Welcome to Our Parkinson's Place

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

Sunday, April 22, 2018

Battling Parkinson’s together

April 22, 2018    ByGregory Philson

Bev said she noticed Steve struggling with balance during a skiing trip before the diagnosis and not noticing certain smells in the kitchen, but she also did not think it was Parkinson’s.
“I was surprised when he was first diagnosed,” Bev said. “But, it did help explain his symptoms.”
Bev also has a medical background and thinks it has made it easier working with Steve.
“I recently retired as an occupational therapist,” Bev said. “I only worked with children, but I think it does help. It is still a challenge everyday. We all have challenges and somehow you just deal with it.”
One of those challenges is the short-term memory loss that Steve deals with because of Parkinson’s. According to the American Parkinson Disease Association, people with Parkinson’s disease “may have trouble recalling information, but in general, memory is less impaired in Parkinson’s Disease compared to Alzheimer’s disease. In PD, people frequently recall information more readily when given cues or choices.”
“I have to keep a schedule, keep track of doctor appointments and take notes for Steve,” Bev said.
Bev also helps Steve keep motivated — which he admits can be hard day-to-day.
“I used to be pretty verbal,” Steve said. “I considered myself pretty articulate with my speech. My speech has been a problem. So, I would want to avoid social situations, but Bev encourages me.”
The couple also tries to keep up with walks and are getting used to a change in responsibilities.
“Now I have to tell myself I need to get the ladder and clean the roof off,” Bev said. “But, I also have to know when to ask others for help.”
They also agree there needs to be a balance in life — which involves understanding when to push it (with verbal or physical exercises) and when to back off. One way the couple tries to keep each other calm is agreeing to “60-second hugs” in stressful moments.
“It helps shift the intensity,” Bev said.
Steve also participates in the Rock Steady Boxing at Pavitt Health and Fitness. Bev said the program helps Steve not only keep up with his fitness — and hopefully slow the progression of the disease — but she also said she believes it helps him cognitively because he has to switch hands and hit certain spots on the heavy bag.
“It really helps in challenging the brain,” Bev said. “It shifts things up for him.”
Steve, like others who participate in the program, also said he likes the camaraderie of working with others in the same physical situation.
“It’s a good social activity because it can be an isolating disease,” Steve said.
Both agree Parkinson’s has not been an easy battle, but staying strong in the fight makes it easier.
“It really helps having the support of my wife,” Steve said. “You have to have that whole fight back attitude.”
“You have to try to stay positive, but there are certainly ups-and-downs.” Bev added. “You have to try your best to both not get down at the same time. It really helps to have support of friends and family. The thing is the caregiver still has to take care of themselves, as well.”

Parkinson’s Disease: By the numbers
• Approximately 1 million Americans live Parkinson’s disease, which is more than the number of people diagnosed with multiple sclerosis, muscular dystrophy and Lou Gehrig’s disease (or Amyotrophic Lateral Sclerosis) combined. Approximately 60,000 American are diagnosed with Parkinson’s every year.
• More than 10 million people worldwide are living with PD.
• Men are 1.5 times more likely to have Parkinson’s disease than women
(Statistics from
Parkinson’s Resources in Juneau
BIG and LOUD Program
Bartlett Regional Hospital, 3260 Hospital Drive
BIG run by Rachelle Cummins, LOUD by Marisha Bourgeois
Contact: 796-8431
Monthly Parkinson’s Support Group
Meetings: Last Tuesday of the month from 6:30-7:30 p.m. at Juneau Pioneers Home main dining room, 4675 Glacier Highway
Run by Southeast Senior Services
Facilitator, Tammy Guiller
Contact: 463-6163
Rock Steady Boxing
Pavitt Health and Fitness, 10004 Glacier Highway
Tuesday and Thursday from 11 a.m.-12:30 p.m. and Saturday 9-10:30 a.m.
Contact: Coaches Janet Valentour, 723-3390 and Keegan Caroll, 723-7925

Penn State Hershey Medical Center drops more than 2,000 neurology patients: Report

By Joe Elias     April 22, 2018

More than 2,000 neurology patients have been dropped by the Penn State Hershey Medical Center and are now searching for new doctors, according to a report from ABC 27 in Harrisburg.
The neurology department at the hospital has lost four doctor's recently, two that retired and two others that moved to other jobs, according to the report.
The department treats patients with disorders of their nerves and the nervous system, such as multiple sclerosis and Parkinson's disease.
The hospital sent patients a letter informing them of the situation. Some patients and their families said the hospital should have done more to help them find another doctor until replacements are hired.
Penn State Health sent the station a response, blaming the problem on a lack of trained specialists.
"We are encountering many of the same challenges being seen by health systems nationwide - namely, a shortage of sub-specialists trained and ready to treat this complex illness," according to the report.

This exercise class can help those living with Parkinson’s disease

Author: Jaime Berg    April 22, 2018

Exercise has been suggested by doctors as a way to help curb tremors. 

Of the one million Americans living with Parkinson’s disease, 17,000 of them live here in Colorado. 

Parkinson's: Targeting new compound slows disease in rats

The condition is neurodegenerative, meaning that the neurons in a brain area tied to motor skills and movement control gradually deteriorate and die.
These brain cells would normally produce dopamine, which is a neurotransmitter key for regulating complex movements as well as controlling mood.
Although current therapies for Parkinson's involve drugs such as Levodopa, which the brain can use to create dopamine, the reason why dopaminergic neurons die in the first place remains unknown.
So, now, a team of researchers led by two professors at Purdue University in West Lafayette, IN, investigated the hypothesis that a product of oxidative stress might be a key player in this cell death and the development of the disease.
Oxidative stress takes place when oxygen radicals are produced in excess, a process that results in a series of damaging effects, such as increased toxicity and damage to our DNA.
Riyi Shi and Jean-Christophe Rochet, who are both professors at the Purdue Institute for Integrative Neuroscience and the Purdue Institute for Drug Discovery, jointly led the research, whose results were published in the journal Molecular and Cellular Neuroscience.

Studying acrolein in rats

Profs. Shi, Rochet, and colleagues used a model of genetically modified rats to induce Parkinson's-like symptoms and study the behavior of their dopaminergic cells, both in vitro and in vivo.
The researchers found that the compound called acrolein tends to build up in the brain tissue of rats affected by Parkinson's.
Acrolein, as the researchers explain, is a toxic byproduct of the brain burning fat for energy. The compound is normally discarded from the body.
Interestingly, however, the study revealed that acrolein raises the levels of alpha-synuclein. This is the clumpy protein that is believed to kill dopamine-producing neurons because it accumulates in unusual amounts in the brain cells of those with Parkinson's or Lewy body dementia.
Additionally, injecting acrolein into healthy rats produced behavioral deficits typical of Parkinson's. So, next, the researchers wanted to see if targeting this compound would stop the disease from progressing.

Blocking acrolein slows down Parkinson's

To this end, the team conducted experiments both in cell cultures and in the animals, evaluating their anatomy and the functionality of their behavior.
They turned to hydralazine, a drug used to treat blood pressure. As Prof. Shi explains, hydralazine is incidentally also "a compound that can bind to the acrolein and remove it from the body."
Remarkably, the scientists found that inhibiting acrolein with hydralazine alleviated Parkinson's-like symptoms in rats, as the study's co-lead author reports.
Acrolein is a novel therapeutic target, so this is the first time it's been shown in an animal model that if you lower the acrolein level, you can actually slow the progression of the disease [...]." 

Prof. Riyi Shi
"This is very exciting," he says. "We've been working on this for more than 10 years."
"We've shown that acrolein isn't just serving as a bystander in Parkinson's disease. It's playing a direct role in the death of neurons," adds Prof. Rochet.

Rats vs. humans: Toward new drugs

Prof. Rochet cautions that, although promising, finding a drug that halts the disease in rats is still a far cry from finding an equivalent compound in humans.
"In decades of research, we've found many ways to cure Parkinson's disease in preclinical animal studies," he says, "and yet we still don't have a disease therapy that stops the underlying neurodegeneration in human patients."
"But this discovery gets us further down the drug discovery pipeline, and it's possible that a drug therapy could be developed based on this information," Prof. Rochet adds.
Although hydralazine is already in use and we know that it has no noxious effects, the researchers say that it may not prove to be the best anti-Parkinson's drug down the line, for various reasons.
"Regardless," Prof. Rochet continues, "this drug serves as a proof of principle for us to find other drugs that work as a scavenger for acrolein."
"It is for this very reason," Prof. Shi explains, that "we are actively searching for additional drugs that can either more efficiently lower acrolein, or do so with fewer side effects."
"The key is to have a biomarker for acrolein accumulation that can be detected easily, such as using urine or blood," he says.
The goal is that in the near future we can detect this toxin years before the onset of symptoms and initiate therapy to push back the disease. We might be able to delay the onset of this disease indefinitely. That's our theory and goal."

Prof. Riyi Shi 

Friday, April 20, 2018

Pies for Parkinson's - A Delicious Way to Help


Table Talk pies and Parkinson Support Network of Cape Cod have joined forces in a yummy way (Courtesy photo)

From the Parkinson Support Network of Cape Cod:
The Pies for Parkinson’s program is a grassroots awareness campaign rather than a fundraiser or particular event. Across the Cape, our board members and local businesses who have sponsored this program are distributing our pie packages (please see the attached images) to local Councils on Aging, Senior Centers, Fire houses, etc. For example, Rose Digregorio, Parkinson Support Network/APDA board member and Pies for Parkinson’s program creator, will be visiting the Barnstable Newcomers Club on April 25. The packages include information about our organization, the services we provide, a schedule of free educational events for individuals with Parkinson’s and their families, as well as how to reach us should they need information and referral services. We encourage anyone who is interested in learning more about the program to contact us.
In recognition of National Parkinson’s Awareness Month (April), the Parkinson Support Network, a branch of the American Parkinson Disease Association, Massachusetts Chapter is pleased to bring Pies for Parkinson’s to the Cape for the second year. We are thankful to Table Talk Pies for supporting this April awareness campaign again this year. We have been supporting the over 2,000 people living with Parkinson’s disease on Cape Cod since 2007. In the eleven years since, PSN has collaborated with health and human service providers, professional organizations and the public to provide access to information for individuals with Parkinson’s and their families. We have offered a variety of educational and wellness programs for our ever growing community, and in joining with the American Parkinson Disease Association Massachusetts Chapter in 2015, we gained the capabilities to help even more individuals with PD.
The American Parkinson Disease Association (APDA) is the largest grassroots network dedicated to fighting Parkinson’s disease (PD) and works tirelessly to assist the more than 1 million Americans with PD live life to the fullest in the face of this chronic, neurological disorder. Founded in 1961, APDA has raised and invested more than $170 million to provide outstanding patient services and educational programs, elevate public awareness about the disease, and support research designed to unlock the mysteries of PD and ultimately put an end to this disease.
With the APDA MA, we are able to provide an Information and Referral Center helpline (800-651-8466) and a website (, along with between four or five signature educational programs annually, funding for the Cape Conservatory’s Sing for Joy group, and an annual Fall Fling Social. To learn more about any of these events or programs, please visit or call 800-651-8466.
If you would like to host your own Pies for Parkinson’s event to spread awareness about Parkinson’s disease, please contact the APDA MA at 800-651-8466.

Do Immune Responses Promote, or Prevent, Parkinson’s Disease?

18 Apr 2018

Researchers keep turning up unexpected links between Parkinson’s disease and the immune system. At the first Advances in Alzheimer’s and Parkinson’s Therapies Focus Meeting (AAT-AD/PD), March 15–18 in Turin, Italy, Michael Schlossmacher of the Ottawa Hospital Research Institute, Canada, reported that the PD-linked gene LRRK2 helps mice fight bacterial and viral infections. Together with previous findings that animals release α-synuclein in response to infection, the data support the idea that microbial exposure could play a role in neurodegenerative disease. And if bad bacteria can hasten PD, could good bacteria delay it? A hint in this direction came from Roberto Grau of Rosario National University, Argentina, who reported that feeding probiotic bacteria to worms prevented α-synuclein accumulation and neurodegeneration. The bacteria turned on longevity genes, which may control α-synuclein folding and degradation, Grau suggested. He is about to test his idea in an upcoming PD trial.
  • A PD risk gene supercharges the immune response to fight off infections.
  • Beneficial bacteria slow the accumulation of α-synuclein in mutant worms.
  • Together, the data suggest that immune responses may modulate PD risk.
If confirmed, the studies imply that microorganisms, and the immune response to them, may modify PD risk, for good or ill. “We think that environmental triggers such as microorganisms interact with the genetic makeup of the host organism to initiate inflammatory responses, and those responses determine the outcome of the illness,” Schlossmacher told Alzforum. His team recently drew attention to this complex disease model of PD pathogenesis and is testing this idea in animal and human studies (Schlossmacher et al., 2017). 
The idea that systemic infections might be at the root of some cases of PD has been gaining some ground in the last decade (July 2011 news series). Researchers recently reported that gut infections stimulate the release and aggregation of α-synuclein (Oct 2016 newsJul 2017 news). The protein is expressed in the peripheral and central nervous system neurons, as well as in red blood cells and platelets (Barbour et al., 2008Scherzer et al., 2008). In mice, the normal gut microbiome accelerates α-synuclein pathology, while in people, the composition of gut microflora changes early in the disease (Dec 2016 newsApr 2017 news). 
B. Subtilis Squelch Synuclein. 
PD model worms (left) accumulate α-synuclein deposits (green), but not when fed probiotic bacteria (right).  [Courtesy of Roberto Grau.]

Why does the body pump out α-synuclein in response to an infection? Last year, Schlossmacher and colleagues reported that the protein helped mice survive a virulent immune challenge, with α-synuclein knockouts succumbing sooner to a deadly virus (May 2017 news). Others have similar findings (Beatman et al., 2015). In Turin, Schlossmacher added new data, proposing a comparable immune modulatory role for LRRK2. This large multifunctional protein is highly expressed in microglia, monocytes, and adaptive immune cells, in addition to its expression in neurons and glia.
To plumb its role in infection, the researchers infected newborn LRRK2 knockout mice with reovirus T3D (Gauvin et al., 2013), and adult knockouts with salmonella bacteria. In both paradigms, the knockouts had evidence of more disease than wild-type, amassing about double the viral or bacterial burden. Female mice lacking LRRK2 were more susceptible to infection than males. Intriguingly, the pathological outcomes of female LRRK2 heterozygotes mirrored those of male knockouts, while male heterozygotes were more likely to be unaffected, responding to infection like wild-type mice. This work is currently in revision (Shutinoski B, Hakimi M, et al.).
PD-linked LRRK2 risk alleles are not knockouts, however. They are mostly gain-of-function variants that increase the protein’s kinase activity. What do those do in response to infection? Schlossmacher and colleagues tested mice that expressed the main PD risk variant, G2019S. In contrast to knockouts, they dealt with infections handily, keeping their viral or bacterial load low. Female mice survived bacterial sepsis better than males but succumbed sooner to a viral brain infection, though the number of mice examined thus far was small. 
The G2019S variant is known to boost myeloid cell recruitment, and a different LRRK2 variant is a known risk factor for an excessive inflammatory response in people with leprosy caused by Mycobacterium leprae (Fava et al., 2016). Schlossmacher speculated that G2019S may augment inflammation, which helps the body fight off a virulent infection but could possibly harm the brain. If so, G2019S’s efficacy against infections may explain why this variant has survived in humans during evolution.
If independently confirmed, LRRK2 would be the first PD gene shown to have a strong gender effect in animal studies. The reason why is unclear, but the sex difference mirrors findings in people. In the Ashkenazi Jewish population, women carrying a G2019S variant are more likely than male carriers to develop PD, and their symptoms appear five years earlier on average (Cilia et al., 2014Marder et al., 2015). This flips the normal gender effect in PD, where men are typically more susceptible.
In future work, Schlossmacher is investigating whether his LRRK2 findings relate to PD. He believes the protein may influence how the body mobilizes α-synuclein in response to an infection. “We think LRRK2 is the horse, and α-synuclein the buggy; where the buggy goes depends on which way the horse pulls,” he told Alzforum. This raises a question for ongoing trials of α-synuclein antibodies, Schlossmacher noted. If the protein helps defend the body against infection, lowering it too much could leave people more vulnerable. “Trialists should monitor patients for signs of infection,” he suggested.
Neuron Protection? 
In PD model worms fed the standard diet of E. coli (left), dopaminergic neurons (green) degenerate; neurons stay healthy when the worms eat probiotics (right).  [Courtesy of Roberto Grau.]

Working in Rosario, Grau focused on good bacteria instead of bad. He previously reported that the probiotic Bacillus subtilis delayed aging in the roundworm C. elegansby reducing insulin signaling (Donato et al., 2017). Because aging is a risk factor for PD, he wondered if the probiotic could protect against it. He used two worm models, one that overexpressed human α-synuclein, and another that expressed a risk variant in the parkin gene. These worms develop several phenotypes mimicking PD, including clumsy movement, constipation, and impairment in dopamine-dependent behaviors such as reproduction and avoiding danger.
When the mutant worms were raised on media containing Bacillus subtilis, however, nearly all these behaviors reverted to wild-type levels. The probiotic suppressed accumulation of α-synuclein into Lewy bodies by 75 percent, and prevented the degeneration of dopaminergic neurons (see images above). The worms lived as long as wild-types. The data suggest that probiotics could possibly prevent the development of PD pathology, Grau said.
The protective effect of Bacillus subtilis depended on its ability to form a biofilm, a slimy sheet of cells surrounded by an extracellular matrix. When the researchers used a mutant strain without that ability, few benefits accrued to the worms. Bacillus lives as a biofilm in the gut, and this organization allows the cells to communicate more efficiently among themselves and with the host, Grau explained.
In his previous study, he found that Bacillus biofilms dialed down insulin-signaling genes such as DAF-2 in the host. This suppression leads to the induction of protective genes, including FOXO and heat shock factor 1. HSF1 in turn mediates the response to cellular stress, and Grau believes it may turn on molecular chaperones that assist in the degradation of α-synuclein.
Grau plans to treat PD patients with the Bacillus subtilis strain DG101, along with their normal medications, to see if the probiotic might improve health, lower symptoms, or extend lifespan. This strain robustly induces FOXO and HSF-1, he noted. The trial is expected to start later this year. He plans to enroll more than 100 people in Argentina who are being treated for PD at private hospitals and follow them for six to 12 months.
In the Alzheimer’s field, treatments that target the aggregation of pathogenic proteins have not worked in symptomatic populations, possibly due to the long prodrome of the disease. This has fueled a push toward preventative trials.
Natto, Anyone? 
This Japanese breakfast food 
fermented soybeans is made 
with B. subtilis.
 [Courtesy of Wikimedia.]

Some people around the world already consume B. subtilis. For example, a Japanese breakfast food called natto is made by fermenting soybeans using the probiotic. The Japanese credit consumption of this food as one reason for their longevity. Grau told Alzforum that natto helped inspire his studies of B. subtilis’ health benefits.
The strain that makes natto produces the protease nattokinase, which degrades amyloid in mice and promotes non-amyloidogenic processing of Aβ (Hsu et al., 2009Fadl et al., 2013). It is unclear if the food affects PD or Alzheimer’s risk. The incidence of Parkinson’s disease in Japan is somewhat lower than in most Western countries (Muangpaisan et al., 2009).

Schlossmacher called Grau’s work elegant, with fascinating implications. He noted that probiotics might trigger shifts in the relative abundance of other species in the gut microbiome, leading to changes throughout the intestine. In theory, such microbiome changes could also help prevent PD by keeping the α-synuclein response to infection in check, he said. Signs of ongoing α-synuclein aggregation occur in healthy people in the GI tract, notably in the appendix (Gray et al., 2013), and chronic constipation is associated with PD risk. Gut motility, which is influenced in part by the GI tract’s microbiome constituents, could thus be a modifiable risk factor, Schlossmacher argues.—Madolyn Bowman Rogers

Never Steady, Never Still review – tough sledding in the snows of Alberta

April 20, 2018

This drama about a mother who has Parkinson’s and her teenage son who is struggling with his sexuality, is unsatisfying despite heartfelt moments

 Conflicted … Jamie (Théodore Pellerin), who plays Shirley Henderson’s son in Never Steady, Never Still.

This is a sincerely intended drama from Canadian writer-director Kathleen Hepburn, and it was a prizewinner on its home turf, but I have to admit to finding it tough sledding. It is plaintive and subdued, with a dual narrative focus that is not as satisfyingly developed or resolved as it might be.
Judy, played by Shirley Henderson, lives near the oilfields of Alberta and has Parkinson’s. She has a supportive if withdrawn husband, Ed (Nicholas Campbell), though she seems also to have an emotional connection with her neighbour Lenny (Lorne Cardinal). Judy is worried and protective about her aimless teen son Jamie (Théodore Pellerin) who, quite aside from worrying about his mother, has his own issues with sexuality and identity, and who occupies half the film’s narrative space. (The feature was developed from an earlier short that was more centred on Jamie.) In the end, I got the feeling I hadn’t quite found out enough about either Jamie or Judy.

The movie comes most alive in Judy’s Parkinson’s therapy group scenes, which have a wit and punch that the rest of the film lacks. There is a terrific exchange in which an older woman fiercely tells the group how annoyed she was when out shopping for socks for her husband, when her wobbly legs would suddenly fail to move at her bidding and she would be stuck making conversation with the town bore. 
There are some heartfelt moments, but this is an opaque and frustrating experience.

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