimental treatment for severe Tourette's in 1999 and has since shown therapeutic promise, but the optimal neural targets have remained unclear.

For this study, researchers at the University of Cologne conducted an open-label trial to treat eight patients with severe Tourette syndrome for whom medication was not beneficial.
Over a one year period, deep brain stimulation targeted at the thalamus significantly improved patients' Tourette-related symptoms, quality of life, and overall functioning. It was also generally well-tolerated. The thalamus is a complex structure deep in the brain that relays sensory and motor signals and is part of the brain network responsible for motor control.
"Tourette syndrome is most commonly associated with the basal ganglia, but the thalamus receives the output from the basal ganglia. It appears that stimulating the thalamus may be helpful when medications have failed," commented Dr. John Krystal, Editor of Biological Psychiatry. "This study suggests that when the basal ganglia are dysfunctional, that one may intervene by altering the activity of a target of the basal ganglia output, such as the thalamus."
Although more research is still necessary, these findings suggest that, despite the risks, thalamic deep brain stimulation may be beneficial for patients with severe Tourette's.


Thursday, March 3, 2016

Tracking the onset of Alzheimer's

March 3, 2016
PET scans can be used to diagnose a health condition, as well as for finding out how an existing condition is developing. PET scans are often used to see how effective an ongoing treatment is.

New research led by scientists at the University of California, Berkeley, shows for the first time that PET scans can track the progressive stages of Alzheimer's disease in cognitively normal adults, a key advance in the early diagnosis and staging of the neurodegenerative disorder.
In the process, the scientists also obtained important clues about two Alzheimer's-linked proteins - tau and beta-amyloid - and how they relate to each other.
The findings, to be published March 2 in the journal Neuron, come from positron emission tomography (PET) of 53 adults. Five were young adults aged 20-26, 33 were cognitively healthy adults aged 64-90, and 15 were patients aged 53-77 who had been diagnosed with probable Alzheimer's dementia.
The stages of tau deposition were established by German researchers Heiko and Eva Braak through postmortem analysis of the brains of suspected Alzheimer's patients.
"Braak staging was developed through data obtained from autopsies, but our study is the first to show the staging in people who are not only alive, but who have no signs of cognitive impairment," said study principal investigator Dr. William Jagust, a professor at UC Berkeley's School of Public Health and at the Helen Wills Neuroscience Institute and a faculty scientist at Lawrence Berkeley National Laboratory. "This opens the door to the use of PET scans as a diagnostic and staging tool."
PET scans are used to detect early signs of disease by looking at cellular-level changes in organs and tissue. The results of the scans in this study paralleled Braak neuropathological stages, which range from 1 to 6, describing the degree of tau protein accumulation in the brain.
Jagust worked with study co-lead authors Michael Schöll, a visiting scholar, and Samuel Lockhart, a postdoctoral fellow, both at UC Berkeley's Helen Wills Neuroscience Institute.

Tau vs. amyloid

Their findings also shed light on the nature of tau and amyloid protein deposits in the aging brain. For many years, the accumulation of beta amyloid plaques was considered the primary culprit in Alzheimer's disease. Over the past decade, however, tau, a microtubule protein important in maintaining the structure of neurons, has emerged as a major player. When the tau protein gets tangled and twisted, its ability to support synaptic connections becomes impaired.
While a number of symptoms exist that signal Alzheimer's disease, a definitive diagnosis has been possible only through an examination of the brain after the patient has died. The availability of amyloid imaging for the past decade has improved this situation, but how Alzheimer's developed as a result of amyloid remains a mystery. Studies done in autopsies linked the development of symptoms to the deposition of the tau protein.
Through the PET scans, the researchers confirmed that with advancing age, tau protein accumulated in the medial temporal lobe - home to the hippocampus and the memory center of the brain.
"Tau is basically present in almost every aging brain," said Schöll, who holds an appointment at Sweden's University of Gothenburg. "Very few old people have no tau. In our case, it seems like the accumulation of tau in the medial temporal lobe was independent of amyloid and driven by age."
The study revealed that higher levels of tau in the medial temporal lobe were associated with greater declines in episodic memory, the type of memory used to code new information. The researchers tested episodic memory by asking subjects to recall a list of words viewed 20 minutes earlier.

Both proteins involved in dementia

One question yet to be answered is why so many people who have tau in their medial temporal lobe never go on to develop Alzheimer's. Likewise, adults may have beta amyloid in their brains and still be cognitively healthy.
"It's not that one is more important than the other," said Lockhart. "Our study suggests that they may work together in the progression of Alzheimer's."
While higher levels of tau in the medial temporal lobe were linked to more problems with episodic memory, it was when tau spread outside this region to other parts of the brain, such as the neocortex, that researchers saw more serious declines in global cognitive function. Significantly, they found that tau's spread outside the medial temporal lobe was connected to the presence of amyloid plaques in the brain.
"Amyloid may somehow facilitate the spread of tau, or tau may initiate the deposition of amyloid. We don't know. We can't answer that at this point," said Jagust. "All I can say is that when amyloid starts to show up, we start to see tau in other parts of the brain, and that is when real problems begin. We think that may be the beginning of symptomatic Alzheimer's disease."
What the study does indicate, the researchers said, is that tau imaging could become an important tool in helping to develop therapeutic approaches that target the correct protein - either amyloid or tau - depending on the disease stage.

Apple Inc.’s ResearchKit Enables iPhone Parkinson’s Disease Study Plus 6 months Study Released by Sage


Apple's ResearchKit enables medical researchers to develop clinical studies that can
reach millions of iPhone users who choose to get involved with the research efforts.
Pictured: Apple's Jeff Williams, March 9, 2015.

Can the iPhone cure disease? That’s the hope behind a landmark study of Parkinson’s disease released Thursday that used Apple’s iPhone to track the progression of the disease among 9,500 people — without the researchers ever seeing a patient in person.
The study, conducted by nonprofit medical research group Sage Bionetworks and Rochester Medical Center with support from the Robert Wood Johnson Foundation, is one of the first big applications of Apple’s ResearchKit, a set of software applications that allows the iPhone to be tool for medical research. 
Participants in the study volunteered to download an app and perform daily tasks that measured dexterity, short-term memory, balance and even speech, all performed with the help of the iPhone’s built-in sensors, such as its accelerometer, microphone and touchscreen. The result is a data set that includes millions of information points gathered over a six-month period beginning last March. 

Short-term spatial memory can be measured via activities performed in the mPower app.

“If you can track an individual on a day-by-day basis, you can see variations in symptoms of 20 to 40 percent even though you only saw a small percentage change over a six-month period,” said Dr. Stephen Friend, president of Sage Bionetworks.
Sage made its findings available widely Thursday to researchers studying the disease and detailed the scale of the project in review journal Nature Scientific Data. For researchers studying Parkinson’s disease, gathering as much data as possible is important in understanding how to treat the symptoms, which afflict 7 million to 10 million people worldwide, causing tremors, speech problems, memory issues and ultimately death.
Motor functions such as tapping speed can be measured via the mPower app.

The study is notable for its size. Traditionally this kind of medical research is done locally in groups that consist of 20 patients on average who travel to a hospital or other physical sites. The iPhone data set, made possible by Sage’s mPower app, includes millions of information points gathered from participants who downloaded the app. 

In a preliminary examination of the data, Sage also spotted some patterns between medication intake and symptoms in participants, which eventually could be used by researchers to find better ways to treat the disease.

By using the iPhone's accelerometer, Sage Bionetworks can measure the balance of a research study participants

Performing a study via an iPhone without any direct human researcher action also poses the dilemma of dealing with occasional participants who sign up and claim they have Parkinson’s even if they do not. But with more than 9,000 participants, it’s much easier for researchers to spot the symptoms common to patients suffering with the disease and those who aren’t affected. Furthermore, the research study wasn’t limited to those with Parkinson’s. Some users were part of a control group.
Participants were also asked whether they wanted to share the data only with Sage Bionetworks or whether to make their data more widely available to third-party researchers. To protect the anonymity of participants, Sage kept their emails and names encrypted and separate from the research data.
While that may be a plus for privacy-minded users, it also prevents researchers from speaking to individual patients for additional feedback. Despite the limitation, it does have its advantages — namely, a larger amount of data that can be gathered on a daily basis via the iPhone app whereas an in-person study would yield results on a monthly or six-month basis through a smaller group of participants.
But with such a large data set available to researchers also comes concerns about privacy. “Even if a researcher has deidentified a health data set, it can be reidentified,” said Pam Dixon, founder of the World Privacy Forum. “It’s kind of a fake promise. You have to add other rules to protect people.”
That said, the responsibility mainly falls on the researchers themselves since Apple only provides ResearchKit to help developers and researchers build out these studies. None of that data is stored in its servers.
“ResearchKit is a perfectly good system in terms of privacy because Apple doesn’t see the data in it,” said Dr. Adrian Gropper, chief technology officer of patient privacy rights. “Apple has the best privacy policy you can have. Apple will not see your data.”
While the study is making the data available for research use, it’s not as easy as just hitting a download button. Researchers interested in the full data set and results are required to sign up for Sage Bionetworks’ Synapse service, have their accounts validated by the Synapse compliance team, submit a statement declaring their intended use of the data and agree to the terms of use for each data set. Researchers who accept the terms agree not to attempt to reidentify research participant data for any reason or use it for commercial purposes. Ethical oversight of the study was obtained from the Western Institutional Review Board.
Researchers using the iPhone in their studies include Mount Sinai, the Dana-Farber Cancer Institute and Stanford Medicine, among others. In addition to Parkinson's disease, the studies conducted also examine autism, epilepsy, melanoma, asthma, diabetes, breast cancer and heart disease.

While Sage's Friend sees ResearchKit as a powerful tool for researchers, he also says it’s

 just getting started. “I think this is the pre-Model-T,” Friend said. “We’re not driving around in 

a Tesla right now. But we’re going that way.”By Aditi Pai 02, 2016