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. This is a free site for all.
Thank you.

Sunday, September 24, 2017

Tai Chi for Parkinson's

Tai Chi Practice for those with Parkinson's Disease.

Lesson One focuses on Balanced Opening Stance and Raise Arms with Breath.
Tai Chi Practice for those with Parkinson's Disease.
Lesson Two focuses on Centered Weight Shifts and Empty Leg Stepping.
Tai Chi Practice for those with Parkinson's Disease.
Lesson Three focuses on Brush Knee Twist Step Practice.
Tai Chi Practice for those with Parkinson's.
Lesson Four focuses on Splashing Hands and Tai Chi Boxing.

Seniors learn how to stay vertical this fall

September 23, 2017

It may have been the first day of fall, but those at Valley Presbyterian Church on Friday learned how to do exactly the opposite.
About 125 attended the lectures, a balance class and Tai Chi demonstrations as part of a three-hour program put on by Valley Assistance Services to teach and demonstrate of a variety of ways to avoid falling. The event was timed to coincide with National Fall Prevention Awareness Month.
Associate Professor Ruth Taylor-Piliae, from the University of Arizona's College of Nursing, spoke about fall risk factors. They include advanced age, a prior fall, muscle weakness, balance problems, poor vision, postural hypotension, fear of falling and chronic conditions including stroke, Parkinson’s disease and dementia.
Taylor-Piliae said one-third of adults 65 and older fall every year and less than half report it to their doctor.
Lunch was provided by Valley Galley, during which Donnie Poling from Tai Chi for Health demonstrated exercises that could be done from a sitting position.
Contact Green Valley freelance reporter Ellen Sussman at

AU neuroscientist’s Parkinson’s disease work showing results

 September 23, 2017  By Tom Corwin

For Joe Kelley and the CSRA Parkinson Support Group, their investment in the research of neuroscientist Bobby Thomas at Augusta University is paying off, not just in the millions of dollars in federal research money Thomas recently received, but in less tangible results.

My initial reaction is good, there’s another chance. There’s another chance that this will be resolved,” said Kelley, a Parkinson’s disease patient for 15 years and vice president of the support group.
Thomas was recently awarded a $1.9 million, five-year grant from the National Institutes of Health to explore ways of stimulating a hotly pursued pathway for regulating genes involved in antioxidants, molecules that reduce free radicals that can cause the oxidative stress, leading to the damage that causes Parkinson’s. Most of the current treatments for Parkinson’s seek to control the symptoms of the disease, such as tremors and balance problems.
Thomas is pursuing a strategy that seeks to protect and preserve the neurons whose slow loss leads to the disease. His research has always focused on a particular pathway, abbreviated as Nrf2, that has received a lot of attention not only from Parkinson’s researchers, but from others for its role as a master regulator of antioxidant response element genes.
Last year, Thomas was pursuing research on a drug used in multiple sclerosis called dimethyl fumarate that appeared to activate the Nrf2 pathway. Unfortunately, Thomas said, he discovered that it did that by modifying another important protein that is abbreviated as Keap, which targets unwanted proteins and gets rid of them through a “garbage disposal” mechanism in the cell.
Without it, “there will be a lot of unwanted proteins in the cell, they will accumulate and eventually it will damage the cell,” he said. “You don’t want to alter that function of the cell.”
While the Nrf2 mechanism has generated a lot of excitement, not just for Parkinson’s but for other diseases, that is a common problem researchers run up against, Thomas said.
“It is very well-known that this pathway is promising from a therapeutic standpoint,” he said. “But the challenge has been how to activate it in a safe manner.”
Clinical trials in the U.S. currently trying to target the mechanism are looking at, oddly enough, broccoli sprout extract or the chemical component of broccoli sprouts that appears to be active, known as sulforaphane, in chronic kidney disease or rheumatoid arthritis. Another one being studied is curcumin, which is found in the spice turmeric. Those approaches might activate the pathway, but they will likely run into the same problem, Thomas said.
“The challenge in the field has been that all activators of Nrf2 modify Keap,” Thomas said. “As part of this project, we are utilizing an alternate approach.”
His research is now focused on a protein called Bach, which normally sits on those antioxidant response genes and suppresses their activity. Blocking the activity of Bach allows Nrf2 to activate those genes, Thomas said. He is working with a company called vTv Therapeutics that already has a Bach inhibitor drug they are trying to develop. Interestingly, in mice bred to lack the Nrf2 gene, the Bach pathway still appears to work in activating the antioxidant genes, Thomas said.
“Targeting Bach may be a much more potent pathway to activate this (antioxidant) pathway,” he said. Because the company already has the inhibitor under development, if Thomas’ preclinical work in animal models shows promise “then the company plans to run clinical trials on patients,” he said.
That outcome is just what the support group hoped when it gave Thomas $10,000 to do the foundation of the work that led to the grant, Kelley said.
“Several of our recipients do that here at Augusta University, use our grant for proof of principle and then give the proof of principle to NIH for larger grant applications,” Kelley said, “because we can’t fund them fully.”

Support group
The CSRA Parkinson Support Group will hold its annual fundraiser walk on Oct. 7 at First Baptist Church of Augusta, 3500 Walton Way Extension. The event, called People of Parkinson’s Walk, will start at 9 a.m., with the walk beginning at 10 a.m. For more information go to

Saturday, September 23, 2017

Palliative Care: Keeping People with PD Comfortable

Palliative care is a specialized medical approach that improves the quality of life of patients and their families facing life-threatening illness. It aims to prevent and relieve suffering by identifying and assessing pain and other problems, including psychosocial and spiritual concerns, as well as physical ailments.
Palliative care grew out of the hospice movement in Great Britain in the 1960s, which continues today to provide care to patients who are terminally ill, generally within the last 6 months of life. But palliative care can be offered to people with serious but non-life-threatening illness, too, including those with Parkinson’s disease (PD). 

How does palliative care work?

The term comes from the Latin root palliare, to cloak or mask pain. As early as the time of diagnosis, a medical team can keep people comfortable, manage pain, and provide support and counseling. Palliative care is generally offered in a medical facility and often administered to complement traditional medical treatment.

Palliative Care in Parkinson’s disease

Palliative care decisions for those with Parkinson’s disease are not that different from those for people with other illnesses: reducing pain and receiving care in a supportive setting. The care team can assist in coordinating the best resources to address needs at each phase of the disease
For some people living with Parkinson’s disease, the non-motor symptoms can be even more severe than movement issues. More than half of people who have PD experience cognitive dysfunction, which means they could even lose their ability to make decisions for themselves or be cared for at home. This is where a palliative care plan can really make a difference for people living with Parkinson’s and for their families as well.

What do people want?

Cultural, religious, and age-related differences affect how people think about death. Not everyone discusses end-of-life issues with his spouse or partner, siblings, children, physician, or spiritual advisor. 
Death has become harder to talk about. Fewer people experience the process at the side of a loved one, family member, or close friend. Just 10% of Europeans over age 80 live with their families; half live alone. By 2020, 40% of Americans are expected to die alone in nursing homes.
End-of-life care is a surging field, especially among the baby boomer population. For anyone with a chronic disease, including those with PD, discussing treatment goals now and understanding wishes for desired degree of medical intervention later can all be part of a palliative care plan.

Writing down your wishes

Advance Directives are legal documents, such as living wills, that allow people to express their wishes for future medical care. A health care proxy allows an individual to name a representative who will make medical decisions for him if he is no longer able to do so on his own. These documents are often created when someone is healthy or first diagnosed. Keeping them handy and updated is important. Family, caregivers, and medical providers should have current copies. 
Sharing treatment goals through advance directives is an important step for people with PD. For those who may experience cognitive dysfunction, establishing advanced directives before this stage eliminates confusion and can help assure that their wishes are honored. Advance Directive forms vary by state and most are available online. Check with a health care provider or attorney to be sure you are accessing the right ones.

Talking to doctors

Today, people increasingly die from chronic disease and old age. Dying has become a medical experience. Death used to be an occasion where friends and family gathered. Today, a changing family structure and geographic dispersion likely contribute to many elderly dying alone or isolated. 
When asked, Americans prefer honesty from their health care providers, regardless of the prognosis. Yet, people have different goals for living with a chronic disease and facing the end of life. Selected concerns include: 
  • Family not financially burdened by their care (54%)
  • Wishes for medical care are followed (49%)
  • Having loved ones around them (48%)
  • Being at peace spiritually (46%)
  • Families not burdened by tough care decisions (44%)
  • Being comfortable and without pain (42%).
  • Living as long as possible (23%)
Providing care at the end of life, as at birth, is part of a journey. It can be made more comfortable. Starting a discussion about palliative care with a care team can provide support and minimize stress for the person who is ill and his loved ones.

Meditation For Beginners: 20 Practical Tips For Understanding The Mind

The most important habit I’ve formed in the last 10 years of forming habits is meditation. Hands down, bar none.

Meditation has helped me to form all my other habits, it’s helped me to become more peaceful, more focused, less worried about discomfort, more appreciative and attentive to everything in my life. I’m far from perfect, but it has helped me come a long way.
Probably most importantly, it has helped me understand my own mind. Before I started meditating, I never thought about what was going on inside my head — it would just happen, and I would follow its commands like an automaton. These days, all of that still happens, but more and more, I am aware of what’s going on. I can make a choice about whether to follow the commands. I understand myself better (not completely, but better), and that has given me increased flexibility and freedom.
So … I highly recommend this habit. And while I’m not saying it’s easy, you can start small and get better and better as you practice. Don’t expect to be good at first — that’s why it’s called “practice”!
These tips aren’t aimed at helping you to become an expert … they should help you get started and keep going. You don’t have to implement them all at once — try a few, come back to this article, try one or two more.
  1. Sit for just two minutes. This will seem ridiculously easy, to just meditate for two minutes. That’s perfect. Start with just two minutes a day for a week. If that goes well, increase by another two minutes and do that for a week. If all goes well, by increasing just a little at a time, you’ll be meditating for 10 minutes a day in the 2nd month, which is amazing! But start small first.
  2. Do it first thing each morning. It’s easy to say, “I’ll meditate every day,” but then forget to do it. Instead, set a reminder for every morning when you get up, and put a note that says “meditate” somewhere where you’ll see it.
  3. Don’t get caught up in the how — just do. Most people worry about where to sit, how to sit, what cushion to use … this is all nice, but it’s not that important to get started. Start just by sitting on a chair, or on your couch. Or on your bed. If you’re comfortable on the ground, sit cross-legged. It’s just for two minutes at first anyway, so just sit. Later you can worry about optimizing it so you’ll be comfortable for longer, but in the beginning it doesn’t matter much, just sit somewhere quiet and comfortable.
  4. Check in with how you’re feeling. As you first settle into your meditation session, simply check to see how you’re feeling. How does your body feel? What is the quality of your mind? Busy? Tired? Anxious? See whatever you’re bringing to this meditation session as completely OK.
  5. Count your breaths. Now that you’re settled in, turn your attention to your breath. Just place the attention on your breath as it comes in, and follow it through your nose all the way down to your lungs. Try counting “one” as you take in the first breath, then “two” as you breathe out. Repeat this to the count of 10, then start again at one.
  6. Come back when you wander. Your mind will wander. This is an almost absolute certainty. There’s no problem with that. When you notice your mind wandering, smile, and simply gently return to your breath. Count “one” again, and start over. You might feel a little frustration, but it’s perfectly OK to not stay focused, we all do it. This is the practice, and you won’t be good at it for a little while.
  7. Develop a loving attitude. When you notice thoughts and feelings arising during meditation, as they will, look at them with a friendly attitude. See them as friends, not intruders or enemies. They are a part of you, though not all of you. Be friendly and not harsh.
  8. Don’t worry too much that you’re doing it wrong. You will worry you’re doing it wrong. That’s OK, we all do. You’re not doing it wrong. There’s no perfect way to do it, just be happy you’re doing it.
  9. Don’t worry about clearing the mind. Lots of people think meditation is about clearing your mind, or stopping all thoughts. It’s not. This can sometimes happen, but it’s not the “goal” of meditation. If you have thoughts, that’s normal. We all do. Our brains are thought factories, and we can’t just shut them down. Instead, just try to practice focusing your attention, and practice some more when your mind wanders.
  10. Stay with whatever arises. When thoughts or feelings arise, and they will, you might try staying with them awhile. Yes, I know I said to return to the breath, but after you practice that for a week, you might also try staying with a thought or feeling that arises. We tend to want to avoid feelings like frustration, anger, anxiety … but an amazingly useful meditation practice is to stay with the feeling for awhile. Just stay, and be curious.
  11. Get to know yourself. This practice isn’t just about focusing your attention, it’s about learning how your mind works. What’s going on inside there? It’s murky, but by watching your mind wander, get frustrated, avoid difficult feelings … you can start to understand yourself.
  12. Become friends with yourself. As you get to know yourself, do it with a friendly attitude instead of one of criticism. You’re getting to know a friend. Smile and give yourself love.
  13. Do a body scan. Another thing you can do, once you become a little better at following your breath, is focus your attention on one body part at a time. Start at the soles of your feet — how do those feel? Slowly move to your toes, the tops of your feet, your ankles, all the way to the top of your head.
  14. Notice the light, sounds, energy. Another place to put your attention, again, after you’ve practice with your breath for at least a week, is the light all around you. Just keep your eyes on one spot, and notice the light in the room you’re in. Another day, just focus on noticing sounds. Another day, try to notice the energy in the room all around you (including light and sounds).
  15. Really commit yourself. Don’t just say, “Sure, I’ll try this for a couple days.” Really commit yourself to this. In your mind, be locked in, for at least a month.
  16. You can do it anywhere. If you’re traveling or something comes up in the morning, you can do meditation in your office. In the park. During your commute. As you walk somewhere. Sitting meditation is the best place to start, but in truth, you’re practicing for this kind of mindfulness in your entire life.
  17. Follow guided meditation. If it helps, you can try following guided meditations to start with. My wife is using Tara Brach’s guided meditations, and she finds them very helpful.
  18. Check in with friends. While I like meditating alone, you can do it with your spouse or child or a friend. Or just make a commitment with a friend to check in every morning after meditation. It might help you stick with it for longer.
  19. Find a community. Even better, find a community of people who are meditating and join them. This might be a Zen or Tibetan community near you (for example), where you go and meditate with them. Or find an online group and check in with them and ask questions, get support, encourage others. My Sea Change Program has a community like that.
  20. Smile when you’re done. When you’re finished with your two minutes, smile. Be grateful that you had this time to yourself, that you stuck with your commitment, that you showed yourself that you’re trustworthy, where you took the time to get to know yourself and make friends with yourself. That’s an amazing two minutes of your life.

Meditation isn’t always easy or even peaceful. But it has truly amazing benefits, and you can start today, and continue for the rest of your life.

FoxFeed Blog: Caregivers Are Impacted by Damaging Health Care Reform, Too

September 22, 2017

Blake, second on right, with his brothers and mother.

Guest blogger Blake Niver, 25, of Wasilla, Alaska, along with his brothers Grant, 28, and Bryce, 22, are caregivers to their mother who lives with Parkinson's. Blake shares his thoughts on the importance of affordable and accessible health care and how to get involved as an advocate for the Parkinson's community.
According to a study from the National Alliance for Caregiving and AARP, nearly 25 percent of all caregivers are millennials, ages 18 to 34. That's not the typical image that comes to mind of a caregiver, but it's the reality for my brothers and me.
My mother, Roberta, was 42 when she was diagnosed with Parkinson's disease. I was in the fourth grade and still remember the exact moment she told me as we drove home from school -- it's a conversation I'll never forget.
It took nearly a decade before my mother's symptoms progressed to the point that it affects her daily activities. Now at 59 years old, she is not able to take the photos she used to love capturing, but she's still working and counts herself lucky that her symptoms have progressed so slowly. However, as each year goes by, the financial and emotional toll looms larger and my brothers and I are concerned for what comes next.
My mother moved from our home state of Alaska and now lives in Minnesota with my brother Grant, a move prompted by access to more affordable health care premiums. She has insurance through her employer, but she might not be able to work for much longer. Soon, she will need to purchase private insurance and her pre-existing condition of Parkinson's could subject her to unsustainably high premiums that my brothers and I will have to help shoulder. Right now, my mother is having issues timing her medications. My fear is that in the near future, she won't be able to visit with a specialist who can help make adjustments to her daily therapies and subsequently, her quality of life will be severely diminished.
Just yesterday, I called Senator Lisa Murkowski's office to tell her to vote "no" on the latest version of damaging health care reform circulating in the Senate. There are a lot tougher conversations to have than calling your senator and sharing your story. I think about what it must have been like for my mother to tell her three young sons about her diagnosis, and I'm heartened to do all I can to help her and others in the Parkinson's community.
We talk openly as a family about the future and try to prepare as much as possible for the financial and emotional effects of my mother's progressing disease. My brothers and I never expected to take care of our mother in our 20s, and we hoped that when our mother needed help, we'd be in a much better financial situation to support her. That's why I feel compelled to do something now to stop legislation that could negatively affect my mother and my family for years to come.
Together, each of us can share our story of what it's like to live with Parkinson's or, in my case, to care for someone living with the disease. Make a phone call, send an email or share a tweet -- tell your representatives how this latest health care proposal will negatively impact our families. Let's open up conversations about the importance of affordable and accessible health care for everyone, especially for the Parkinson's community.

Restless Legs Syndrome

Restless legs syndrome (RLS) is a neurological movement disorder characterized by a compelling urge to move the legs usually accompanied by an uncomfortable and unpleasant sensations.
Symptoms begin or worsen during periods of rest or inactivity, are partially or totally relieved by movement, and are worse in the evening or at night. Despite being a common disorder, RLS is generally underdiagnosed. The prevalence of RLS in the general population is 5%–10%, making it the most common movement disorder.
Prevalence increases with advancing age and the condition is observed more frequently in women. Delayed sleep onset, multiple awakenings, and a reduction in sleep efficiency all contribute to significant sleep disturbance in these patients. RLS can be idiopathic and begin at any age, or secondary to conditions such as, iron deficiency, renal failure, neuropathy, and normal pregnancy.
Although the etiology of RLS is still unclear, evidence suggests that the symptoms result from central dopaminergic dysfunction. Although results should be interpreted with caution, brain-imaging studies have shown abnormal dopamine receptor binding and dopamine hypoactivity. Iron deficiency has also been implicated in the etiology of RLS.
Dopamine agonists and l-dopa have demonstrated efficacy in the management of RLS and in contrast, certain agents that block the dopaminergic system aggravate RLS symptoms. Other known treatments for RLS include gabapentin, benzopdiazepines, and opiates.

Contributed by Marcelo Merello, MD
Director, Neuroscience Department
Head Movement Disorders Section
Institute for Neurological Research Raul Carrea (FLENI)
Buenos Aires, Argentina

HomeFeatured Better Think Twice About Spice: Synthetic Cannabis’ Impact on Brain Health


Summary: A new study reports on the dangers of using synthetic cannabis products on a person’s brain and general health.

Source: University of Tsukuba.

Considering the recent irreversible spread of synthetic cannabinoids and their impact on human health, their data should serve as a public alert. image is credited to the DEA and is in the public domain.

Marijuana is the most commonly abused drug in the world, and the advent of synthetic cannabinoids creates additional challenges to the society because of their higher potency and ability to escape drug detection screenings. Scientists from Japanese sleep institute have a warning for the society about a danger coming from cannabinoid abuse.

Research led by Olga Malyshevskaya and Yoshihiro Urade of International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba, discovered that seizures, a life-threatening condition, can be induced by natural Δ9-tetrahydrocannabinol (Δ9-THC, main constituent of marijuana) or the synthetic cannabinoid JWH-018 (main component of synthetic blend “Spice”) in mice. This was demonstrated by continuous recording of animals’ electric brain activity (electroencephalogram, EEG), video and movement activity tracking. Based on their data they propose potential treatment in case of cannabinoid overdose with the cannabinoid-1-receptor (CB1R) specific antagonist (AM-251), because in their study pretreatment prevented cannabinoid-induced seizures.

“Our study is quite important because unaware of the particularly severe effect by those cannabinoids, people see marijuana as a soft drug, without dangerous health effects,” Malyshevskaya says. Use of synthetic cannabinoids and the associated complications in humans are on the rise and spreading all-over the world. People are synthesizing different variants of cannabinoids to evade regulatory agents, producing structures with minimal information on their pharmacology and potential harm.

Considering the recent irreversible spread of synthetic cannabinoids and their impact on human health, their data should serve as a public alert. It is critically important for health-care professionals and policy makers to be aware of the serious adverse effects, as shown in this report. Clinicians in the emergency departments should always suspect seizure activity in patients who have a history of cannabinoid intoxication. The number of clinical cases involving marijuana intoxication has been steadily increasing due to increase in cannabis potency over the last two decades.

Reflecting the scientific debate on the action of cannabinoids, there are numerous disputes regarding the legal status of marijuana. As several governments proceed with legalization for both medical and recreational use, there will always be public health concerns, as marijuana overdose often results in direct adverse reactions.
Source: Joseph Caputo – University of Tsukuba
Image Source: image is credited to the DEA and is in the public domain.
Original Research: Full open access research for “Natural (∆9-THC) and synthetic (JWH-018) cannabinoids induce seizures by acting through the cannabinoid CB1 receptor” by Olga Malyshevskaya, Kosuke Aritake, Mahesh K. Kaushik, Nahoko Uchiyama, Yoan Cherasse, Ruri Kikura-Hanajiri & Yoshihiro Urade in Scientific Reports. Published online September 22 2017 doi:10.1038/s41598-017-10447-2


Natural (∆9-THC) and synthetic (JWH-018) cannabinoids induce seizures by acting through the cannabinoid CB1 receptor

Natural cannabinoids and their synthetic substitutes are the most widely used recreational drugs. Numerous clinical cases describe acute toxic symptoms and neurological consequences following inhalation of the mixture of synthetic cannabinoids known as “Spice.” Here we report that an intraperitoneal administration of the natural cannabinoid Δ9-tetrahydrocannabinol (10 mg/kg), one of the main constituent of marijuana, or the synthetic cannabinoid JWH-018 (2.5 mg/kg) triggered electrographic seizures in mice, recorded by electroencephalography and videography. Administration of JWH-018 (1.5, 2.5 and 5 mg/kg) increased seizure spikes dose-dependently. Pretreatment of mice with AM-251 (5 mg/kg), a cannabinoid receptor 1-selective antagonist, completely prevented cannabinoid-induced seizures. These data imply that abuse of cannabinoids can be dangerous and represents an emerging public health threat. Additionally, our data strongly suggest that AM-251 could be used as a crucial prophylactic therapy for cannabinoid-induced seizures or similar life-threatening conditions.
“Natural (∆9-THC) and synthetic (JWH-018) cannabinoids induce seizures by acting through the cannabinoid CB1 receptor” by Olga Malyshevskaya, Kosuke Aritake, Mahesh K. Kaushik, Nahoko Uchiyama, Yoan Cherasse, Ruri Kikura-Hanajiri & Yoshihiro Urade in Scientific Reports. Published online September 22 2017 doi:10.1038/s41598-017-10447-2

Study Combines Music and Brain Stimulation to Improve Memory


Summary: Combining non-invasive brain stimulation with a person’s favorite music from the past may help to activate old memories and improve mood for older patients with MCI, a new study reports.

Source: Baycrest.

There are few treatments available to improve or slow down memory decline among MCI patients. image is adapted from the Baycrest news release.

Baycrest will embark on the first study combining music therapy with brain stimulation to improve memory among patients with Mild Cognitive Impairment (MCI).

This study could pave the way to developing an affordable and easy-to-use treatment for MCI patients, who face a higher risk of developing Alzheimer’s disease.

Dr. Claude Alain, assistant director and senior scientist at Baycrest’s Rotman Research Institute (RRI), will work with MCI patients to study the benefits of listening to music they enjoyed in the past, paired with Transcranial Direct Current Stimulation (tDCS) – a non-invasive and painless form of brain stimulation that transmits a very low-intensity current through the skull.

Research has demonstrated that listening to music improves the mood and well-being of older adults with dementia, and may also stimulate social interaction by “bringing back” past memories for these patients.

“Somehow music activates memories in dementia patients, which in turn leads to more social engagement and interaction with caregivers,” says Dr. Alain, who is also a psychology professor at the University of Toronto. “Brain stimulation has also been shown to temporarily improve a person’s memory and attention, but the reason it helps is still unclear.

“By combining personalized music choices with tDCS, we aim to strengthen the unique brain pathway music uses to activate memories and improve the effectiveness of this musical intervention among patients who are starting to experience memory issues.”
There are few treatments available to improve or slow down memory decline among MCI patients.
Currently, the study is recruiting older adults with mild cognitive impairment. Anyone interested in participating can visit here or leave a message at: 416-785-2500 ext. 2080.

Funding: This research is supported by the Lorraine Johnston Foundation, which aided in the study’s development and contributed funds towards hiring staff and conducting testing in older adults with MCI.
With additional funding, researchers could pursue studying the brain mechanisms behind brain stimulation. Depending on the study’s results, there is the potential to develop a treatment program for patients with more severe types of dementia.

Source: Jonathan MacIndoe – Baycrest

Image Source: image is adapted from the Baycrest news release.

Bicycling 'overloads' movement networks with Parkinson's

September 23, 2017

HealthDay)—Bicycling suppresses abnormal beta synchrony in the Parkinsonian basal ganglia, according to a study published online Sept. 11 in the Annals of Neurology.

Lena Storzer, Ph.D., from Heinrich Heine University Düsseldorf in Germany, and colleagues compared bicycling and walking in Parkinson's disease  (five patients with and eight patients without freezing of gait) with electrodes implanted in the subthalamic nuclei for . Low (13 to 22 Hz) and high (23 to 35 Hz) beta power changes were analyzed in 13 patients (57.5 years; four female).
The researchers found that in patients without freezing of gait, both bicycling and walking led to a suppression of subthalamic beta power (13 to 35 Hz), and this suppression was stronger for bicycling. For those with freezing of the gait, a similar pattern was observed, in general. However, a movement-induced, narrowband power increase around 18 Hz was evident even in the absence of freezing.
"Abnormal ~18 Hz oscillations are implicated in the pathophysiology of  of , and suppressing them may form a key strategy in developing potential therapies," the authors write.
Several authors disclosed financial ties to the medical device industry.
Journal reference: Annals of Neurology

Friday, September 22, 2017

Tom's Top Tips for Living Well with Parkinson's

Changes in Olfactory Bulb Explain Loss of Smell in Early Stages of Parkinson’s Disease, Study Finds


The olfactory bulb is significantly smaller in Parkinson’s disease patients compared to healthy individuals, a new study found, providing an anatomical explanation for the loss of the sense of smell in the early stages of the disease.
The discovery, “A ventral glomerular deficit in Parkinson’s disease revealed by whole olfactory bulb reconstruction,” was published in the journal BrainIt results from joint work of two research teams, one based in New Zealand and other from Germany.
The olfactory bulb is a part of the brain that receives neural signals from olfactory sensory neurons, which detect smells in the environment. Smell signals are transmitted via axons (long, slender projections of a nerve cell) of the sensory neurons to the glomeruli (thousand of structures located on the olfactory bulb). The olfactory bulb processes these smell signals and relays them to several other parts of the brain.
In the study, the team compared the olfactory bulbs of Parkinson’s disease patients with those of healthy subjects. They found that the glomeruli distribution was significantly altered. While 70 percent of the glomerular component was in the bottom part of the olfactory bulb in normal cases, this dropped to 44 percent in Parkinson’s patients.
Additionally, the volume taken up by the glomeruli was reduced by more than half in Parkinson’s patients.
Results support the theory that Parkinson’s disease begins with viruses, bacteria, or environmental toxins entering the brain via the nose, affecting the olfactory bulb first. According to this hypothesis, the disease then gradually spreads through other regions of the brain.
The team also calculated the joint volume of all glomeruli in the olfactory bulb. They then compared the values between olfactory bulbs from people with and without Parkinson’s disease. Findings showed that the number of glomeruli in Parkinson’s patients was reduced by more than half.
Following up on the study, researchers are already working to unravel what causes glomeruli deterioration in Parkinson’s disease and whether there are any other changes in the olfactory bulb in this neurodegenerative disease.

Explainer: what are mitochondria and how did we come to have them?

 September 21, 2017

We’ve probably all heard of mitochondria, and we may even remember learning in school that they are the “powerhouses of the cell” – but what does that actually mean, and how did they evolve? To answer this question, we have to go back about two billion years to a time when none of the complexity of life as we see it today existed. 

Where did mitochondria come from?

Our primordial ancestor was a simple single-celled creature, living in a long-term rut of evolutionary stagnation. Then something dramatic happened – an event that would literally breathe life into the eventual evolution of complex organisms. One of the cells engulfed another and enslaved it as a perpetual source of energy for its host. 
The increase in available energy to the cell powered the formation of more complex organisms with multiple cells, eyes, and brains. Slowly, the two species became intertwined – sharing some of their DNA and delegating specific cellular tasks – until eventually they became firmly hardwired to each other to form the most intimate of biological relationships. Two separate species became one. 

These energy slaves are the mitochondria, and there are hundreds or even thousands of them inside every one of your cells (with the exception of red blood cells) and in every other human alive. They still resemble their bacterial origin in appearance, but we can no longer exist without them, nor they without us. The evolutionary explosion powered by mitochondria is evident by the fact they are found in every complex multicellular organism that has ever existed, from giraffes to palm trees, mushrooms and dinosaurs. 
As vestiges of their ancient origin, mitochondria still have their own genome (although some of their DNA has been transferred to our genome). It’s alien in appearance and composition when compared with our own nuclear genome (the DNA inside each of your cell’s nuclei that contains about 20,000 genes). In fact, our nuclear genome shares more in common with that of a sea sponge than with the mitochondrial genome inside our own cells. 
Unlike the nuclear genome, the mitochondrial genome is small (containing just 37 genes), circular, and uses a different DNA code. The mitochondrial genome slinks its way across generations by stowing away within mitochondria harboured in each egg, and as such, is passed down from the mother only. This is different to the nuclear genome, half of which is inherited from your father and the other half from your mother. 

What do the mitochondria do?

The mitochondrial genome is vital for the mitochondria’s main role: burning the calories we eat with the oxygen we breathe to generate the energy to power all of our biological processes. But this amazing source of energy is not without its cost.
Like any powerhouse, mitochondria produce toxic byproducts. Free radicals (highly reactive oxygen molecules with an odd number of electrons that can cause ageing and health problems) can be created by accidents that happen during energy production. 
So in essence, mitochondria power and imperil our cells.
Because the mitochondrial genome is in close proximity to the source of free radicals, it’s more susceptible to their damaging effects. And the mitochondrial genome undergoes replication thousands of times more than the nuclear genome, simply because you have so many in each cell. Making copies of copies introduces mistakes. 
A combination of these two effects results in the mitochondrial genome mutating up to 50 times faster than the nuclear genome, which is meanwhile kept safely in the nucleus. These mutations can be passed down to maternal offspring, causing devastating metabolic disorders in the next generation.

What happens when something goes wrong?

Only as recently as 1988 was the first disease caused by such a mutation in the mitochondrial genome identified. Now, we know about many such disorders, called mitochondrial diseases, which can be traced to mutations in the mitochondrial genome. These diseases can manifest at any age and result in a wide range of symptoms including hearing loss, blindness, muscle wasting, stroke-like episodes, seizures, and organ failure.
These diseases are currently incurable. But multiple lines of investigation are currently underway to treat and prevent transmission to subsequent generations.
Despite this, during life, it’s inevitable that mutations will occur in the mitochondrial genome in an individual’s neurons, muscle, and all other cells. Compelling work now suggests that the accumulation of these mistakes may contribute to the progressive nature of late-onset degenerative diseases such as Alzheimer’s and Parkinson’s. 
The health of this seemingly alien genome is inextricably linked to that of our own bodies. As we come to grips with mitochondria’s importance in disease, we continue to uncover the intimate secrets of a two-billion-year relationship that has given complex life to the planet.