Brian Grant says Karl Malone helped him raise funds in bout with Parkinson’s disease

 by Paolo Songco      September 8, 2018

Despite being ferocious rivals on the basketball court during their playing years, Biran Grant and Hall of Famer Karl Malone have now formed a precious bond as friends. In fact, when Grant’s Parkinson’s disease became public nearly a decade ago, the Utah Jazz legend was one of the first who reached out to him.

Grant recently sat down with TMZ Sports to discuss how his condition has impacted his life, and how Malone was there for him in his time of need.

“When I was diagnosed, I received a call from [Karl Malone] two weeks after [the report on Grant’s diagnosis] aired on ESPN with Ric Bucher,” explained Grant. “He just said, ‘Brian, this is Karl. I’d like to help.'”

Grant went on to explain how an infamous on-court incident involving himself and Malone, in which Grant sustained a cut near his eye, led to the idea of doing a fundraiser.

“I said, ‘You know what we can do? We can go on that fishing trip,'” Grant said.

That fishing trip, which Grant and Malone set up and auctioned off, earned them a cool $107,000 which was used for the benefit of Grant’s treatment.

This just proves that no matter how fierce the competition between players may get on the court, everyone remains to be part of one big NBA family.

Now at 46 years old, Grant continues to fight his battle against his crippling disease.

Here is Grant’s full TMZ Sports interview:  

https://clutchpoints.com/jazz-news-brian-grant-says-karl-malone-helped-raise-funds-parkinsons/

Several supporters at seventh Parkinson SuperWalk

By Shawna O'Neill, TC Media   September 8, 2018

From left-to-right: Penny Eccles, Vernon Eccles, Denise Babb, Henri Roy and Carolyn Roy showing their support at the Parkinson SuperWalk 2018. (Shawna O'Neill/TC Media).

CORNWALL, Ontario – Over 100 participants gathered at the Cornwall Civic Complex this morning in anticipation of the city’s seventh annual Parkinson SuperWalk.

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Walkers set out at 11 a.m. and could choose between a 3.5 km route or 5 km route. All walkers who raised over $50 received a free shirt.  

“There’s lots of people here, everyone seems to be enjoying the day so far and we have beautiful weather for the walk,” said Ginette Trottier, Community Development Coordination of Parkinson Canada for Eastern Ontario. “It has grown every year.”

Last year the walk raised over $9,000. This year, the goal is to reach $10,000. According to Trottier, funds raised go towards national research, and bringing education events to the area for community members and health care professionals. It will also fund a support group that meets in the area.

Trottier expected to see a crowd of about 125 to 150 attendees, and thinks that 20 to 30 of those involved have Parkinson’s disease.

“One of the things that’s difficult for the people who have Parkinson’s is they tend to be isolated,” explained Trottier. “When they come out, they get to meet other people and other families who are coping. It’s nice for them to know they’re not alone and a lot of people support them.”

Penny Eccles, of Team Eccles, said that after three weeks of fundraising, her team garnered over $6,000. Friends from Montreal and Toronto attended the walk today to support Penny and her husband Vernon who has Parkinson’s disease.

“We’re small but mighty!” said Penny, reflecting on her close-knit team of friends. 

https://www.cornwallseawaynews.com/news/local/2018/9/8/several-supporters-at-seventh-parkinson-superwalk.html

Certain MicroRNAs Could Help Diagnose Parkinson’s, Study Suggests

SEPTEMBER 7, 2018 BY JOSE MARQUES LOPES, PHD 

Specific microRNAs that are contained in tiny, cell-derived vesicles called exosomes may be biomarkers of Parkinson’s disease, according to a study.

The study, “Circulating exosomal miRNAs as diagnostic biomarkers in Parkinson’s disease,” was published in the journal European Review for Medical and Pharmacological Sciences.

MicroRNAs (miRNAs) are tiny bits of RNA that bind to messenger RNA (mRNA) — a molecule generated from DNA that contains the information to make proteins — to regulate gene expression, which is the process by which information in a gene is synthesized to create a working product, like a protein.

Abnormal plasma levels of miRNAs have been found in Parkinson’s patients. For example, while miR-505 — also implicated in cancer and hypertension — was reduced, miR-331-5p — also involved in cancer and chemotherapy resistance — was elevated in these patients.

In the cerebrospinal fluid, which fills the brain and spinal cord, miRNAs contained in exosomes may have diagnostic value for Parkinson’s patients. However, little is known about exosomal miRNAs from blood plasma, which have been suggested as a useful approach to diagnose Alzheimer’s.

Aiming to address this, researchers at Cangzhou Central Hospital in China collected blood from 52 Parkinson’s patients and 48 healthy participants used as controls. Parkinson’s patients included 28 men, at a mean age of 65.6 years with a mean disease duration of 5.3 years. Healthy individuals included 26 men, at a mean age of 61.2 years.

All patients had taken Parkinson’s medications for at least two weeks and had Mini-Mental State Examination cognitive scores within the normal range.

Among the used Parkinson’s medications, a levodopa/carbidopa combination was taken by all patients. Comtan (entacapone) was also common, taken by 20 patients (38.5%), while Zelapar (selegiline) was taken by 10 (19.2%), and Requip (ropinirole) taken by nine (17.3%).

Exosomes were isolated from blood samples, which were then analyzed for their levels of protein and miRNAs.

The exosomes were round or oval-shaped and contained the exosomal protein markers CD9, CD63, and Tsg101, confirming the presence of these tiny vesicles in plasma.

Among nine different miRNAs, the level of exosomal miR-331-5p was significantly higher and that of miR-505 was significantly lower in Parkinson’s patients than in healthy controls. In patients, miR-331-5p was mainly packaged in exosomes, which, according to the researchers, may mean it is later transferred to Parkinson’s-related cells to influence disease development.

In turn, miR-505 was essentially found in the plasma, indicating it may not be transferred to Parkinson’s by exosomes, but rather by other cells. However, this theory needs to be further studied, the team said.

These results provide “solid evidence that exosomal miR-331-5p and miR-505 could be biomarkers for [Parkinson’s],” the researchers wrote, and that “exosomal miR-331-5p and miR-505 have diagnostic values for [Parkinson’s].”

https://parkinsonsnewstoday.com/2018/09/07/specific-micrornas-may-help-diagnose-parkinsons-study/

Site-Seeker supports Parkinson’s foundation

Published Sep 7, 2018

NEW HARTFORD — Site-Seekeer, a digital marketing agency based in New Hartford, raised more than $5,000 for the Michael J. Fox Foundation at its 2018 Putts for Parkinson’s golf tournament, the company announced.

To date, Site-Seeker has donated more than $13,000 to research into Parkinson’s disease. 

The mother of company founders Eddie and Brian Bluff died in 2017 after suffering with the disease more than 20 years.

“We watched Parkinson’s disease slowly take pieces of our mother from us: her ability to walk, her ability to speak and care for her family,” CEO Brian Bluff said. 

The Michael J. Fox Foundation is a patient-focused research group dedicated to finding a cure for Parkinson’s disease and improving treatments and therapies.

The tournament, Aug. 24 at Kanon Valley Country Club, had nearly 50 guests and gave away nearly $4,000 in cash and prizes, with many cash winners donating prizes to the Michael J. Fox Foundation, according to Site-Seeker. 

Tax-deductible donations to Team Fox on behalf of Site-Seeker may be made online at https://fundraise.michaeljfox.org/tf-2018/Team/View/59252/Site-Seeker.

http://romesentinel.com/business/site-seeker-supports-parkinsons-foundation/QBqrie!vRAv9KsdVMklMWXNFeLR8g/

Apomorphine Benefits Finally Confirmed in Parkinson's

Sue Hughes September 07, 2018

The benefits of the dopamine agonist apomorphine in Parkinson's disease have finally been confirmed in a randomized controlled trial, although the drug has been used in the condition for many years.

The new trial — known as TOLEDO — showed that subcutaneous apomorphine infusion "has beneficial clinical effects on motor fluctuations in patients with Parkinson's disease that persist despite optimization of oral or transdermal medication," conclude the authors, led by Regina Katzenschlager, MD, Danube Hospital, Vienna, Austria.

"Additionally, continuous subcutaneous administration of apomorphine might allow the dose and number of doses of short-acting oral antiparkinsonian medication to be reduced," they add.

The trial is published in the September issue of the Lancet Neurology. The findings were first presented and reported by Medscape Medical News at the American Academy of Neurology 2017 Annual Meeting.

Equivalent to Levodopa

Katzenschlager and colleagues explain that apomorphine was first licensed in the United Kingdom for use in the treatment of Parkinson's in 1993 on the basis of findings from an open-label study showing that apomorphine had antiparkinsonian efficacy equivalent to that of levodopa, and it remains the only available medication with the same symptomatic efficacy as levodopa.

Subcutaneous apomorphine infusion is licensed for severe motor fluctuations and is reimbursed by several healthcare systems across the world.

They note that in more advanced Parkinson's disease, patients can experience long troublesome periods of immobility, and attempts to control fluctuations with oral medication can lead to disabling dyskinesia. Persistent motor complications can be managed with deep-brain stimulation or continuous dopaminergic drug delivery using subcutaneous infusion of apomorphine or intestinal infusion of levodopa-carbidopa gel.

While high-level evidence supports the efficacy of deep-brain stimulation and levodopa-carbidopa gel, both treatments are invasive and associated with certain risks.

Although numerous uncontrolled studies have shown the efficacy of apomorphine in reducing "off" time, when the patient's medication is not working optimally and parkinsonian symptoms return, and most have also shown an improvement in dyskinesias and concomitant reductions in oral levodopa doses, the researchers report that the drug has never been tested in a randomized controlled trial. They say this is "an important weakness in the formal evidence base for this treatment option."

They therefore conducted the TOLEDO trial, in which 107 patients with Parkinson's disease who had motor fluctuations not adequately controlled by medical treatment were randomly assigned to receive 3 to 8 mg/h apomorphine or placebo saline infusion during waking hours (16 hours a day) for 12 weeks.

After completing the 12-week double-blind phase, patients could enter the 52-week open-label phase of the trial, during which all patients received apomorphine infusion.

The primary efficacy endpoint was the absolute change in off time (derived from patient diaries) from baseline to the week 12 visit. 

Results showed that off time (which was around an average of 6 hours per day at baseline) was reduced by an average of 0.58 hours per day in the placebo group vs 2.47 hours in the apomorphine group, a significant difference (P = .0025).

Apomorphine was well tolerated without any unexpected safety signals, although six patients in the apomorphine group withdrew from the study because of treatment-related adverse events.

"Our study aimed to reflect actual clinical practice, including regional differences, and to fairly represent the population of patients with Parkinson's disease who are routinely offered this treatment," the researchers write. The results provide high-level evidence that apomorphine infusion leads to a pronounced improvement in off time, which is associated with an increase in good on time and is clinically meaningful from the patient's perspective.

"We hope that treatment guidelines will be developed to guide physicians, and apomorphine infusion will be offered and reimbursed more widely as an effective treatment option."

They add that although comparative randomized studies of apomorphine vs levodopa-carbidopa gel have not yet been done, "both infusion treatments have similar effect sizes, and apomorphine infusion is easily reversible and less invasive than levodopa-carbidopa gel, which requires the insertion of a gastric tube."

They also point out that while most patients started treatment as inpatients, outpatient initiation of treatment was also possible, "which, depending on the health-care system and circumstances, might mean more convenience to patients and health-care providers and a reduced need for use of inpatient hospital resources."

Before Invasive Therapies

In an accompanying Comment, Peter A. LeWitt, MD, Henry Ford Hospital, Detroit, Michigan, says the TOLEDO study should help guide clinicians in making decisions about management of patients with advanced Parkinson's disease, particularly when considering use of deep-brain stimulation or intestinal infusion of levodopa-carbidopa gel.  

"In view of its efficacy and safety profile, apomorphine infusion should be considered before embarking on other invasive therapies," he states.

LeWitt notes, however, that this study highlights that despite treatment with apomorphine, high doses of levodopa, and other adjunctive medications,

many patients continue to be burdened by substantial daily off time fluctuations.

"A final question unanswered by this study is the effectiveness of apomorphine monotherapy, which has been previously tested in only a few studies. Future studies might investigate this question and what benefit, if any, is offered by concomitant levodopa treatment," he concludes.

This study was funded by Britannia Pharmaceuticals. Katzenschlager reports personal fees, nonfinancial support, and grants from Britannia Pharmaceuticals during the conduct of the study. LeWitt has served as a consultant or advisor for Abide, Acorda, Biogen, Britannia, Cavion, Sunovion, Intec, Jazz, Merz, NeuroDerm, Pfizer, Sage, SynAgile, Titan, and US WorldMeds, and has received speaker honoraria from Acadia, Lundbeck, and US WorldMeds. He is compensated for services as editor-in-chief of Clinical Neuropharmacology. The Parkinson’s Disease and Movement Disorders Program that he directs has received clinical research grant support for conducting clinical trials from Acorda, Adamas, Biotie, Cavion, Intec, Lundbeck, NeuroDerm, The Michael J Fox Foundation for Parkinson’s Research, The Parkinson Study Group, Roche, Sunovion, and US WorldMeds.

Lancet Neurol  Published 2108;17:749-759, 732-733.  

https://www.medscape.com/viewarticle/901709?src=rss

In the Pipeline-Parkinson's Disease: Alpha-Synuclein Antibody Therapy Is Safe, Setting the Stage for an Efficacy Trial

Robinson, Richard    September 6, 2018

A monoclonal antibody infusion targeting alpha-synuclein (AS) lowered the level of serum AS by up to 97 percent in people with Parkinson's disease, with greater and long-lasting reductions seen at higher doses in a small safety trial, setting the stage for a larger phase 2 study.

A monoclonal antibody targeting aggregated alpha-synuclein (AS) is safe and tolerable, and enters the central nervous system in people with Parkinson's disease (PD), according to a study published June 18 online in JAMA Neurology.

The results set the stage for a larger efficacy trial, according to experts, although the lack of an AS imaging marker presents serious challenges to tracking the efficacy of this or other therapies targeting the aggregated protein.

The antibody treatment is meant to interrupt the prion-like spread of misfolded AS, which many researchers believe is central to the neurodegenerative process. That hypothesis is based on over a decade of work in animal models and autopsy studies in people with PD, suggesting that, as with the prion diseases themselves, misfolded AS from one neuron can be released and taken up by another, where it induces misfolding in endogenous AS.

“The notion that alpha-synuclein plays a central role in the pathogenesis of Parkinson's disease is well accepted,” the lead study author Joseph Jankovic, MD, FAAN, professor of neurology and director of the Parkinson's Disease Center and Movement Disorders Clinic at Baylor College of Medicine in Houston, told Neurology Today. “There is good evidence that misfolding and aggregation of alpha-synuclein are toxic, and while there is some controversy about the role of prion-like spreading, I think the prevalent view among Parkinson [researchers] is that aggregated alpha-synuclein propagates from cell to cell.”

Several biotechnology and pharmaceutical companies are developing antibody-based treatments for AS aggregates, including Prothena Biosciences in partnership with Hoffmann-La Roche, the sponsors of the current study.

****

STUDY DETAILS

The trial enrolled 80 people with PD, who were randomized approximately 2:1 to placebo or the humanized monoclonal antibody PRX002, infused monthly for three months. Patients receiving active treatment were grouped into six cohorts, with each successive cohort receiving a higher dose, to a maximum of 60 milligrams per kilogram. 

The treatment was safe and well tolerated, with no serious or severe treatment-emergent adverse events. Treatment-emergent adverse events that were more common in those receiving active treatment included rash at the infusion site, one acute allergic reaction, and dysgeusia.

The antibody was cleared as expected over time, at a rate indicating that monthly infusions would maintain the desired minimum concentration in the bloodstream. Lumbar punctures at approximately week nine indicated that the antibody was present in cerebrospinal fluid at 0.3 percent of the concentration in the serum, roughly the same as seen in antibody trials of Alzheimer's disease, Dr. Jankovic noted.

Antibody infusion lowered the level of serum AS by up to 97 percent, with greater and long-lasting reductions seen at higher doses. That was not true in the cerebrospinal fluid, Dr. Jankovic noted, where there were no statistically significant changes compared to placebo for free AS; total AS declined only in one of the intermediate-dose groups, and there was no dose-dependent trend.

“This is the first pathogenesis-targeted study in Parkinson's disease,” Dr. Jankovic said. “If you accept the hypothesis that aggregation of alpha-synuclein plays a role in the disease, then targeting it is the next logical step. I think that's the most important message of the study. The fact there is some target engagement, as shown by a reduction in serum alpha-synuclein, and that the antibody is getting into the central nervous system, is also encouraging.” These positive results, combined with a good safety profile, “support going forward with a larger study to test efficacy,” he said.

That trial, called Pasadena (https://clinicaltrials.gov/ct2/show/NCT03100149) is underway, and is expected to be completed in 2021. The study includes multiple clinical and pharmacokinetic endpoints, and will include dopamine receptor imaging. But it will not include any direct measurement of AS aggregation clearance, because there is not yet any imaging marker for any form of the protein, Dr. Jankovic said.

“We hope some of the outcome measures in the trial will indicate a trend toward benefit,” Dr. Jankovic said, “but there is currently no way to measure levels of the aggregated protein in the body.”

****

EXPERT COMMENTARY

“I think this trial represents important progress in development of antibody therapies for Parkinson's disease,” commented David Standaert, MD, PhD, professor and chair of neurology at the University of Alabama at Birmingham. “The results demonstrate safety and tolerability, and they have shown that the antibody gets into the central nervous system. However, this doesn't tell us whether this changes alpha-synuclein in the brain. An imaging marker would really change the game in that respect. Without that, there isn't any other way to further establish the likelihood of success without going ahead with an efficacy trial.”

Patrik Brundin, MD, PhD, professor and director of the Center for Neurodegenerative Science at the Van Andel Research Institute in Grand Rapids, MI, agreed. “It is important to have a good surrogate marker for alpha-synuclein, which we currently do not have,” despite much research, he said. “Nonetheless, the results in animal models, with reduction in AS and improvements in motor and behavioral measures, are promising.”

“I think of all the animal models of Parkinson's disease, the synuclein-based ones are the most compelling ones, and the effects in those models of the various immunotherapies being developed are consistent, that reducing alpha-synuclein is beneficial.”

Dr. Brundin noted that the recent announcement by Biogen that their antibody targeting amyloid-beta fibrils appears to both reduce amyloid and improve clinical measures gives more hope that this is a worthwhile approach. “One has to know one is targeting the right molecule, and in Parkinson's disease, we are confident that alpha-synuclein is the right molecule.”

However, Dr. Standaert noted, one must also target the right conformation of that molecule. “The whole question of what exactly is the form of misfolded synuclein that is toxic is still not completely settled,” he said.

Success also depends on getting the antibody to the right place at the right time, and there is much that is still unclear about prion-like spread of AS in the human brain, Dr. Standaert said. “If the antibody clears only extracellular aggregates, rather than acting intracellularly, it may slow spreading, but not have much effect on the death of neurons already afflicted with aggregated protein. But slowing the disease would still be a groundbreaking accomplishment.

“My patients will all tell me that they are more worried about how their disease will progress, rather than their current symptoms. If we could simply stop the progress of the disease, a lot of patents would be really happy.”

Neurology Today: September 6, 2018 - Volume 18 - Issue 17 - p 6–8

doi: 10.1097/01.NT.0000546220.05241.70

https://journals.lww.com/neurotodayonline/Fulltext/2018/09060/In_the_Pipeline_Parkinson_s_Disease_.5.aspx

WVU expert available for comment on Parkinson’s disease and its impact on daily life

 Article ID: 700181   7-Sep-2018   West Virginia University 

WVU's Ann Murray

Parkinson’s disease has reached new notoriety in the last decade as celebrities have spoken up and stepped up to support research and reduce stigma. From everyone’s favorite former teen wolf, Michael J. Fox, to Alan Alda of M*A*S*H fame. And while the spotlight has helped to further the cause, there is still plenty of misinformation about the disease, which impacts nearly 10 million people worldwide.

Ann Murray, M.D.

Assistant Professor, Neurology

American Board of Psychiatry and Neurology certified

WVU School of Medicine

What is Parkinson’s disease?

“Parkinson’s is a multifaceted disease that stems from a problem in deep brain structures.  This problem leads to loss of dopamine in the brain which results in problems with all aspects of movement for patients affected.

“Many people associate some of the dance-like movements of Michael J. Fox to Parkinson’s disease itself, but those movements are most frequently side-effects of medications used to treat the disease. 

“Parkinson’s is not only a physical disease – although that is the predominant feature – it can also cause slow thinking, mood changes and sleep problems. This disease impacts all aspects of patients’ lives and that’s why it’s so important to see a specialist who can identify the best treatment options and address all these needs.”

How does it impact a patient?

“This disease can truly affect every aspect of a patient's life and some of the biggest impacts are much less visualized -- like slow movement, and difficulty talking and living their day-to-day life. That’s the part of the disease that can be so disabling.”

More common than one might think

“This disease is common. I tell patients that I'm sure they know someone with Parkinson’s, but may never actually be aware of that person’s diagnosis, because the goal of therapy is to keep all Parkinson's patients maintaining their lifestyle as best they can."

 A passion and commitment to care

“My goal is for them to live their life doing the things they want to do with this disease – so this disease will never become their life

“We still don't have a cure, but the good news is we have so many amazing treatment options patients can usually continue doing the things they love with the people they love and that’s our goal.”

https://www.newswise.com/articles/expert-pitch-wvu-expert-available-for-comment-on-parkinson-s-disease-and-its-impact-on-daily-life

Parkinson’s WA fundraiser A Walk in the Park for Hamersley resident

Written by Laura Pond       September 6th, 2018

 Warwick Senior High School teacher Belinda Hall and her father Peter Dee. Picture: Andrew Ritchie.

HAMERSLEY resident Peter Dee shares a commonality with some high profile entertainers that he wishes he did not.

The popular Perth musician and comedian, who toured Australia with band Hi-Way 1 in the 1970s and supported Michael Bubl in the 2000s, has had to stop performing since being diagnosed with Parkinson’s disease four years ago.

He said it was “more prevalent than you think”, listing Neil Diamond, Billy Connolly and Robin Williams as famous performers with the disease.

“It’s a terrible disease; from nose to toes, somewhere it’s attacking you,” he said.

“You don’t die from it, you die with it.”

Despite this, Mr Dee said he was an optimist and wanted to help raise awareness of the disease.

He and daughter Belinda Hall, deputy principal at Warwick Senior High School, are taking part in A Walk in the Park on September 16 in Floreat, to fundraise for Parkinson’s WA.

“I want to help get more acceptance for the disease and more understanding,” he said.While most people associated tremors with Parkinson’s, Mr Dee said other symptoms he experienced included losing his sense of smell, unintentionally falling asleep and being unable to sit down for more than 30 minutes at a time.

Mrs Hall said she was proud to join him in the walk.

“My dad has been a superstar to me my whole life,” she said.

“He took us on trips all over the world as kids with his work, and also did crazy things like hire a light plane to Rotto for lunch.

“These days he is finding some things a little more challenging and we have really appreciated the information and support provided by Parkinson’s WA.

“That is why I am participating in A Walk in the Park – so that I can support the organisation that helps support my dad.”

The family and dog-friendly event kicks off at Perry Lakes Reserve from 9.30am, with the 2km and 5km walks starting at 11am.

There will be performances by Flamenco dancers Casa Del Comps and Brazilian-style Wasamba drummers, as well as refreshments, homemade produce and children’s entertainment.

Register at www.parkinsonswa.org.au.

https://www.communitynews.com.au/stirling-times/news/parkinsons-wa-fundraiser-a-walk-in-the-park-for-hamersley-resident/

This Energy Drink Claims It Helps With Alzheimer's And Parkinson's

MAYA MCDOWELL

SEP 6, 2018

Monster Energy is calling B.S.

When you think of energy drinks, you might think of pulling an all-nighter in college, or trying to wake yourself up during a long drive. You're probably not thinking "good for my health", let alone "helps with diseases." Vital Pharmaceuticals (VPX Sports) begs to differ, though. The company has marketed the energy drink Bang as being able to possibly "reverse mental retardation" and "help with all forms of dementia", including Alzheimer's Disease, Parkinson's Disease, and Huntington's Disease, per a marketing video on YouTube. 

Monster Beverage Corporation (behind Monster Energy) is not having it. The company filed a lawsuit in a California district court against VPX Sports, alleging that the company uses "deceptive advertising and marketing", according to the Miami Herald. 

The lawsuit lists four complaints, based on violation of California laws for unfair competition, false advertising, and trade libel, Miami Herald reports. The suit states, "Monster is likely to suffer, has suffered, and will continue to suffer damages to its business and goodwill, the loss of sales and profits it would have made but for [VPX's] wrongful acts, and increased advertising and marketing costs, all in an amount to be proven at trial."

Jack Owoc, owner of VPX, calls himself the CSO (Chief Scientific Officer), and states on the website, "I intended to hold myself and the company to a higher standard than other company on the planet. In fact, I wanted to run VPX like a pharmaceutical company and adhere closer to their higher standards."

Monster's suit references videos Jack has posted on social media, including YouTube and Instagram that promote Bang and suggest that the "Super Creatine" ingredient in the product is "20 times more effective at reaching the brain than other forms of creatine," according to Miami Herald. 

In addition, Monster's suit challenges VPX's claims that drinking Bang can "reverse mental retardation ... can also help cure Alzheimer's Disease, Parkinson's Disease, Huntington's Disease and other forms of dementia," and that Bang is "the healthiest energy drink," per Miami Herald. 

According to the suit, even if the drink could deliver the promised benefits, "the ingredients at the heart of [VPX's] claims — Super Creatine are sprinkled into Bang in such low amounts that none of the purported benefits could ever be delivered through safe consumption of Bang."

You can watch one of the promotional videos for Bang yourself:

https://youtu.be/_hYcTX9jYr0

To each their own, but I won't be drinking energy drinks anytime soon for my health.

https://www.delish.com/food-news/a23008821/energy-drink-claims-helps-with-alzheimers-parkinsons/