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Saturday, December 12, 2015

Alaska artist's graphic novel about Parkinson's disease part of innovative series of medical texts


Mike Dunham

Singaporean students create device to help fight Parkinson's symptoms

Dec. 10, 2015

A group of students from the National University of Singapore has invented a device that helps prevent falls resulting from impaired walking associated with the disease.

This wearable device for people with Parkinson's Disease won the Intel Invent 50 competition this week.
One dangerous aspect of Parkinson's Disease is the impeded ability to walk, which causes people to fall and injure themselves. A team of Singaporean students is hoping to use technology to prevent such accidents.
PD Loggers, a group of three students at the National University of Singapore, has invented an Internet-connected device that tracks a person's movements, detects when the walking problem, known as freezing of gait, is about to kick in and then helps prevent a fall. This week, the invention won the Invent 50 competition, a Singapore-wide student tech-invention contest sponsored by electronics giant Intel
The device consists of three sensors, which are placed on each ankle and at the back of the neck, that work together to acquire data on a person's walking patterns. The team created an algorithm that runs on an Intel Edison chip and analyzes the wearer's gait cycle. When the device senses a fall is imminent, it vibrates vigorously to warn the person and applies biofeedback techniques to attempt to re-initiate movement.

Parkinson's Disease is caused by the deterioration of neurons, which hampers the movement of dopamine out of the brain. This leads to stuttering, impaired movement and other physical maladies. The affliction is incurable. According to the Parkinson's Disease Foundation, more than 10 million people around the world have the disease.
The student team took five months to develop the device and assert that it is nearly market-ready. For now, the group intends to continue R&D on the device. Winning the Invent 50 competition scored the team 10,000 Singapore dollars ( $7,000, AU$10,000, ‎£4,500) and internships with Intel.

http://health.einnews.com/article/301350249/T_HFNZreTyM_vlgi

Friday, December 11, 2015

6 Things I Wish People Knew About Being Chronically Ill During the Holidays


Most people would say the holiday season can be stressful, and when you are chronically ill, this time of year can offer added stress and exhaustion.
In the online communities I’m part of, I start to see the anxiety levels increasing with questions like, “How will I prepare a meal?” or “How do I get my house ready for guests?” 
This is a list for the chronically ill and their loved ones to help them not just survive the holiday season and family gatherings but to enjoy the celebrations as well. This is what we need our friends, family and the wider community to understand about our challenges during this time of year.
1.  We have to plan ahead carefully.
I’m sure many with chronic illnesses are like me: I have a careful plan whenever I leave the house, and I try to prepare for all contingencies. Going to family gatherings or parties requires even more planning. This may mean bringing medication, mobility aids and fluids with us. If we’re going to a friend or family member’s house, we may need to discuss our needs with the host or family members.
Many of us wish we could participate in holidays the way we used to, including cooking, decorating and hosting gatherings. To do these things, many of us have to prepare over a few days or weeks. If we try to do it all in one day, we won’t be able to enjoy ourselves or could end up bedridden.
If we have to travel, it’s important to have emergency supplies on hand with us. It’s important to prepare for the worst and hope for the best. Traveling is also extra taxing on the chronically ill, so it may require more time for rest. Each of us knows how much energy we have, so it’s important to conserve and use it judiciously. And we need understanding from others that rest is an essential part of managing an illness.
2. We may need to ask for your help.
During the holidays, it’s easy to set unrealistic expectations for ourselves, whether you’re healthy or chronically ill. If we know an activity will sink us, we may need to ask for your help. Maybe we’ll have to delegate cleaning or cooking. Maybe we’ll have to explain complex dietary needs. Asking for help is hard. Please understand when we ask for help, we’re not asking out of laziness or trying to seek attention. Asking for help is against my nature, but I’ve learned the hard way that when I didn’t ask for help when I should have, I ended up not succeeding.
We know more than anyone else what we’re capable of, so when we communicate our challenges, it’s a declaration of trust. We all need people in our lives who we can rely on when we’re facing challenges. This is especially true for those who live with illness.
3. We have to set realistic expectations.There can be so much pressure this time of year to create perfect memories with our family and friends. We want our house to look perfect. We want to have the perfect holiday dinner, the perfect party and the perfect gift wrapped in effortless ribbon and glitter. Who can do this? Our holiday doesn’t have to look like it was immaculately conceived in a Pinterest lab. Perfection isn’t realistic for anyone.
I believe it’s especially unrealistic for the chronically ill. It’s easy to ignore our own needs to maintain the appearance of functionality, but our self-preservation is of the utmost importance. We need our friends and family to help us enjoy this time of year without setting ourselves up for failure.
4. Include us in conversations at gatherings.
I often think about how I’m not sure what to say at gatherings. I’m not working, I usually only leave the house for appointments and I spend most of my time managing symptoms and rewatching “Downton Abbey” for the thousandth time. What do I have to discuss with anyone? Sometimes illness can be the elephant in the room when you’re with friends and family, but it doesn’t have to be a focal point. Although some with chronic illness don’t have a vibrant external life, this often strengthens a person’s internal life. We still have much to share.
It can be difficult not to feel sad or even resentful when we hear others discuss working, traveling or exciting social lives. These feelings can take us out of the present and make us feel worse about our quality of life. But I’ve found a lot of joy in just listening to others discuss what they’re doing and living through those experiences vicariously. I think illness has given me the gift of being a better listener and living more in the present. It has made me more compassionate as well. Even though we live on a different scale than most, we want to share ideas and thoughts or just enjoy listening. Include us in the conversation, because we would love to participate and share your company.
5. We have to celebrate on our own terms.
There are a variety of reasons someone with chronic illness has to spend the holiday alone or limit their holiday plans. Health issues can create rifts between family members, and just the sheer physical stress of traveling or going to gatherings is too much for some. I’ve seen some use their online health communities to celebrate with others and feel less alone this time of year.
Sometimes dietary restrictions or energy levels can make participating in gatherings challenging. If we can’t fully participate, please understand we need to celebrate on our own terms. When I go to a gathering, I make sure there’s a place for me to sit or lie down when I need to take breaks. Celebrating on our own terms means we can have a comfortable holiday without extra stress or pressure.
6. We need to celebrate in spite of our challenges.
Maybe the overwhelming stress of cooking a turkey, the sight of singing Santas or having to hear Paul McCartney’s “Wonderful Christmastime” one more time is putting you over the edge, but it’s easy to lose sight of the fact that this is a time of year for all of us to celebrate, reflect and feel gratitude. 
It’s easy to focus on what we have lost because of illness, but it’s also important to find something to celebrate, whether it’s spending time with friends and family, cheating by eating food we normally wouldn’t allow ourselves to eat or wearing something sparkly, even if we aren’t leaving our couch.
We need to have some fun and carve out some celebration and enjoyment for ourselves, because we’re seldom truly able to indulge. For many of us with illness, leaving the house and participating in a gathering can be a rare treat, and we often try to participate despite the toll it might take on our bodies. This time of year can make taking that risk worth it.
We are survivors and warriors, and this time of year is a reminder that we made it through another year of battling illness with dignity and grace. That, more than anything else, deserves celebration.
http://healthcurecorner.com/6-things-i-wish-people-knew-about-being-chronically-ill-during-the-holidays/

Cell-free circulating mtDNA identifies Parkinson's disease

Dec. 10, 2015

(HealthDay)—Cell-free circulating mitochondrial DNA (ccf-mtDNA) from cerebrospinal fluid (CSF) is reduced in patients with Parkinson's disease (PD), according to research published in the December issue of the Annals of Neurology.

Angela Pyle, Ph.D., from the University of Newcastle Upon Tyne in the United Kingdom, and colleagues examined whether ccf-mtDNA was an early indicator of PD pathology. Fifty-six CSF samples from patients with PD were selected with 10 age-matched asymptomatic control CSF samples.
The researchers observed a significant reduction in ccf-mtDNA in PD cases versus controls, when analyzing two mtDNA targets: MTND1 and MTDN4 copy number. In receiver operating characteristic curve analysis, MTND1- and MTND4-calculated ccf-mtDNA strongly predicted PD status (area under curve, 0.81 and 0.84, respectively). There was no significant correlation for ccf-mtDNA with CSF-tau, -phosphorylated tau, and -α-synuclein.
"Given the severity of the reduction in CSF ccf-mtDNA in PD, and supported by both subsequent measurement and remarkably similar data observed in Alzheimer's Disease, we conclude that ccf-mtDNA is a viable biomarker for the early detection of neurodegenerative disease," the authors write.
 Explore further: Study examines immunotherapy and cerebrospinal fluid biomarkers in patients with Alzheimer's The identification of cell-free circulating mitochondrial DNA (ccf-mtDNA) in early-stage Alzheimer's disease (AD) raised the possibility that the same neurodegenerative effect could be observed in Parkinson's disease (PD). Here, and for the first time, we investigated the role of ccf-mtDNA in PD, identifying a significant reduction of ccf-mtDNA in PD patient cerebrospinal fluid (CSF) when compared to controls. Our data demonstrates that CSF ccf-mtDNA is not only a powerful biomarker for PD, but, given that the effect is also observed in AD, is likely a biomarker for neurodegeneration. Ann Neurol 2015;78:1000–1004
http://medicalxpress.com/news/2015-12-cell-free-circulating-mtdna-parkinson-disease.html

In home health care for Parkinson's

In home health care can improve a clients quality of life.
Dec. 9, 2015

According to statistics, Parkinson’s disease affects more than a million people in the United States. Symptoms often appear after the age of 40 but some people are affected younger, most famously the actor Michael J. Fox. Around one percent of seniors over the age of 60 have Parkinson’s.
Parkinson’s, which currently has no cure, is caused when the brain stops producing sufficient dopamine. The lack of this chemical interferes with the body’s ability to control movement and gets progressively worse over time, although some recent treatments do show some promise.
Initial symptoms of Parkinson’s include shaking or tremors of a limb at rest, slow movement (bradykinesia), problems with balance and falling, and stiffness in the arms, legs or trunk. Secondary symptoms as Parkinson’s progresses include such things as dragging the foot on the affected side, freezing in place when walking, loss of facial expression, decreased automatic reflexes like blinking and swallowing, and a tendency to fall backwards.
When adults with Parkinson’s, particularly seniors, experience more severe difficulty with their mobility and a greater tendency to fall it may be wise to have Comfort Keepers home caregivers of Northern MI offer additional support to foster independence and offer respite to family members who have been providing primary care.
Many times the senior or adult with Parkinson’s feels happier at the thought of continuing to live at home, but needs some help with basic care. .
Comfort Keepers home care Northern MI services include:
Meal preparation
Assisting with personal care
Light housekeeping
Providing transportation
Medication management
Companionship
Respite care

Even if the home requires changes to accommodate devices such as lift chairs, bedside toilet or a wheelchair or safety devices such as handrails, these modifications are usually less expensive than moving to assisted living or nursing facilities. Although the biggest benefit is not the financial savings your family member or loved one can remain in their own home, keeping independence and having the ability to be active with the help of in home care. Families are often very pleased by the positive impact the companionship that home care can have on a client.
Hiring home care Northern MI through Comfort Keepers can help when family members need to work or be away from home, if the primary caregiver needs a break, or if the senior or family members want help with personal care.

http://www.examiner.com/article/in-home-health-care-for-parkinson-s

Apigenin transformed human stem cells into neurons in 25 days

Dec. 11, 2015
The team applied apigenin to human stem cells - cells that have the ability to develop into different cell types - in a laboratory dish. 

They found that after 25 days, these stem cells transformed into neurons - an effect the researchers say was not seen in the absence of apigenin.


The team found apigenin-treated neurons (right) developed stronger synapses than untreated neurons (left).
Image credit: Rehen et al.

What is more, the researchers found  the connections that developed between the newly formed neurons - known as synapses - were stronger and more sophisticated. "Strong connections between neurons are crucial for good brain function, memory consolidation and learning," notes Rehen.
Further investigation revealed that apigenin boosts neuron formation and connections by binding to estrogen receptors (ERs), which influences the development, progression, function and plasticity of the nervous system.
While studies have shown the hormone estrogen may delay development of Alzheimer's, schizophrenia, depression and Parkinson's, among other neurodegenerative conditions, Rehen and colleagues note the use of estrogen therapy is hampered by the risks of tumor growth and cardiovascular problems it poses.
However, the team says their findings suggest apigenin could offer a promising future treatment alternative for a number of neurodegenerative disorders.
"An alternative approach would be to mimic estrogenic-mediated positive effects by modulating specific ERs with other estrogenic compounds, such as some flavonoids classified as selective ER modulators (SERMs)," they explain.
In addition, Rehen says their study suggests the possibility of a simple brain-boosting strategy we can all adopt:

Flavonoids are present at high amounts in some foods and we can speculate that a diet rich in flavonoids may influence the formation of neurons and the
way they communicate within the brain."

http://www.medicalnewstoday.com/articles/303977.php?tw 

Signaling from dysfunctional mitochondria induces a distinct type of senescence

Finding provides alternative explanation for the free-radical theory of aging and suggests new role for mitochondria in affecting physiology.

 
Buck Institute faculty Judith Campisi, PhD, says age researchers need to stop thinking of cellular senescence, now accepted as an important driver of aging, as a single phenotype that stems from genotoxic stress. Research from her lab reveals that cellular senescence, a process whereby cells permanently lose the ability to divide, is also induced by signaling from dysfunctional mitochondria - and that the arrested cells secrete a distinctly different "stew" of biologically active factors in a process unrelated to the damaging free radicals that are created in mitochondria as part of oxygen metabolism. The results are published in Cell Metabolism.
"We don't yet know how much this process contributes to natural aging," said Campisi, adding that those studies are currently underway. "But we do think the findings are important in addressing mitochondrial diseases, and those age-related diseases, such as some forms of Parkinson's, which involve mitochondrial dysfunction."
The discovery was unexpected and was made by postdoctoral fellow Christopher Wiley, PhD, who (in collaboration with Eric Verdin, PhD, from the Gladstone Institute) was eliminating sirtuins, a class of proteins long linked to longevity, one by one in human cell cultures. "The senescent phenotype only occurred when we eliminated the mitochondrial sirtuins," said Wiley. In addition, Wiley saw that the senescent cells secreted a different SASP (senescence-associated secretory phenotype) than expected - one that lacks the IL-1-dependent inflammatory arm - a major factor in the SASP originally identified in the Campisi lab in 2008. The authors dubbed this new phenomenon MiDAS - mitochondrial dysfunction-associated senescence.
Along with identifying MiDAS, Wiley also found that mitochondrial dysfunction upset the balance of NAD+ (an enzyme that is a co-factor for sirtuins), which arrested cell growth and prevented the IL-1-associated SASP. "The NAD+ balancing act happens outside the mitochondria in the cytoplasm of the cell," said Wiley. "This really highlights a signaling role for mitochondria, something understudied in the context of disease. And it identifies a new type of SASP, underscoring the existence of different types of senescence."
Wiley also identified the MiDAS SASP in mice genetically engineered to develop progeria in response to mitochondrial mutations, which causes rapid aging. The MiDAS SASP suppressed adipogenesis, which plays a vital role in metabolism and the creation of fat cells. He says the work provides a link to lipodystrophy, a medical condition characterized by abnormal or degenerative conditions involving fat tissue, adding that early HIV drugs (which are still being used in third world countries) deplete mitochondrial DNA and that patients receiving the drugs often show a particular loss of subcutaneous fat, especially in their face.
"For any disease that has a mitochondrial component this research adds a potential explanation for the real driver of the dysfunction -- and it's not free radicals, which we ruled out in our study" said Campisi. "Our finding suggest a new role for mitochondria when it comes to affecting physiology."
http://www.medicalnewstoday.com/releases/303946.php?tw

How eating herbs could boost your brain


Written by  Fri 11 December 2015
Adding a sprig of thyme or a pinch of parsley to your next home-cooked meal may do more than boost its flavor - it could boost your brain, too. New research reveals how a substance present in such herbs - apigenin - triggers formation of human brain cells and boosts connections between them.

Researchers found the flavonoid apigenin - found in parsley, thyme and other plants and herbs - triggered the formation of human brain cells and strengthened their connections.
Lead author Stevens Rehen, of the D'Or Institute for Research and Education (IDOR) and the Federal University of Rio de Janeiro (UFRJ),and colleagues publish their findings in the journal Advances in Regenerative Biology.
The team says their findings suggest apigenin - also found in red pepper, chamomile and many other plants and herbs - shows promise as a treatment for numerous neurodegenerative disorders, including Alzheimer's diseaseParkinson's disease and schizophrenia.
Previous animal studies have shown that substances from the same flavonoid group as apigenin may benefit memory and learning, and other research has demonstrated that flavonoids have the potential to preserve and boost brain function.
For this latest study, Rehen and colleagues set out to gain a better understanding of how apigenin affects human brain cells, or neurons.
http://www.medicalnewstoday.com/articles/303977.php?tw