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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.

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Saturday, July 15, 2017

From diagnosis to clinical trial: my worldwide Parkinson’s journey

PERSPECTIVES  Author: Ben StecherPublished: 13 July 2017

After his initial despair at being diagnosed with young-onset Parkinson’s, Ben Stecher sought to understand his condition by speaking to experts around the world – and taking part in a clinical trial. He tells us how his emotional – and inspiring – research trips to the US, Canada, the UK and Israel helped him navigate what he calls “the fine line between hope and hype”

I was diagnosed with Parkinson’s disease in 2013 at the age of 29 years old. Like all that hear such news, I have felt the fear, anxiety and despair that goes along with it. But I realised at some point that much of that stemmed from not understanding what was going on, why my feet and hands were shaking and why I could not move with ease. Over time, much of that negativity subsided as I learned about the disease, how to treat it, how to live with it, and what future therapies might be in store for me. This knowledge also kindled an almost childlike curiosity to see what else was going on in the Parkinson’s world and over the last year I have allowed that curiosity to be a driving force in my life
I lived in Shanghai for the first couple of years after my diagnosis and was lucky enough to find Dr Hung Zuo Xing at the WA Optimum Health Care clinic in Shanghai, China, who introduced me to functional medicine and hammered home the importance of looking at this disease as not just the result of dysfunction in the brain but as the result of a complex interaction of environmental, nutritional and hormonal factors.
Bon voyage
In 2016, I embarked on the first leg of my journey and headed to the USA.
At the invitation of Sherrie Gould­ – a Parkinson’s a nurse practitioner and co-founder of research organisation ‘Summit For Stem Cell: Victory Over Parkinson’s’ – who I had never met, I went down to San Diego to learn about the latest stem cell therapies being developed for Parkinson’s disease. While there, I met Dr Jeanne Loring, the head of the lab, and Dr Andres Bratt-Leal, the lead scientist. It was in San Diego where I got my first real sense of the immense progress science has made lately towards one day putting an end to neurodegeneration.

“For all the complexity surrounding Parkinson’s disease, it is a relatively easy disease to define as it is primarily the death of dopamine producing neurons”

The team there introduced me to the medical marvel that is IPS cells, and the idea that one day stem cells will be used to restore dopamine producing neurons to patients. Too often there is a disconnect between researchers, physicians and patients, no centre I have visited does a better job of integrating all three and that is due in large part to the work of Sherrie, Jeanne and Andres.
World Parkinson Congress 2016
I saw Dr Steven Finkbeiner speak at the World Parkinson’s Congress in September 2016 and I was captivated by the work he’s doing with Dr Gaia Skibinski and Dr Julia Kaye at the Gladstone Institutes, California, US, figuring out better disease models, and by his application of machine learning to our understanding of disease. The biggest limitation we have when studying the brain is that it’s not so easy to crack open people’s heads and see what is going on inside. We use models like rodent brains, or neurons in petri dishes to test new therapies on but they just aren’t able to mimic the incredible complexity of the human brain.
For all the complexity surrounding Parkinson’s disease, it is a relatively easy disease to define as it is primarily the death of dopamine producing neurons, so, it makes sense to develop therapies to try and replace these neurons. There are currently five labs around the world working on stem cell therapies. Dr Lorenz Studer at the Rockefeller University, New York, US leads the lab that is closest to running human trials. It can be hard for researchers and patients alike to walk the fine line between hope and hype with any promising new therapy – this is especially true with these new stem cell therapies.
Stem cell treatments
There are a number of other labs also working to ensure the safe and effective transplant of the cells. Dr Tilo Kunath at the MRC Centre for Regenerative Medicine at the University of Edinburgh, Scotland is working diligently on just that. Stem cells have a lot of potential to be the next big breakthrough therapy in Parkinson’s but without groups like his testing and refining the techniques being applied we may fall short of our goal. I am also thankful for his openness and willingness to work with other researchers – I wish more scientists shared his enthusiasm for collaboration.
Dr Tilo Kunath and Ben Stecher at Arthur’s seat, Edinburgh, Scotland
Earlier this year, in Vancouver I met a team of researchers at the University of British Columbia that left an indelible impression on me, starting with Dr Katie Dinelle who took the time to take me through the inner working of fMRI and SPECT scans and elucidated the hope surrounding a new line of such machines coming out soon that will blend these techniques together, and give us new tools to peer into the inner-workings of the brain.

“I’m also very hopeful that the mountains of data they are collecting on the patients involved in the study, will reveal something soon about the biomarkers involved in Parkinson’s”

Through the Parkinson’s Progression Markers Initiative (PPMI) study – run by the Michael J Fox Foundation – I was placed under the care of Debra Smejdir and Dr David Russell in New Haven, Connecticut, US. The study is the best-run clinical trial I have been a part of due to it’s the patient-centred approach. I’m also very hopeful that the mountains of data they are collecting on the patients involved in the study will reveal something soon about the biomarkers involved in Parkinson’s.
Back to my homeland, Israel
At the Ichilov Hospital in Tel Aviv, Israel this year I met Dr Tanya Gurevich, the director of the country’s largest Parkinson’s disease programme, and Dr Avner Thaler, a spirited young researcher playing a leading role in some of what is going on there. Ichilov is also a centre for a number of clinical trials, most promising among which are those for genetic cohorts of the disease such as LRRK2 and GBA carriers. For those ‘lucky’ enough to have one of these mutations there is good news as the first batch of clinical trials targeting those genetic variations are set to begin soon.
This article is an edited version of posts that originally appeared on ‘Tomorrow Edition’ and is re-published with the permission of Ben Stecher.

Study: Professions linked to Lou Gehrig’s Disease and Parkinson’s

    July 13, 2017

In this photo a scientist in Florida, Matthew Disney, works on potential cures for neurodegenerative diseases like ALS. In an unrelated study, the CDC in July announced a link between certain professions and mortality from ALS and Parkinson’s disease. (Bruce Bennett/Palm Beach Post)

Scientists investigating why people die from Lou Gehrig’s disease and Parkinson’s have found a new factor: high-paying or highly educated administrative jobs.
A study released Thursday afternoon by the U.S. Centers for Disease Control and Prevention analyzed data from several states. It found that workers in certain occupations were more likely to die from the two neurodegenerative conditions. Those occupations included computer and mathematical fields, lawyers, architects, engineers, and teachers.
Previous research has often focused on victims’ exposure to poisons at work, such as in factories, farming or the military, the study said. But this study pulled back and looked at jobs in general, and did not find a link between those professions and Parkinson’s disease or Lou Gehrig’s (also known as Amyotrophic Lateral Sclerosis, or ALS).
Other factors were already recognized, such as being older, or being male. Pesticide exposure is a factor for Parkinson’s, and cigarette smoking is a factor for ALS.

The study encouraged further investigation of the finding. For one thing, it acknowledged that they couldn’t separate what effects might come from actually having those jobs, or from simply being of a higher socioecononic status.

Friday, July 14, 2017

Scientists develop imaging method for measuring glutathione in real time

July 13, 2017

Glutathione is the most abundant natural antioxidant in cells. It protects them from damage and regulates a number of important functions, including cell proliferation and death, the synthesis of the genetic material and proteins and the activation of gene expression. These functions are regulated by changes in the concentration of glutathione, but the current methods do not allow for real-time measurements of glutathione levels inside cells. 

Researchers at Baylor College of Medicine, Texas Children's Hospital and Rice University have moved the field of glutathione research a step forward by developing a fluorescent probe - they called it RealThiol - that can measure real-time changes of glutathione concentration in living cells. Published in Nature Communications, this study offers a new tool to investigate the roles glutathione plays in aging, health and diseases such as cancer, Alzheimer's and Parkinson's, cardiovascular conditions and diabetes, among others.

Until now, methods for measuring glutathione levels inside cells only allowed for one time point measurements," said corresponding author Dr. Jin Wang, associate professor of pharmacology and chemical biology and of molecular and cellular biology at Baylor. "We wanted to develop a method that would allow biologists to measure how glutathione concentration inside cells changes in ."
How to measure glutathione changes in real time
Previous methods are based on irreversible chemical reactions that capture all the glutathione that is inside the cells, providing a one-time snapshot of its amount. Wang, who was trained as a physical organic chemist, and his colleagues looked for reversible chemical reactions that would capture and release glutathione, allowing for multiple measurements inside the same cell.
"Other researchers had succeeded at developing chemical probes for measuring the dynamic changes of calcium and zinc in cells using reversible chemical reactions," Wang said. "However, some researchers thought that the same could not be accomplished for glutathione."
In 2015, Wang and his colleagues published a proof of concept that a reversible reaction could be used to measure glutathione. Further research led to the current publication.
"The key contribution of the current study is that we optimized the  and made the reaction much faster; both the forward and the reverse  can be completed within one minute, allowing us to follow the dynamic changes on glutathione in living cells," Wang said. "Our method requires very small amounts of the probe, which results in little toxicity and poses minimal perturbance of the antioxidant capacity in the , and the probe can be used in various applications, from microscopy to cell sorting experiments."
Using RealThiol, the researchers measured enhanced antioxidant capability of activated neurons and dynamic glutathione changes during ferroptosis, a form of cell death. The Wang group is currently developing glutathione probes with different sub-cellular specificities. This new tool set can potentially generate knowledge that could help develop new strategies to treat diseases involving -mediated processes.
More information: Nature Communications (2017). DOI: 10.1038/NCOMMS16087 
Journal reference: Nature Communications

Thursday, July 13, 2017

Missing Link Discovered Between Immune Cells and Alzheimer’s Disease


Summary: Researchers at Cornell University have discovered a new pathway that involves immune cells which may contribute to the development of Alzheimer’s disease.

Source: Cornell University

Immune cells called perivascular macrophages (green) are observed in close contact with blood vessels in the brain (red). When activated by plaque deposits from the peptide amyloid-beta, a hallmark of Alzheimer’s disease, perivascular macrophages produce damaging free radicals that paralyze blood vessels and deprive the brain of the needed supply of nutrients and oxygen. image is credited to the researchers.

By studying the effects of immune cells that surround blood vessels in the brain, Weill Cornell Medicine researchers have discovered a new pathway involving these cells that may contribute to the cause of Alzheimer’s disease.

One of the hallmarks of Alzheimer’s disease is the accumulation of plaque deposits, or abnormal protein fragments, from a peptide called amyloid-beta. Amyloid-beta destroys neurons and damages brain blood vessels with the help of highly reactive molecules, called free radicals, which are derived from oxygen. 

For their study, published May 17 in Circulation Research, the researchers sought to determine which cells in the brain were responsible for producing the free radicals, also known as reactive oxygen species (ROS).

“These free radicals are nasty molecules that paralyze the vessels so that they can’t function normally. As a result, brain cells are deprived of the blood supply of oxygen and glucose they need to function properly,” said senior study author Dr. Costantino Iadecola, director of the Feil Family Brain and Mind Research Institute and the Anne Parrish Titzell Professor of Neurology at Weill Cornell Medicine.

In their study, the investigators examined cells in the brain called perivascular macrophages (PVM), which surround blood vessels and pick up and remove damaging metabolic byproducts floating around the brain. The team focused on these cells because amyloid-beta tends to accumulate in the vascular space where PVM are located.

“We saw that when cells are exposed to amyloid beta, these PVM start producing free radicals like crazy,” Iadecola said.

To determine whether the PVM were involved in the ROS production, the researchers removed PVM by injecting into the brains of mice spherical lipid droplets called liposomes that contained the drug clodronate.

“The liposomes acted as a kind of Trojan horse,” said Laibaik Park, assistant professor of research in neuroscience in the Feil Family Brain and Mind Research Institute, and first author of the study. “The PVM digest the lipids and sets the drug loose into the cell, forcing them to die.”

Park and Iadecola administered the liposomes in mice with Alzheimer’s disease; ROS paralyzed the blood vessels in the rodents. Remarkably, the team found that the blood vessels in these mice appeared to work normally once rid of PVM, despite the presence of amyloid-beta. “This showed that without the PVM, amyloid-beta was unable to exert its damaging effects on brain blood vessels,” Park said.

The researchers then sought to learn what caused the PVM to produce ROS. Previous studies showed that macrophages have innate immune receptors on their surface called CD36 that help them bind and interact with other immune cells and proteins. The next step was to determine what happens when CD36 was not present, Iadecola said.

To remove the CD36 receptors from PVM, the researchers first used radiation to destroy the PVM. Then, old PVM were replaced through a bone marrow transplant with new PVM that did not have the receptor.

“When we did that, it was as good as getting rid of the whole macrophage, proving that the presence of CD36 on PVM was necessary for the ROS production and vascular damage to occur,” Iadecola said.

The researchers ultimately discovered that when amyloid beta binds to the CD36 receptor of PVM, a signaling pathway is triggered, which causes an enzyme called NADPH oxidase to produce free radicals.

“It was previously thought that amyloid-beta was going to work its way from the brain into the wall of blood vessels, reaching endothelial cells, which would be the source of the radicals,” Iadecola said. “But in reality, amyloid-beta globs onto the macrophages to activate them. This makes perfect sense because endothelial cells are inside the vessels away from brain amyloid-beta, while PVM are outside the vessel continuously bathed by amyloid-beta coming from the brain.”

Genetic studies have long suggested that the brain’s innate immune cells, like microglia and macrophages, contribute to Alzheimer’s disease, but how these cells damaged the brain was not known. “Our study identifies a novel way in which immune cells could contribute to Alzheimer’s disease, and provide a new therapeutic approach to suppress their damaging effects,” Iadecola said.

Researchers will now seek to develop methods that block CD36 or NADPH oxidase in the cells, which may reduce the amount of amyloid-beta in the brain and potentially slow the progression of Alzheimer’s disease. “Delaying the process may give you more years with a healthy mind,” Iadecola said.

He also added that the maintenance of blood vessel health is crucial for a wide variety of brain diseases. “Our research shows that even in a disease that doesn’t start with a blood vessel, by making the vessels work better, there may be a beneficial effect,” Iadecola said. “Beside Alzheimer’s disease, our study provides us with a new way to look at vascular risk factors that cause stroke and dementia, like hypertension and diabetes, because in these conditions these PVM cells were not previously considered as major players.”
Source: Molly Schulson – Cornell University
Image Source: image is credited to the researchers.
Original Reserch: Abstract for “Brain Perivascular Macrophages Initiate the Neurovascular Dysfunction of Alzheimer Aβ Peptides” by Laibaik Park, Ken Uekawa, Lidia Garcia-Bonilla, Kenzo Koizumi, Michelle Murphy, Rose Pitstick, Linda H Younkin, Steven G Younkin, Ping Zhou, Geroge A Carlson, Josef Anrather, and Costantino Iadecola in Circulation Research. Published online May 17 doi:10.1161/CIRCRESAHA.117.311054


Brain Perivascular Macrophages Initiate the Neurovascular Dysfunction of Alzheimer Aβ Peptides

Rationale: Increasing evidence indicates that alterations of the cerebral microcirculation may play a role in Alzheimer’s disease (AD), the leading cause of late-life dementia. The amyloid-β peptide (Aβ), a key pathogenic factor in AD, induces profound alterations in neurovascular regulation through the innate immunity receptor CD36, which, in turn, activates a Nox2-containing NADPH oxidase leading to cerebrovascular oxidative stress. Brain perivascular macrophages (PVM) located in the perivascular space, a major site of brain Aβ collection and clearance, are juxtaposed to the wall of intracerebral resistance vessels and are a powerful source of reactive oxygen species (ROS).

Objective: We tested the hypothesis that PVM are the main source of ROS responsible for the cerebrovascular actions of Aβ, and that CD36 and Nox2 in PVM are the molecular substrates of the effect.

Methods and Results: Selective depletion of PVM using intracerebroventricular injection of clodronate abrogates the ROS production and cerebrovascular dysfunction induced by Aβ applied directly to the cerebral cortex, administered intravascularly or overproduced in the brain of transgenic mice expressing mutated forms of the amyloid precursor protein (Tg2576 mice). In addition, using bone marrow chimeras we demonstrate that PVM are the cells expressing CD36 and Nox2 responsible for the dysfunction. Thus, deletion of CD36 or Nox2 from PVM abrogates the deleterious vascular effects of Aβ, whereas wild-type PVM reconstitute the vascular dysfunction in CD36-null mice.

Conclusions: The data identify PVM as a previously unrecognized effector of the damaging neurovascular actions of Aβ and unveil a new mechanism by which brain-resident innate immune cells and their receptors may contribute to the pathobiology of AD.
“Brain Perivascular Macrophages Initiate the Neurovascular Dysfunction of Alzheimer Aβ Peptides” by Laibaik Park, Ken Uekawa, Lidia Garcia-Bonilla, Kenzo Koizumi, Michelle Murphy, Rose Pitstick, Linda H Younkin, Steven G Younkin, Ping Zhou, Geroge A Carlson, Josef Anrather, and Costantino Iadecola in Circulation Research. Published online May 17 doi:10.1161/CIRCRESAHA.117.311054

What’s the Difference Between Alzheimer’s Disease and Dementia?


Summary: A common misconception is that Alzheimer’s disease and dementia are the same thing. Alzheimer’s disease is simply one form of dementia. Researchers from Texas A&M describe how Alzheimer’s and other forms of dementia impact the lives of both patients and their families, and provide new insights into minimizing the risks of developing neurodegenerative conditions.

Source: Texas A&M.

Two of the most common risk factors for Alzheimer’s and dementia are age and genetics. Most individuals with Alzheimer’s are 65 or older, and those who have a parent or sibling with Alzheimer’s are more likely to develop the disease. However, there is evidence to suggest that there are other factors that people can influence. image is adapted from the Texas A&M news release.

Not all dementia is Alzheimer’s—but it can be just as devastating when it affects loved ones.
While often used interchangeably, dementia and Alzheimer’s disease are not the same. Dementia is a general term for a decline in mental ability severe enough to interfere with daily life. Alzheimer’s disease is a specific type of dementia that causes memory loss and impairment of other important mental functions. An expert from the Texas A&M School of Public Health describes how these conditions can impact the lives of both patients and those around them, and provides insights into ways of minimizing risks.

Dementia (and Alzheimer’s)
“Dementia is an umbrella term for a serious decline in mental ability that impacts one’s overall health and functioning,” said Marcia Ory, PhD, MPH, head of the Center for Population Health and Aging and Regents and Distinguished Professor at the Texas A&M School of Public Health. “There are different types of dementia, and the most common type of dementia is Alzheimer’s.”

Alzheimer’s disease makes up between 60 to 80 percent of dementia cases. It is a progressive disease, which means that the symptoms gradually worsen over a number of years. Alzheimer’s is also the sixth-leading cause of death in the United States, and those with Alzheimer’s live an average of eight years after their symptoms became noticeable to others.

Other specific types of dementia include vascular dementia and mixed dementia. Vascular dementia is considered the second-most common form of dementia after Alzheimer’s disease and is usually the result from injuries to the vessels supplying blood to the brain—often after a stroke or series of strokes.

Other less-common types of dementia come from frontotemporal disorders and Lewy body dementia. Frontotemporal disorders are a form of dementia caused by a family of brain diseases known as frontotemporal lobar degeneration (FTLD), and Lewy body dementia is caused by abnormal deposits of a protein—called alpha-synuclein—in the brain.

Mixed dementia is a term that describes having multiple types of dementia, such as both Alzheimer’s disease and vascular dementia. In a person with mixed dementia, it may not be clear which symptoms are attributed to one type of dementia over the other. Researchers are still working to understand how the disease processes influence one another in mixed dementia patients.

In some cases, it’s not known what type of dementia someone has or if it’s not a specific, named type at all. The causes of dementia are not always known, and some older people may develop age-associated memory impairment—which is different than dementia and Alzheimer’s disease.

Risk factors for dementia
Two of the most common risk factors for Alzheimer’s and dementia are age and genetics. Most individuals with Alzheimer’s are 65 or older, and those who have a parent or sibling with Alzheimer’s are more likely to develop the disease. However, there is evidence to suggest that there are other factors that people can influence.

According to research from the University of Cambridge, one-third of Alzheimer’s disease cases were attributed to preventable risk factors. The seven main risk factors for Alzheimer’s disease are diabetes, hypertension, obesity, physical inactivity, depression, smoking and low educational attainment.

“Minimizing the risk of these factors can potentially minimize the onset of dementia, but to an unknown degree,” Ory said. “We know that physical activity, a healthy diet and healthy lifestyle can help reduce the symptomology of many major diseases, and similarly these can affect the onset and progression of dementia symptomatology.”

If you’re looking for a start to reducing the risk for dementia or Alzheimer’s, a healthy diet and getting enough exercise is a good start. Exercise has been shown to increase blood flow and help connections between neurons, which is important with cognitive functioning.

“Systematic review of all the studies of physical activity conclude that it’s a modifiable risk factor,” Ory said. “We don’t know what type, how much or how often we should exercise. Further, the newest frontier is to go beyond a single risk factor approach and identify all the good behaviors—such as diet, exercise and cognitive exercises—and examine how the combination can lower the risk or symptomology of dementia.”

Overall, because there are multiple risk factors, the solutions should be multi-pronged intervention programs. “Similar to how there are a lot of risk factors for falls, there are a lot of risk factors that increase likelihood of dementia,” Ory said. “It’s complicated to minimize the risk, but you’ll do best with multi-dimensional approach.”

Talking with your health care provider
Aging is a difficult process for many people, and talking to your health care provider about your concerns can be very beneficial. They can provide you with information and resources to help ease your concerns or improve your quality of life if you have any of these conditions.

“There are simple screening tests that health care professionals can perform during routine medical visits,” Ory said. “Knowing the signs and symptomatology of dementia is important as there are medications that can reduce your symptomatology, and, along with being more active and engaging in other healthy lifestyles, can improve your quality of life.”

Although there are no medications or treatment that can cure dementia or Alzheimer’s, medications and a healthy lifestyle will help you process your condition as well as possible. Ask your physician about safety and limitations. There is nothing shameful about having dementia.

“Before people talked about dementia in medical terms, they’d say that the patient was ‘crazy’ or ‘senile,’” Ory said. “People don’t use those terms now because they recognize it’s a medical condition and not about personality or willpower. Alzheimer’s and dementia are far too common and are not something we can ignore.”

Ory also recommended that caregivers of someone with dementia look into programs or support groups. “Don’t ignore your own care when you are caring for someone with dementia,” she said. “It takes a group effort sometimes, and joining a program or being able to discuss the difficulties with others or experts, can help immensely.”
Source: Holly Shive – Texas A&M
Image Source: image is adapted from the Texas A&M news release.

White Collar Workers at Higher Odds of Death From ALS, Parkinson's

By Steven Reinberg, HealthDay   |   July 13, 2017

Study found richer, better-educated folks with these brain diseases are more likely to die

Typically, better-paying jobs and those that require higher education are thought more desirable, but a new study suggests white collar workers have a higher risk of death from two neurodegenerative diseases.
The research found that richer, better-educated people with Parkinson's disease or amyotrophic lateral sclerosis (ALS, also called Lou Gehrig's disease), appear more likely to die from these diseases than those in lower paying or less educationally demanding work.
Workers in these "high socioeconomic" occupations include mathematicians, architects, engineers, lawyers and managers, according to a new report from the U.S. Centers for Disease Control and Prevention.
"This is kind of an unexpected finding," said lead author John Beard, a research officer at the CDC's National Institute for Occupational Safety and Health.
Most prior studies have focused on environmental exposures to chemicals, such as pesticides or solvents, or electromagnetic fields that seem to occur more frequently in lower socioeconomic occupations, like military service, farming or construction, he said.
The researchers looked at 26 different occupations and deaths from ALS and Parkinson's disease and, overall, found that workers in occupations associated with higher education and income had an increased risk from dying from these diseases, Beard said.
"We see these higher rates of deaths from ALS and Parkinson's in people with higher socioeconomic status, but we don't understand the reasons for it," he said.
"It's hard to know if these deaths are related to environmental exposure or to socioeconomic status," Beard added.
More research is needed to replicate this result and to try to figure out what is going on, he said.
Beard said this study has limitations that have to be accounted for before any recommendations can be made. For example, the current study only shows an association, it doesn't prove a cause-and-effect relationship.
He said studies that look at environmental exposures in various jobs and the levels of exposure and their relationship to these diseases also need to be done. 
It may not be the job itself that increases the risk of dying from these conditions, but other factors, such as smoking, Beard said.
One neurologist speculated that people in lower socioeconomic jobs might die at younger ages from other causes.
"People with lower socioeconomic jobs may die earlier from heart or respiratory disease and not have the chance to develop these diseases that are much more likely to happen in older people," said Dr. Sami Saba, a neurologist from Lenox Hill Hospital in New York City.
Saba doesn't think the type of job or the size of income accounts for this finding. "There is some possibility that these researchers are not accounting for," he said.
Beard, however, doesn't think age is a factor, because the researchers adjusted their findings for age, he said.
The researchers looked at data from more than 12 million adult death certificates from 1985 to 1999, 2003 to 2004, and 2007 to 2011 in 30 states.
Job classifications were grouped into 26 categories based on similar job duties and ordered from high-paying management occupations to lower-paying transportation and material-moving work.
The analysis included nearly 27,000 ALS deaths, more than 115,000 Parkinson's deaths and nearly 159,000 deaths from heart failure.
The report was published July 14 in the CDC's Morbidity and Mortality Weekly Report.
More information
For more information on ALS, visit the ALS Association.
SOURCES: John Beard, Ph.D., research officer, National Institute for Occupational Safety and Health, U.S. Centers for Disease Control and Prevention; Sami Saba, M.D., neurologist, Lenox Hill Hospital, New York City; July 14, 2017, Morbidity and Mortality Weekly Report, online

10 Quotes to Help You When You’re Feeling Down


We know dealing with a condition such as Parkinson’s disease can sometimes feel, both for the patients and the caregivers. You feel like you’re not doing enough or as if the disease is taking up all your time and attention.
To help you on your journey, we’ve gathered a few quotes we thought might help pick you up during those moments when everything feels a bit bleak.
1. “Always remember you are braver than you believe, stronger than you seem, smarter than you think and twice as beautiful as you’ve ever imagined.” – Dr. Seuss
2. “Never believe that a few caring people can’t change the world. For, indeed, that’s all who ever have.” – Margaret Mead
3. “A hundred years from now, it will not matter what kind of car I drove, what kind of house I lived in, how much money I had in the bank…but the world may be a better place because I made a difference in the life of a child.” – Forest Witcraft
4. “Live so that when your children think of fairness, caring, and integrity, they think of you.” – H. Jackson Brown, Jr.
5. “Too often we underestimate the power of a touch, a smile, a kind word, a listening ear, an honest compliment, or the smallest act of caring, all of which have the potential to turn a life around.” – Leo Buscaglia
6. “Our greatest weakness lies in giving up. The most certain way to succeed is always to try just one more time.” – Thomas Edison
7. “Act as if what you do makes a difference. It does. – William James
8. “You’ve survived 100 percent of everything in your life so far, so there’s a pretty good chance that you’ll survive whatever is next.” – Timber Hawkeye
9. “How wonderful it is that nobody need wait a single moment before starting to improve the world.”1 – Anne Frank
10. “Courage doesn’t always roar. Sometimes courage is the quiet voice at the end of the day saying, ‘I will try again tomorrow.'” – Mary Anne Radmacher
Parkinson’s News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website.

U.S. Government Researchers Develop Tool to Predict Cognitive Decline in Parkinson’s Patients


U.S. government researchers have developed a computerized mathematical model for predicting and testing cognitive decline in Parkinson’s patients.
The team from the National Institute of Neurological Disorders and Stroke used information on 3,200 Parkinson’s cases in North America and Europe to develop the algorithm.
The model could help doctors do a better job of addressing the cognitive decline associated with the disease. It could also help them predict patient outcomes.
Data on the patients came from the years 1986 to 2016. Researchers applied statistical methods to the information to identify predictors of cognitive decline. They included the age when the disease showed up, a patient’s gender, movement scores, a patient’s formal years of education, whether a patient had experienced depression, and whether a patient had any genetic mutations.
“This study includes both genetic and clinical assessments from multiple groups of patients, and it represents a significant step forward in our ability to effectively model one of the most troublesome non-motor aspects of Parkinson’s disease,” Dr. Margaret Sutherland, program director of the National Institute of Neurological Disorders and Stroke, said in a news release.
The patients in the study had experienced movement problems as well as cognitive loss.
“By allowing clinical [trial] researchers to identify and select only patients at high-risk for developing dementia, this tool could help in the design” of trials that require a manageable number of participants, said Clemens Scherzer, a senior researcher in the study.
An interesting finding was that patients with more years of formal education were at lower risk of developing cognitive loss over the years.
“This fits with the theory that education might provide your brain with a ‘cognitive reserve,’ which is the capacity to potentially compensate for some disease-related effects,” Scherzer said. “I hope researchers will take a closer look at this. It would be amazing if this simple observation could be turned into a useful therapeutic intervention.”
An ethical issue with using the algorithm with patients is telling them that it is predicting cognitive decline when scientists have yet to develop treatments for the problem, researchers said.
But the model could help improve the design of clinical trials, which could be a plus in the development of therapies, they said.
Doctors could also use the algorithm to help predict which patients need to be treated against cognitive decline once therapies are available.
“Prediction is the first step,” Scherzer said. “Prevention is the ultimate goal, preventing a dismal prognosis from ever happening.”

Study identifies source of cell-specific change in Alzheimer's disease

July 13, 2017

Researchers led by Arizona State University (ASU) and the Translational Genomics Research Institute (TGen) have identified altered expression of a gene called ANK1, which only recently has been associated with memory robbing Alzheimer's disease, in specific cells in the brain.

Using an extremely precise method of isolating cells called "laser capture microdissection," researchers looked at three specific cell types - microglia, astrocytes and neurons - in the brain tissue of individuals with a pathological diagnosis of Alzheimer's disease, and compared them to brain samples from healthy individuals and those with Parkinson's disease.

Following sequencing of each of these cell types, the ASU-TGen led team found that altered ANK1 expression originates in microglia, a type of immune cell found in the brain and central nervous system, according to the study published today in the scientific journal PLOS ONE.

"Although previous genetic and epigenetic-wide association studies had shown a significant association between ANK1 and AD, they were unable to identify the class of cells that may be responsible for such association because of the use of brain homogenates. Here, we provide evidence that microglia are the source of the previously observed differential expression patterns in the ANK1 gene in Alzheimer's disease," said Dr. Diego Mastroeni, an Assistant Research Professor at Biodesign's ASU-Banner Neurodegenerative Disease Research Center, and the study's lead author.

All three of the cell types in this study were derived from the hippocampus, a small looping structure shaped like a seahorse (its name derives from the Greek words for horse and sea monster).  The hippocampus resides deep inside the human brain and plays important roles in the consolidation of both short-term and long-term memory, and in the spatial memory that enables the body to navigate.

In Alzheimer's disease - and other forms of dementia - the hippocampus is one of the first regions of the brain to suffer damage, resulting in short-term memory loss and disorientation. Individuals with extensive damage to the hippocampus are unable to form and retain new memories.

"Using our unique data set, we show that in the hippocampus, ANK1 is significantly increased four-fold in Alzheimer's disease microglia, but not in neurons or astrocytes from the same individuals," said Dr. Winnie Liang, an Assistant Professor, Director of TGen Scientific Operations and Director of TGen's Collaborative Sequencing Center, and one of the study's authors. "These findings emphasize that expression analysis of defined classes of cells is required to understand what genes and pathways are dysregulated in Alzheimer's."

Alzheimer's features many signs of chronic inflammation, and microglia are key regulators of the inflammatory cascade, proposed as an early event in the development of Alzheimer's, the study said.

Because the study found that ANK1 also was increased two-fold in Parkinson's disease, "these data suggest that alterations in ANK1, at lease in microglia, may not be disease specific, but rather a response, or phenotype associated with neurodegeneration … more specifically, neuroinflammation."

More than 5 million Americans have Alzheimer's, an irreversible and progressive brain disorder that slowly destroys memory, thinking skills and eventually the ability to conduct even the simplest of tasks. For most patients, symptoms first appear in the mid-60s. For older Americans, it is the third leading cause of death, following heart disease and cancer, according to the National Institutes of Health.

"The success of this, and many other studies, owes a great deal to the support and collaborative nature of the people of the Arizona Alzheimer's Consortium.  The results obtained in this work emphasize the importance of methods that enable us to characterize the molecular profile of defined cells, either as a group or as single cells, that have been defined by any of several means," said Dr. Paul Coleman, Research Professor at Biodesign's ASU-Banner Neurodegenerative Disease Research Center, and the study's senior author.

Dr. Eric Reiman, Director of the Arizona Alzheimer's Consortium and Clinical Director of Neurogenomics at TGen, said: "This study demonstrates the value of bringing together talented researchers from different disciplines and organizations to advance the scientific fight against Alzheimer's disease."

Journal reference: PLoS ONE