Number of years in NFL plus certain positions portend greater risk for cognitive and mental health problems

NEUROSCIENCE NEWS    AUGUST 30, 2019

Longer career length and playing specific positions put NFL players at greater risk of developing cognitive problems and mental health issues. Playing for 10 or more seasons increased the risks for depression, anxiety, and cognitive impairment twice as much than those who played for a single season. For every five seasons of play, the risks increase 20% for cognitive impairment. Those most at risk are running backs, linebackers and those who played special teams positions.

Source: Harvard

The study is believed to be the first to explore the interplay between career length, position and cognitive and mental health outcomes among professional football players. The image is in the public domain.

Longer NFL careers and certain playing positions appear to each spell greater long-term risk for serious cognitive problems such as confusion, memory deficits, depression and anxiety in former football players, according to a new report published Aug. 30 in The American Journal of Sports Medicine.

The study is believed to be the first to explore the interplay between career length, position and cognitive and mental health outcomes among professional football players.

The analysis — based on a survey of nearly 3,500 former NFL players — was conducted by investigators at the Harvard T.H. Chan School of Public Health and Harvard Medical School as part of the ongoing Football Players Health Study at Harvard University.

The study results show that players who experienced concussions had elevated risk for serious cognitive problems, depression and anxiety, which persisted over time, as long as 20 years following injury. The investigators caution that their analysis relied on players’ memories of experiencing concussion rather than on diagnosis at the time of injury. And the findings do not mean that everyone with concussion will necessarily experience cognitive or mental health problems, they add. Contrary to previous reports, the new research did not find a link between starting football at a young age and cognitive problems in adulthood.

On one level, the researchers say, many of their findings make intuitive sense and confirm what some might have already suspected: The longer players remain in the game, the more likely they are to suffer a head injury, which increases the risk for neurocognitive problems. It also affirms that certain positions are more prone to concussions and, therefore, players in them face greater risk for experiencing the downstream of effects of head injury.

Nonetheless, the researchers said, the analysis is the first to document and quantify the risk that stems from lengthier careers and certain high-impact positions.

Specifically, the analysis showed that players who reported the most concussion symptoms had 22-fold risk of reporting serious long-term cognitive problems and six times the risk of having symptoms of depression and anxiety, compared with those who reported the fewest symptoms.

“Our findings confirm what some have suspected — a consistently and persistently elevated risk for men who play longer and who play in certain positions,” said study lead investigator Andrea Roberts, a research scientist at the Harvard T.H. Chan School of Public Health.

“Our results underscore the importance of preventing concussions, vigilant monitoring of those who suffer them and finding new ways to mitigate the damage from head injury.”

For the study, former players, average age 53, were asked about the number of seasons played in the NFL, their positions and any history of blows to the head or neck followed by symptoms of concussion such as dizziness, confusion, vision problems, loss of consciousness, nausea, headaches and seizures, among other symptoms. Based on the number and severity of symptoms, players were given a concussion score.

Overall, one in eight players (12 percent) reported signs of serious cognitive problems. By comparison, about 2 percent of people in the general population in the United States report such problems. Age made no difference in the interplay between concussion and cognitive problems, the study showed. Those under age 52 reported serious cognitive problems at a similar rate as the rest (13 percent), a finding that suggests neurocognitive decline was likely not a function of mere aging. Alarmingly, that risk remained magnified even in those 45 and younger. Indeed, 30 percent of players 45 and younger who had the most concussions reported serious cognitive problems.

To gauge whether the number of seasons played and position type were linked to depression, anxiety and cognitive problems, the researchers used standard questionnaires commonly used to screen for the presence of such disorders. The researchers compared the proportion of players with serious cognitive problems among individuals with various career lengths — one season, two to four seasons, five to six seasons, seven to nine seasons and 10 seasons or more. Overall, those with the longest careers — 10 seasons or more — were twice as likely to report severe cognitive problems compared with players who’d played a single season — 12.6 percent in the 10-plus season group reported signs of severe cognitive problems, compared with 5.8 percent in the single-season category. The risk crept up proportionally with the number of seasons played, growing progressively higher as the number of years increased. Every five seasons of play carried a nearly 20 percent increase in risk for serious cognitive problems.

Which position one played also mattered. To evaluate the risk-position link, the researchers divided players into three groups based on the average concussion symptoms per year that players reported in each position. Kickers, punters and quarterbacks had the fewest symptoms per year, followed by wide receivers, defensive backs, linemen and tight ends. The groups with the highest number of symptoms included running backs, linebackers and special teams.

Those in the group with the most concussion symptoms had twice the risk for serious cognitive problems — 15 percent of those in this group had cognitive difficulties — compared with those reporting the fewest concussion symptoms (6 percent). Those with the most concussions also had a nearly 50 percent greater risk for depression and anxiety, compared with those playing in the group with the fewest concussion symptoms. One in four in the first group had symptoms indicative of depression, compared with 15 percent of players reporting problems in the latter one, while 27 percent had signs of anxiety, compared with 16 percent in the group with the fewest concussions. Those who played in the mid-range group had a 75 percent higher risk of cognitive problems and a 40 percent elevation in risk for depression and anxiety, compared with players in the group with the fewest symptoms.

Nearly one in four players reported symptoms of anxiety (26 percent) and depression (24 percent), and nearly one in five (18 percent) reported symptoms of both conditions. Career length influenced risk for depression, with every five seasons boosting the risk by 9 percent. The number of seasons, however, was not linked to greater anxiety risk.

The age at which an individual started playing organized football did not affect risk. Indeed, outcomes were similar between those who began playing the game before age 12 and those who began later. The findings, however, pertain solely to former NFL players and not necessarily to the general population, the researchers caution. The question of when a child should start playing organized football remains very much open, and should be made by each individual family, the researchers said.

“The overarching goal of the Football Players Health Study is to unravel risk factors and disease mechanisms and to inform interventions that preserve and optimize player health and wellness,” said study senior author Marc Weisskopf, the Cecil K. and Philip Drinker Professor of Environmental Epidemiology and Physiology at the Harvard T.H. Chan School of Public Health. “These latest findings confirm much of what we know but they add much needed granularity and specificity to risk magnitude by career length and position.”

“Clearly, not everyone who sustains a concussion is destined for cognitive trouble, but the results of the research highlight just how critical it is to continue to find ways to prevent head injuries from occurring in the first place because of the many downstream and long-lasting effects on physical, cognitive and mental health,” said Ross Zafonte, the Earle P. and Ida S. Charlton Professor of Physical Medicine and Rehabilitation and head of the Department of Physical Medicine and Rehabilitation at Harvard Medical School. Zafonte is also principal investigator of the Football Players Health Study.

Funding: The research was supported by National Football League Players Association (NFLPA).

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Source:

Harvard

Media Contacts: 

Ekaterina Pesheva – Harvard

Image Source:

The image is in the public domain.

Original Research: Closed access

“Exposure to American Football and Neuropsychiatric Health in Former National Football League Players: Findings From the Football Players Health Study”. Andrea L. Roberts, Alvaro Pascual-Leone, Frank E. Speizer, Ross D. Zafonte, Aaron L. Baggish, Herman Taylor, Lee M. Nadler, Ann Connor, Rachel Grashow, Alexandra M. Stillman, Dean A. Marengi, Marc G. Weisskopf, Theodore K. Courtney.

American Journal of Sports Medicine. doi:10.1177/0363546519868989

Abstract

Exposure to American Football and Neuropsychiatric Health in Former National Football League Players: Findings From the Football Players Health Study

Background:

Former American football players have a higher prevalence of cognitive impairment than that of the US general population. It remains unknown what aspects of playing football are associated with neuropsychiatric outcomes.

Hypothesis:

It was hypothesized that seasons of professional football, playing position, and experience of concussions were associated with cognition-related quality of life (QOL) and indicators of depression and anxiety.

Study Design:

Descriptive epidemiology study.

Methods:

The authors examined whether seasons of professional football, playing position, and experience of concussions, as measured by self-report of 10 symptoms, were associated with cognition-related QOL and indicators of depression and anxiety in a cross-sectional survey conducted 2015 to 2017. Cognition-related QOL was measured by the short form of the Quality of Life in Neurological Disorders: Applied Cognition–General Concerns. The Patient Health Questionnaire–4 measured depression and anxiety symptoms. Of 13,720 eligible men with apparently valid contact information, 3506 players returned a questionnaire at the time of this analysis (response rate = 25.6%).

Results:

Seasons of professional play (risk ratio [RR] per 5 seasons = 1.19, 95% CI = 1.06-1.34) and playing position were associated with cognition-related QOL. Each 5 seasons of play was associated with 9% increased risk of indicators of depression at borderline statistical significance (P = .05). When compared with former kickers, punters, and quarterbacks, men who played any other position had a higher risk of poor cognition-related QOL, depression, and anxiety. Concussion symptoms were strongly associated with poor cognition-related QOL (highest concussion quartile, RR = 22.3, P < .001), depression (highest quartile, RR = 6.0, P < .0001), and anxiety (highest quartile, RR = 6.4, P < .0001), even 20 years after last professional play.

Conclusion:

The data suggest that seasons of play and playing position in the NFL are associated with lasting neuropsychiatric health deficits. Additionally, poor cognition-related QOL, depression, and anxiety appear to be associated with concussion in the long term.

https://neurosciencenews.com/nfl-cognition-positions-mental-health-14839/

Creation of new brain cells plays an underappreciated role in Alzheimer’s disease

NEUROSCIENCE NEWS   AUGUST 30, 2019

Microglia may play a significant role in disrupting neurogenesis in those with Alzheimer’s disease. When mice were given drugs which caused microglial cells to die, neurogenesis returned to normal.

Source: University of Chicago

Much of the research on the underlying causes of Alzheimer’s disease focuses on amyloid beta (Aß), a protein that accumulates in the brain as the disease progresses. Excess Aß proteins form clumps or “plaques” that disrupt communication between brain cells and trigger inflammation, eventually leading to widespread loss of neurons and brain tissue.

Aß plaques will continue to be a major focus for Alzheimer’s researchers. However, new work by neuroscientists at the University of Chicago looks at another process that plays an underappreciated role in the progression of the disease.

In a new study published in the Journal of Neuroscience, Sangram Sisodia, PhD, the Thomas Reynolds Sr. Family Professor of Neurosciences at UChicago, and his colleagues show how in genetic forms of Alzheimer’s, a process called neurogenesis, or the creation of new brain cells, can be disrupted by the brain’s own immune cells.

Some types of early onset, hereditary Alzheimer’s are caused by mutations in two genes called presenilin 1 (PS1) and presenilin 2 (PS2). Previous research has shown that when healthy mice are placed into an “enriched” environment where they can exercise, play and interact with each other, they have a huge increase in new brain cells being created in the hippocampus, part of the brain that is important for memory. But when mice carrying mutations to PS1 and PS2 are placed in an enriched environment, they don’t show the same increase in new brain cells. They also start to show signs of anxiety, a symptom often reported by people with early onset Alzheimer’s.

This led Sisodia to think that something besides genetics had a role to play. He suspected that the process of neurogenesis in mice both with and without Alzheimer’s mutations could also be influenced by other cells that interact with the newly forming brain cells.

Focus on the microglia

The researchers focused on microglia, a kind of immune cell in the brain that usually repairs synapses, destroys dying cells and clears out excess Aß proteins. When the researchers gave the mice a drug that causes microglial cells to die, neurogenesis returned to normal. The mice with presenilin mutations were then placed into an enriched environment and they were fine; they didn’t show any memory deficits or signs of anxiety, and they were creating the normal, expected number of new neurons.

He feels that this discovery about the microglia’s role opens another important avenue toward understanding the biology of Alzheimer’s disease. The image is in the public domain.

“It’s the most astounding result to me,” Sisodia said. “Once you wipe out the microglia, all these deficits that you see in these mice with the mutations are completely restored. You get rid of one cell type, and everything is back to normal.”

Sisodia thinks the microglia could be overplaying their immune system role in this case. Alzheimer’s disease normally causes inflammation in the microglia, so when they encounter newly formed brain cells with presenilin mutations they may overreact and kill them off prematurely. He feels that this discovery about the microglia’s role opens another important avenue toward understanding the biology of Alzheimer’s disease.

“I’ve been studying amyloid for 30 years, but there’s something else going on here, and the role of neurogenesis is really underappreciated,” he said. “This is another way to understand the biology of these genes that we know significantly affect the progression of disease and loss of memory.”

Additional authors include Sylvia Ortega-Martinez, Nisha Palla, Xiaoqiong Zhang and Erin Lipman from the University of Chicago.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Source:

University of Chicago

Media Contacts: 

Matt Wood – University of Chicago

Image Source:

The image is in the public domain.

Original Research: Closed access

“Deficits in Enrichment-Dependent Neurogenesis and Enhanced Anxiety Behaviors Mediated by Expression of Alzheimer’s Disease-Linked Ps1 Variants Are Rescued by Microglial Depletion”. Sylvia Ortega-Martinez, Nisha Palla, Xiaoqiong Zhang, Erin Lipman and Sangram S. Sisodia.

Journal of Neuroscience. doi:10.1523/JNEUROSCI.0884-19.2019

Abstract

Deficits in Enrichment-Dependent Neurogenesis and Enhanced Anxiety Behaviors Mediated by Expression of Alzheimer’s Disease-Linked Ps1 Variants Are Rescued by Microglial Depletion

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that presently affects an estimated 5.7 million Americans. Understanding the basis for this disease is key for the development of a future successful treatment. In this effort, we previously reported that mouse prion protein-promoter-driven, ubiquitous expression of familial AD (FAD)-linked human PSEN1 variants in transgenic mice impairs environmental enrichment (EE)-induced proliferation and neurogenesis of adult hippocampal neural progenitor cells (AHNPCs) and in a non-cell autonomous manner. These findings were confirmed in PS1M146V/+ mice that harbor an FAD-linked mutation in the endogenous PSEN1 gene. We now demonstrate that CSF1R antagonist-mediated microglial depletion in transgenic male mice expressing mutant presenilin 1 (PS1) or PS1M146V/+ “knock-in” mice leads to a complete rescue of deficits in proliferation, differentiation and survival of AHNPCs. Moreover, microglia depletion suppressed the heightened baseline anxiety behavior observed in transgenic mice expressing mutant PS1 and PS1M146V/+ mice to levels observed in mice expressing wild-type human PS1 or nontransgenic mice, respectively. These findings demonstrate that in mice expressing FAD-linked PS1, microglia play a critical role in the regulation of EE-dependent AHNPC proliferation and neurogenesis and the modulation of affective behaviors.

SIGNIFICANCE STATEMENT 

Inheritance of mutations in genes encoding presenilin 1 (PS1) causes familial Alzheimer’s disease (FAD). Mutant PS1 expression enhances the levels and assembly of toxic Aβ42 peptides and impairs the self-renewal and neuronal differentiation of adult hippocampal neural progenitor cells (AHNPCs) following environmental enrichment (EE) that is associated with heightened baseline anxiety. We now show that microglial depletion fully restores the EE-mediated impairments in AHNPC phenotypes and suppresses the heightened baseline anxiety observed in mice expressing FAD-linked PS1. Thus, we conclude that the memory deficits and anxiety-related behaviors in patients with PS1 mutations is a reflection not just of an increase in the levels of Aβ42 peptides, but to impairments in the self-renewal and neuronal differentiation of AHNPCs that modulate affective behaviors.

https://neurosciencenews.com/alzheimers-brain-cell-creation-14838/

My Memory Worx Fund established to support Parkinson's programs and services

August 30, 2019

EFFINGHAM -- The MyMemoryWorx Fund at Southeastern Illinois Community Foundation provides a way for donors, individuals, and local businesses to provide charitable grants to MyMemoryWorx. The fund will specifically support the programs and services which are open to local people and their families affected by Parkinson’s disease. Any clinical or for-profit portions of MyMemoryWorx will not be eligible for support from this fund.

MyMemoryWorx opened in 2016 and is a brain health & education center specializing in interventions not found inside a pill bottle. Kelly Willenborg is the Founder and President of MyMemoryWorx which offers certified cognitive coaching and assessments. She is certified in several fitness programs geared to the senior population and has opened a resource center called the Parkinson’s Institute of Effingham which manages programs such as Rock Steady Boxing and SPEAK OUT! Voice Therapy to improve the lives of those facing the disease. Her work with the aging population began over 10 years ago after launching The Healing Jukebox: an arm for delivering musical engagement and education to long-term care and memory care residents/staff. The Healing Jukebox has placed 120+ iPods in over 10 facilities. Kelly continues to advocate for music therapy as a board member of Tri-Music, a non-for-profit agency in Central Illinois. She received her Master’s in Aging Studies/Gerontology from Eastern Illinois University.

The Parkinson’s Institute of Effingham (PIE) originated in November of 2018 as an extension of the existing neuro health interventions. The institute’s goal is three-fold: educate, stimulate and support. They practice peer connection, reassuring that no participant feels alone or are defined by the disease. Kelly acknowledges that the peer connection is a vital part of their involvement with the program: “They are all up against the same battle.” Kelly saw the formation of PIE as a natural progression from the early services she provided. PIE’s services currently include monthly support group meetings, specialty workshops (falling, pain management, etc), voice therapy and the new Rock Steady Boxing program.

Rock Steady Boxing’s mission is to empower people with Parkinson’s disease, and improve their quality of life through a non-contact boxing curriculum. Although Rock Steady Boxing in Effingham is one of over 800 locations, this program offers a unique opportunity for monitoring mental improvements through a clinical cognitive testing system. Members are screened free of charge every three months, giving them personal data that incorporates both mental and, like other Rock Steady programs, physical achievements. In the few months it has been in operation, it has received incredible feedback from its members. Kelly spoke highly of their progress: “I can tell a difference from their ability to move, their balance, and their camaraderie.”

MyMemoryWorx will open their office at 710 West Jefferson Avenue in the new LiveWell center in September 2019. Their space will be shared with Mika Yoga and Tri-Music. “The new location represents the realization of a dream come true... music, mindfulness and mental fitness all under one roof.”

MyMemoryWorx is currently seeking class volunteers and a paid coach to assist her with the boxing program as well as donations to support the Parkinson’s community. We encourage learning collaborations with college programs as well. Kelly Willenborg can be reached for general inquiries or to explore partnerships at: willenborgkelly@gmail.com

Southeastern Illinois Community Foundation manages more than 140 affiliated funds for the immediate and long-term benefit of communities in southeastern Illinois. For more information, contact Amanda Lessley, President/CEO of Southeastern Illinois Community Foundation, at 217.342.4988 or amanda@enrichingourcommunity.org.

https://jg-tc.com/lifestyles/health-med-fit/my-memory-worx-fund-established-to-support-parkinson-s-programs/article_82c8c540-0231-5dc6-8ee3-e05ae3046311.html

Explaining, Not Complaining: A New Approach to Pain

August 30, 2019 In Columns, Dr. C's

Pain visits me all the time now. There are multiple days when high pain levels make me nauseated. I am sick and tired of having to say how sick and tired I feel. I’m experimenting with a new approach: responding to the pain in a dispassionate way, making observations, and providing explanations.

Neo (my neocortex, mentioned in a previous column) snickers, “Who are you kidding? You can’t sit with five days of high pain without the Grouch showing up and leaving behind a trail of consequences.” Neo tends to be a bit of a naysayer, much like Eeyore in the books about Winnie-the-Pooh, by A.A. Milne.

“Not true,” I quickly retort. “For the last two five-day stretches of bad pain, I did not let the Grouch speak in public. My partner shared her sincere gratitude on this accomplishment. It makes it easier on her and makes the home less stressful, decreasing my total pain level.”

Neo replies, “I’m not talking about just zipping the lip. I’m talking about that inner dialog, the way you speak about the high levels of pain to yourself. What happened the other night after five days with high pain?”

I let out a deep sigh. “That was a difficult night, following a difficult week. It seemed like so many events were crashing around me. I tried to quiet my thoughts, but the pain was too loud, overpowering. Eventually, it consumed me.”

Neo challenges my perception. “Did you hear how you talked to yourself about this high-pain experience?”

Reflecting, I admit, “Yep. With every pain surge, I complained about how miserable I felt. There wasn’t an external Grouch for others to see, but he showed up in my thoughts — a lot!”

“Exactly!” Neo exclaims. “It is the Grouch you have to change if you seek improved well-being. It’s easy to complain, and you have plenty of company on social media. But finding a different path, implementing healthy solutions — that’s where the hard work happens.”

I’ve seen glimmers of a different inner dialog. Rather than reacting to the high pain, I should be sitting in the “pause between” and observing it with as little emotion as possible; analyzing the pain and reporting back to Neo like a journalist covering a story. A new inner dialog needs to develop to keep the Grouch at bay. It’s a dialog about being caressed by calmness, about knowing this is possible at any time and making calmness the focus of my attention.

“Nice idealism,” Neo says, waving his brain neurons at me. “You know you haven’t been fully successful at this yet.”

I sigh, “True, I haven’t achieved a perfect day. Maybe I never will. But I am trying to improve every day.” Taking a deep breath to calm the emotions Neo has stirred by pointing out my failings, I continue, “I also find that seeking quietude in the pause between helps me. I’m facing one day at a time while doing all I can to implement a new pattern of thought and behavior. I’m just taking small, incremental steps right now, but I’m happy with the progress.”

Neo reminds me in that Eeyore tone, “You know how hard this is to accomplish.”

I stand, move to the windows and look out on the perennial gardens. The summer colors are starting to diminish, but the plants still have plenty of blooms. “You know, Neo,” I say calmly, “Life is like gardening in many ways. Take a shovelful of dirt, arrange plants by complementary colors, and lay a broad, level path to walk, pause, and enjoy. Showing up and accomplishing those baby steps every day eventually brings forth a garden of wonder and delight.”

Neo and I are quiet together while we walk the garden path.

***

Note: 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. The opinions expressed in this column are not those of Parkinson’s News Today or its parent company, BioNews Services, and are intended to spark discussion about issues pertaining to Parkinson’s disease.

https://parkinsonsnewstoday.com/2019/08/30/new-approach-explaining-not-complaining/

Phase 3 Trial to Test Continuous Pump Delivery of Levodopa in Treating Motor Fluctuations

AUGUST 30, 2019  BY MARISA WEXLER IN NEWS.

A new Phase 3 clinical trial, called the “BouNDless study,” will soon compare continuous administration of ND0612 to oral immediate-release carbidopa/levodopa (CD/LD) in people with Parkinson’s disease who are experiencing motor fluctuations, Mitsubishi Tanabe Pharma America (MTPA) announced.

Both of the above-mentioned treatments work by increasing the level of the neurotransmitter dopamine in the brain — their key distinction is delivery. Unlike the conventional oral medication, ND0612 is given in continuous injections via a subcutaneous (under the skin) pump, not unlike how insulin might be delivered to people with diabetes.

“While oral CD/LD is the established standard for treating motor symptoms in Parkinson’s disease, many patients experience a decline in benefit as their disease advances, requiring them to take multiple doses throughout the day in an effort to control symptoms, often with unpredictable results,” Atsushi Fujimoto, the president of MTPA, said in a press release.

“We look forward to researching the potential efficacy and safety of continuous subcutaneous treatment with ND0612 on managing motor fluctuations and other complications of Parkinson’s disease, through the BouNDless study.”

The Phase 3 trial (NCT04006210), now getting underway, will compare ND0612 to immediate release CD/LD treatment in people with Parkinson’s whose symptoms are not being controlled by conventional treatments, defined as an average of 2.5 hours (or more) of motor fluctuation each day, with at least two hours per day during which motor symptoms are not under control (off time) while the person is awake.

Following a screening period, all participants will go through an open-label oral immediate release CD/LD adjustment period, followed by an open-label ND0612 conversion period. They will then be randomly assigned to either ND0612 or its matching placebo, plus immediate release CD/LD. After this 12-week main study, all have the option to continue in open-label extension period for one year.

The study’s main goal is to determine the effect of ND0612 on daily “good” on time, defined as time without dyskinesia (involuntary movement) or with non-troublesome dyskinesia.

BouNDless is set to soon start enrolling about 300 people at some 120 different sites around the globe. More information is available here.

The study is being funded by the pharmaceutical company NeuroDerm, which is developing ND0612; if the treatment is approved, MTPA will be the company selling it in North America. Both NeuroDerm and MTPA are owned by Mitsubishi Tanabe Pharma Corporation.

“Given the limitations of current therapeutic options for Parkinson’s disease, we recognized the importance of developing a potential non-surgical continuous treatment that may stabilize CD/LD plasma levels and alleviate the disabling motor fluctuations that are often exacerbated with disease progression,” said Sheila Oren, MD, MBA, chief medical officer at NeuroDerm. “We are excited that the Phase 3 study of ND0612 is underway, and we may be one step closer to potentially bringing a much-needed treatment option to patients.”

https://parkinsonsnewstoday.com/2019/08/30/phase-3-trial-tests-continuous-pump-levodopa-delivery-on-parkinsons-motor-fluctuations/

Phase 2 Trial of Parkinson’s Psychosis Therapy Enrolling Across U.S. D

AUGUST 30, 2019 BY JOSE MARQUES LOPES, PHD

A Phase 2 clinical trial of SEP-363856, an oral treatment candidate for patients with Parkinson’s psychosis, is recruiting participants throughout the U.S.

The Sunovion-funded SEP361-203 study (NCT02969369) will be conducted at 24 U.S. sites and will include approximately 36 participants, 24 on SEP-363856 and 12 on placebo.

Trial locations and their contacts can be found here.

Eligible patients are at least 55 years old, received a Parkinson’s diagnosis at least one year prior to the study and have been experiencing symptoms such as visual hallucinations (to see, hear or feel things that do not exist) and/or delusions, which refers to holding false and typically paranoid beliefs.

Women may be eligible if they are postmenopausal. All participants need to have a caregiver able to attend all study visits. Full details on inclusion and exclusion criteria are given here.

Following a screening/washout period lasting up to two weeks, Sunovion’s SEP361-203 will be given in oral capsules at 25, 50, or 75 mg once daily for six weeks, followed by 12 weeks of an open-label extension phase and one week of follow-up.

The study will test the safety, tolerability and effectiveness of SEP-363856, via changes in the Scale for Assessment of Positive Symptoms – Parkinson’s Disease (SAPS-PD) total score, which addresses hallucinations and delusions.

Other assessments include the Clinical Global Impression-Severity of Illness (a measure of disease severity), the Neuropsychiatric Inventory (composed of an interview of the caregiver), and the Mini Mental State Evaluation of cognitive function, which measures memory, orientation, concentration, and language. Blood and urine tests also will be performed.

All study visits, tests and trial-related medication will be provided at no cost. Participants also may be reimbursed for travel and other expenses. The study is expected to be completed by May 2020.

Parkinson’s psychosis is one the non-motor symptoms of the disease. Its most common manifestations are hallucinations and delusions, but illusions (misinterpreting existing things), panic attacks, and vivid dreams also may occur.

Currently, Nuplazid (pimavanserin), developed by Acadia, is the only U.S. Food and Drug Administration (FDA)–approved medication for treating hallucinations and delusions associated with Parkinson’s disease.

Suncoast Neuroscience Associates in St. Petersburg, Florida is one of the locations enrolling participants for the SEP361-203 study. Patient care there is led by Alberto Vasquez, MD, a neurologist and lead principal investigator at Suncoast. 

To contact the researchers at Suncoast:https://cdn.newswire.com/files/x/ec/6e/ebfc42b5224c1020ea20ae1cf3b2.pdf

https://parkinsonsnewstoday.com/2019/08/30/phase-2-trial-of-parkinsons-psychosis-therapy-enrolling-across-us/

"Catch" this Parkinson's event Saturday

 Aug 30, 2019 

https://youtu.be/44AOZWDmT78

CORPUS CHRISTI, Texas — It is that time of year again -- time to pull out your kayak, your stand-up paddle board, or whatever you have that floats, to take part in the annual Catch the Cure-Paddle for Parkinson’s. 

The event is held to raise money to help find a cure for Parkinson’s Disease.

Crystal Ybanez helped organize a fishing tournament fundraiser in 2007. During the tournament's first three years, it raised close to $5,000 at each event.

“In 2006, my father, Ed Ybanez, was diagnosed with Parkinson’s Disease at the age of 54," Ybanez said. "As a family we struggled with how to cope with the diagnosis and how we could take bad news and try to make the best of the situation. My aunt, Ramona Singleterry, suggested that we start a local support group and have a fundraiser to help support Parkinson’s Disease research in hopes that a cure will one day be discovered."

The organization decided to try something different in 2010 and held its first Paddle for Parkinson’s event. 

“Paddle for Parkinson’s is a kayak/stand up paddle board race that starts at the Billish Park boat ramp on Padre Island," Ybanez said. "Paddlers race one another to the yacht club and back, either doing one 2.5 mile loop or two loops depending on the category they choose. The race is open to anyone who wants to participate. Anyone under 18 must have a parent or guardian present." 

For those who do not have their own kayak or stand-up paddle board, Wind and Waves can be contacted at 361-937-9283 for rentals. Registration takes place Friday from 5-7 p.m. at Snoopy’s Pier, or on-site at the event from 7:30-8:30 am on Saturday.

“Each year the number of participants and funds raised has grown," she said. "The last few years, we’ve had 50-60 registrants for the event and hope to have the same amount this year."

This year the group is optimistic the event will bring its fundraising efforts to new heights, and at the same time, continue to unify community members in an effort to raise money for finding a cure for Parkinson’s disease, which is a debilitating neuro-degenerative disorder. 

“The 2018 'Paddle' raised $13,500 which brings the total amount over 13 years to approximately $143,500," Ybanez said. 'That money has gone to support the Parkinson’s Foundation and Michael J. Fox Foundations, as well as helped support the local patients and caregivers through support group meetings, exercise classes, and more."

The 2019 event does have some changes from the past years. Previously they have had a post-race barbecue-and-band event immediately following the race and awards. This year, the race and awards will still take place, but the Coastal Bend Parkinson’s Support Group will be hosting an educational seminar at The Waves Resort instead. 

The race begins at 9 am on Saturday on the canals at the Billish Park boat ramp in Padre Island, and will last until the final participant has finished. 

Awards will be announced and handed out. The seminar will start at 12:30 p.m. and will have a combination of exhibitors and speakers.

From 12:30-1:00 p.m., attendees can visit exhibitors and have appetizers. There will be numerous speakers from 1-5 p.m. to discuss how to manage Parkinson’s disease and what options are available for patients and caregivers.

Support group meetings are open to anyone who would like to attend, and take place the third Saturday of the month. More information can be found on the website: https://www.catchthecure.org/

https://www.kristv.com/news/local-news/catch-this-parkinsons-event-saturday