Parkinson's disease meds not likely related to cirrhosis

• BY KEITH ROACH, M.D.
 
• Sep 13, 2018 

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• DEAR DR. ROACH: My dad recently passed away as a result of cirrhosis of the liver. He also had Parkinson’s disease for 10 years. Several other people we know who have Parkinson’s also have cirrhosis. Is it possible that his Parkinson’s medication could have caused the cirrhosis? My dad was 78. He did drink beer up until about 10 years ago, mainly socially and nothing real extensive. He was a little overweight, probably by 30 or 40 pounds. The medication that he was on was carbidopa/levodopa. It just seems like it would be too much of a coincidence that there are several people with the exact circumstances as my dad. — E.S.

  ANSWER: I am sorry to hear about your dad passing.

  Carbidopa/levodopa (Sinemet) is a common, well-established treatment for Parkinson’s disease. While it’s impossible to say with certainty in any given person, carbidopa/levodopa is almost never associated with serious liver damage, so cirrhosis related to this drug would be exceedingly unlikely.

  In your dad’s case, it’s much more likely that he had fatty liver disease, which is associated with being overweight (and especially in people with diabetes, if your dad had that). This is a much more likely cause of cirrhosis, in my opinion. Although he may not have consumed a lot of beer, any alcohol increases the risk of liver damage in a person who already has some liver problem, including fatty liver.

  The only definitive treatment for fatty liver is a better diet and weight loss (and, of course, alcohol abstinence, at least in people with abnormal liver enzymes by blood testing). A diet of mostly plants with little meat, almost no refined sugar or processed carbohydrates, and with nuts and whole grains, can help control diabetes and foster weight loss, which can sometimes reverse the damage to the liver.

  To answer your question directly, Parkinson’s disease and cirrhosis both are common, and it’s not too much of a coincidence to see several people with that combination.

  DEAR DR. ROACH: I recently opened up some stored tuna that my son had saved for me. He loves to hunt his own food. When I ate it, I realized that when he had gone to Alaska, he had not only hunted tuna but also black bear. He had used the black bear grease to cure the tuna. I was mortified that he had used a protected animal to preserve his tuna. I reluctantly ate it anyway. Now, I am worried about my health. Will anything happen to me healthwise because I have eaten the grease from a black bear from Alaska? The bear was wild, so could it have had a disease, like rabies? I’m sure it has never been vaccinated. — Anon.

  ANSWER: Black bears are hunted in many states, and although it is regulated (you need a license) in Alaska, they are not a protected species under the Endangered Species Act. Black bears are hunted for both sport and meat. The major health risk from consuming bear meat is trichinella, a muscle parasite. The meat must be heated to a high temperature to be sure of killing the parasite. Grease from the bear should not have trichinella risk.

  Another concern is rabies. Rabies is possible but rare in bears. I doubt it could be transmitted from grease, though, as rabies virus lives in nervous tissue, not fat.
https://www.marshallnewsmessenger.com/parkinson-s-disease-meds-not-likely-related-to-cirrhosis/article_ff2aa71e-b769-11e8-b5e1-4f0bf1b54b1d.html 

Parkinson’s Disease and the Uric Acid Sweet Spot

By: Dr. Michael Greger  September 14, 2018

Parkinson’s disease, the second most common neurodegenerative disorder after Alzheimer’s, is characterized by a slowness of movement, rigidity, tremor, and stooping posture, all of which worsen over time. Non-movement symptoms such as cognitive impairment and sleep, smell, and mood disturbances occur as the disease spreads to other areas of the brain.

The cause of Parkinson’s is perhaps “one of the important questions posed by the neurobiology [science] of aging.” For example, why is the consumption of dairy products associated with increased risk of Parkinson’s? Perhaps because they contribute to our exposure to pesticides and other neurotoxins like dieldrin, which continues to be found in the autopsied brains of Parkinson’s victims. Even though dieldrin was banned decades ago, it lingers in the environment and we “continue to be exposed to the pesticide through contaminated dairy and meats…”

The cause of Parkinson’s “is unlikely to be due to milk compounds such as calcium, vitamin D, total fat, or total protein as these compounds are not associated with [the disease] when derived from other sources.” However, it could be lactose, the milk sugar, perhaps accounting for the increased associated risk of death and bone fractures, as well as Parkinson’s. There is, however, a third possibility.

Milk lowers uric acid levels, and uric acid may be protective against Huntington’s and also slow the decline caused by Parkinson’s. More importantly, it may lower the risk of getting Parkinson’s in the first place. Why? Perhaps because uric acid is an important antioxidant in the brain, something we’ve known for more than 30 years. We can demonstrate uric acid’s importance directly on human nerve cells in a petri dish. When the pesticide rotenone is added, oxidative stress goes up. Add the pro-oxidant homocysteine, and it goes up even more. But, when uric acid is added, it completely suppresses the oxidative stress caused by the pesticide.

Drinking milk, however, has a uric acid-lowering effect. In the paper making this assertion, a study they cited was “A cute effect of milk on serum urate concentrations,” but that was just a cute typo. The correct title is “Acute effect of milk…” Indeed, drink cow’s milk, and, within hours, uric acid levels drop 10 percent. Drink soymilk, and, within hours, they go up 10 percent. Now, for gout, a painful arthritic disease caused by too much uric acid, the uric acid-lowering effect of dairy is a good thing—but uric acid is “a double-edged sword.”

If our uric acid levels are too high, we can get gout, but, if they’re too low, it may increase our risk of neurodegenerative diseases, such as Alzheimer’s, Huntington’s, Parkinson’s, and multiple sclerosis.

Incidence rates of gouty arthritis over five years indicate that if our uric acid is over 10.0 mg/dl, we have a 30 percent chance of suffering an attack of gout within the next 5 years. However, at levels under 7.0 mg/dl, our risk is less than 1 percent, so it might make sense to have levels as high as possible without going over 7.0 to protect the brain without risking our joints. But having excessive uric acid in the blood puts more than just our joints in jeopardy. Yes, having levels that are too low may increase our risk of MS, Parkinson’s, Alzheimer’s, and even cancer, but having levels that are too high may increase our risk of gout, kidney disease, and heart disease.

In fact, having a uric acid level over 7.0 mg/dl isn’t only associated with an increased risk of gout, but also an increased risk of dying from all causes. However, having a low uric acid level may also shorten our lifespan by increasing mortality. High uric acid levels are associated with increased risk of death from heart disease, but low uric acid levels are associated with increased risk of fatal stroke. So, keeping uric acid at optimum levels, the sweet spot between 5.0 and 7.0 mg/dl, may protect the brain in more ways than one.

If we measure the uric acid levels in patients with Parkinson’s, they come in around 4.6 mg/dl, which can explain why dairy consumption may increase risk for Parkinson’s since milk pushes down uric acid levels. Dairy intake may also explain the differences in uric acid levels among meat-eaters, vegetarians, and vegans. In the graph in my video, you can see that vegan men have significantly higher uric acid levels at 5.7 mg/dl than vegetarians, presumably because vegans don’t drink milk, and those who both eat meat and consume milk fall between the vegans and vegetarians.

https://youtu.be/mc_IrKSNnVc

https://www.care2.com/greenliving/parkinsons-disease-and-the-uric-acid-sweet-spot.html

Terrible timing: After Ampyra loss, Acorda's much-needed Inbrija hits snag at FDA

 by Eric Sagonowsky | Sep 13, 2018 

Acorda was hoping to secure an approval for Inbrija in October, but on Thursday, the FDA moved its decision deadline back to January. (Pixabay

Acorda Therapeutics just got its second bad-news blow of the week. First, it lost an appeal that could have fended off generic copies of its primary sales generator, Ampyra. And now, instead of approving the Parkinson's drug Inbrija just in time to give Acorda a lifeline, the FDA pushed back its decision to January.

The FDA had originally expected to decide on Inbrija by Oct. 5, but the agency extended that deadline to Jan. 5 to review Acorda's recent submissions on “chemistry, manufacturing and controls.” 

The delay comes at a terrible time for Acorda. Earlier this week, a federal appeals court upheld a lower court's decision to invalidate patents on its multiple sclerosis drug Ampyra, which pulled in $150.3 million of the company's $153.3 million in second-quarter sales. With the decision, two generic makers should be able to enter the market, Jefferies analyst Michael Yee wrote, ready to take a bite out of Acorda's share. 

In a statement, Acorda CEO Ron Cohen said his company looks “forward to continuing our constructive dialogue with FDA” and remains committed to Inbrija. The company has said the Parkinson’s drug could pull in more than $800 million.

All told last year, Ampyra generated $542 million for Acorda. After a patent loss in district court, the company laid off 100 staffers and moved to advance Inbrija. Acorda has guided for Ampyra sales of $300 million to $350 million this year.

Acorda's shares were down about 18% on Thursday morning ahead of the market open.

https://www.fiercepharma.com/pharma/after-ampyra-setback-acorda-s-much-needed-inbrija-hits-a-snag-at-fda

Gene therapy shown to remove core component of Parkinson's disease

September 14, 2018,  Rush University Medical Center

Photomicrograph of regions of substantia nigra in a Parkinson's patient showing Lewy bodies and Lewy neurites in various magnifications. Top panels show a 60-times magnification of the alpha synuclein intraneuronal inclusions aggregated to form Lewy bodies. The bottom panels are 20 × magnification images that show strand-like Lewy neurites and rounded Lewy bodies of various sizes. Neuromelanin laden cells of the substantia nigra are visible in the background. Stains used: mouse monoclonal alpha-synuclein antibody; counterstained with Mayer's haematoxylin. Crdit: Suraj Rajan

An international team led by Rush researcher Jeffrey Kordower, Ph.D., has moved a step closer to developing a treatment to clear brain cells of a protein that is an integral cause of Parkinson's disease. The team published the findings of their study in the Aug. 22 issue of Nature Parkinson's Disease.

Parkinson's disease is a chronic, progressive movement disorder that affects the body's ability to control movement. The condition is a result of damage to brain cellsthat produce dopamine, a chemical that relays messages to the parts of the brain that control movement, resulting in trembling, stiffness, slow movement and poor balance and coordination.

Working with rats induced with a simulation of Parkinson's disease, Kordower's team showed that a genetically engineered fragment of an antibody—called a nanobody—cleared away toxic clumps of the protein alpha-synuclein after the team injected the nanobody into the rats' brains.

The hope is that once this therapy is introduced, it will continue to keep brain cells clear of the alpha-synuclein for the rest of the person's life, said Kordower, a professor in Rush Medical College's Department of Neurological Sciences, where he also is director of the Section of Neurobiology.

Fixing cells from within

Alpha-synuclein, abbreviated as α-syn, occurs naturally in the brain and elsewhere in the body. In neurological disorders, however, the protein clusters in misfolded (abnormally clumped together) and disordered forms. In Parkinson's disease—known as PD for short—malformed α-syn accumulates in distinctive formations called Lewy bodies, which is considered an integral part of PD.

"We're looking for ways to reduce alpha-synuclein levels, accumulation and toxicity resulting from the spread of alpha-synuclein around the nervous system," Kordower said.

The treatment his team is testing is part of a rapidly evolving approach that deploys therapeutic nanobodies to invade cells as part of genetically-altered viruses. In this study, once inside the cell, the nanobody appears to have stopped the clumping of the dysfunctional α-syn that leads to a loss of nerve cells and, eventually, full-blown PD. Stopping the clumping should prevent the progression of the disease.

This study is the first to use nanobodies for PD. Some previous research has shown promise with clearing α-syn in areas outside the cells, but Kordower believes an intracellular approach could be even more effective, because the amount of α-syn within cells is more plentiful than the amount outside them. "If you reduce intracellular levels, chances are that the a-synuclein won't get extracellular, so it won't spread," Kordower elaborated.

Letting PESTs inside

His team created an "overexpression" (overabundance) of α-syn in the test rats' brains. They then tested two types of the gene therapy, each on a different group of rats, and used saline in a control group, to see if the nanobodies could clear away the clutter inside those cells. The nanobodies were custom-made for the study by the University of North Carolina Vector Core.

One of the treatments, VH14*PEST, clearly worked best. It improved dopamine levels and reduced motor-function symptoms significantly better than the saline given the control group. VH14*PEST measurably improved the symptoms by one measure, the stepping test, and somewhat by another measure called the cylinder test.

VH14*PEST accomplished these results by reducing the levels of an amino acid in α-syn called Serine-129 that had undergone a chemical reaction called phosphorylation (the addition of a phosphate). Amino acids are the building blocks of proteins, and Serine-129 is a normal component of α-syn, but phosphorylated Serine-129 causes the deformities in α-syn that are seen in PD.

"The decrease in serine 129 phospho synuclein demonstrates the success of the nanobodies in reducing pathological alpha synuclein in the brain," Kordower said.

The second nanobody the team tried, NbSyn87*PEST, was effective, but less so overall, and had side effects like increased inflammation. PEST refers to a sequence of the amino acids proline, aspartate or glutamate, serine and threonine, which targets proteasomes – combinations of proteins that work to break down unneeded or damaged proteins. This PEST sequence has been found to be an effective intervention against disordered proteins such as the excessive α-syn found in Parkinson's.

'Humanizing' a PEST

Given the promising results of the VH14*PEST treatment, Kordower and his team plan to pursue it further. First, though, the group has to fully "humanize" the compound it used in the rat model. That is, they have to make it safe for people.

"Then we have to repeat these studies, in rats, with the humanized version to make sure it is as effective as the ones we've been testing," which were compatible with a rodent's physiology, Kodower explained. Only then can the team consider using the therapy in clinical trials in humans.

Down the road, this nanobody treatment could have implications for other parts of the brain as well, including the cortex, where misfolded α-syn may cause dementia, Kordower added.

More information: Diptaman Chatterjee et al. Proteasome-targeted nanobodies alleviate pathology and functional decline in an α-synuclein-based Parkinson's disease model, npj Parkinson's Disease (2018). DOI: 10.1038/s41531-018-0062-4

https://medicalxpress.com/news/2018-09-gene-therapy-shown-core-component.html

Advantages and Difficulties of Telemedicine in Parkinson’s Analyzed in Review Study

SEPTEMBER 13, 2018    BY MARTA FIGUEIREDO 

Telemedicine has the potential to become a critical component of healthcare in people with Parkinson’s disease, but larger studies are required to determine its role, a review study contends.

The study, “Current perspectives on the role of telemedicine in the management of Parkinson’s disease,” was published in the journal Smart Homecare Technology and TeleHealth.

While it has been established that Parkinson’s patients benefit significantly from specialty care, the number of patients who receive this type of care is still limited, and people in rural areas or in developing countries face even greater challenges to access it.

Telemedicine offers advanced clinical resources and expertise to patients who otherwise would not have access to specialized care. It allows healthcare professionals to evaluate, diagnose, treat, and follow patients at a distance using telecommunications technology.

While it may not be the most appropriate method to make an initial diagnosis of Parkinson’s disease, several studies have suggested that telemedicine is as effective as — and more convenient and economically advantageous than — in-person follow-up visits, for both patients and healthcare providers.

Researchers now have evaluated the advantages and constraints of telemedicine in Parkinson’s disease management in the U.S. after the establishment of a patient-provider relationship and a definitive diagnosis through an in-person appointment.

After an extensive search of published studies, researchers identified and further analyzed 13 suitable studies (conducted between 2006 and 2017) that focused on video conference, also known as virtual visits, as a form of telemedicine.

The team found that telemedicine has several advantages in Parkinson’s management, both in an at-home and nursing home setting.

Telemedicine has elevated feasibility — more than 90 percent of telemedicine visits were found to be completed as scheduled — saves time and money, and shows high satisfaction among Parkinson’s patients and healthcare providers (more than 85 percent of those participating were satisfied).

Also, patient satisfaction increased over time, suggesting that as technology advances, less technical problems are occurring in virtual visits.

The researchers noted that a modified version of the Unified Parkinson’s Disease Rating Scale (UPDRS) — a valid measure of disease severity — was developed to simplify virtual assessment of disease status, and to exclude the need of hands-on assessment, which may improve virtual assessment.

Notably, patients followed-up with telemedicine showed similar clinical improvements to those followed-up with in-person appointments, suggesting that “treatment outcomes for telemedicine, based on improvement in motor functioning, are objectively as good as they are for in-person care,” researchers said.

However, they noted that current published studies have some limitations, and that there is an urgent need for larger and long-term studies involving patients of all races and educational status, and with more severe disability.

The widespread use of telemedicine is limited by technological barriers, as patients with no access to high-speed internet or who live too far from centers with that technology, are unable to get this type of care. Also, some studies have suggested that current video conferencing quality may not allow clinicians to effectively access subtle motor dysfunctions.

“It remains unclear whether the home assessment is more accurate because it reflects a patient’s natural environment, or if an office assessment is more accurate because clinicians can see the patients more clearly,” the team wrote.

Bureaucracy- and legal-related issues, such as difficulties in negotiating reimbursement for virtual visits with insurance companies and in medical licensing throughout the U.S., also are two major barriers for telemedicine visits.

The authors believe that an ideal telemedicine program should be based on the development of a remote clinic with the resources to have reliable video conferencing.

Although telemedicine will not replace the traditional “hands-on” examination, “we are closer than ever to making virtual visit assessment as good as in-person examination with wider access to care, increased convenience for patients, and seamless communication between members of the treatment team,” they concluded.

https://parkinsonsnewstoday.com/2018/09/13/advantages-difficulties-telemedicine-parkinsons-reviewed/

Early Study Identifies at Least 6 Compounds That Might Prevent Alpha-Synuclein Clumping

SEPTEMBER 13, 2018 BY JOSE MARQUES LOPES, PHD IN NEWS.

Using a new screening strategy, researchers have identified compounds that block the clumping of alpha-synuclein protein, a key event in Parkinson’s.

The study, “Potent α-Synuclein Aggregation Inhibitors, Identified by High-Throughput Screening, Mainly Target the Monomeric State,” appeared in the journal Cell Chemical Biology.

Aggregated alpha-synuclein is the main component of Parkinson’s hallmark Lewy bodies. Screening of compounds that may prevent alpha-synuclein from clumping has been hampered by its slow and random aggregation pattern and the difficult detection of early-stage alpha-synuclein oligomers. These oligomers consist of a few units (or monomers) and are suggested to be the most toxic form of alpha-synuclein.

Researchers at Aarhus University, Denmark, developed a high-throughput screening assay using Förster Resonance Energy Transfer (FRET), a common technique for measuring tiny distances between molecules, close enough for molecular interactions to occur.

High-throughput screening is a method commonly used in drug discovery that uses robotics, data processing, and sensitive detectors — among other tools — to quickly conduct millions of chemical, genetic, or pharmacological tests.

“It is in our common [Parkinson’s]-combating interest to obtain as many leads as possible to maximize the likelihood of a successful [treatment] candidate,” the researchers wrote.

The team first developed a way to make alpha-synuclein clump more rapidly and predictably by using sodium dodecyl sulfate (SDS), a widely used detergent molecule in chemical analysis and biotechnology.

The combination of SDS-induced aggregation with FRET enabled the screening of 746,000 compounds, 58 of which markedly inhibited early alpha-synuclein clumping and lessened oligomers-induced cell membrane interactions.

These identified inhibitors were structurally diverse. The six most effective were derivatives of the same molecule. All interacted strongly with the first portion of alpha-synuclein monomers, known as the N-terminal region. Proteins are composed of several amino acids and have two distinct regions: N-terminus, the start of the protein, and C-terminus, the end of its amino-acid chain.

Several compounds reduced the oligomers’ toxicity in nerve cells grown in laboratory dishes. Although the inhibitors introduced chemical modifications in clumped alpha-synuclein, these changes were not necessary for their beneficial (inhibitory) activity.

The team also discovered compounds that boosted the protein’s aggregation, or “proaggregators” that share the same structural core. The researchers suggested they may be useful to modulate and study alpha-synuclein clumping at the cellular level.

Overall, the new clumping inhibitors “have the potential to further elucidate the mechanisms underlying the pathophysiology of [alpha-synuclein]” in models such as stem cell-derived neurons from patients, “which will provide necessary insights for future therapies,” the researchers wrote.

While these findings are in the context of Parkinson’s, “this FRET-based assay can screen for compounds affecting the aggregation behavior of any protein,” they added.

https://parkinsonsnewstoday.com/2018/09/13/early-study-identifies-at-least-6-compounds-that-might-prevent-alpha-synuclein-clumping/

Parkinson's disease and Medicines

EDUCATIONAL SUPPLEMENT 

The manufacturers of these medications may not list Parkinson’s disease as an absolute contraindication; however, better choices within a medication class may be suggested. Some of these medications alter the brain ‘s dopamine system causing an increase in Parkinson’s symptoms, others may chemically interact with Parkinson’ s medications and cause side effects. This is not intended to be a complete list and additional brand names may occur for each medication. If you have any questions about this list, please talk to your physician or pharmacist. 

Medications That Should Be Avoided 

Medication	Chemical Name	Brand Name	Mechanism of Interaction
Older Antipsychotics  (used to treat behavioral disorders)	Chlorpromazine Fluphenazine Haloperidol* Loxapine Thioridazine Thiothixene Trifluoperazine Pimozide	Thorazine® Prolixin® Haldol® Loxitane® Mellaril® Navane® Stelazine® Orap®	Block dopamine receptors in the brain, worsening PD symptoms
Antiemetics  (used to treat nausea or vomiting)	Chlorpromazine Droperidol Metoclopramide Prochlorperazine Promethazine	Thorazine® Inapsine® Reglan® Generics® Generic	Block dopamine receptors in the brain, worsening PD symptoms
Antihypertensives  (used to decrease blood pressure)	Reserpine Methyldopa	Serpalan® Aldomet®	Decrease dopamine stores and activity, worsening PD symptoms
Antidepressants  (used to treat depression)	Phenelzine Tranylcypromine	Nardil® Pamate®	Inhibit monoamine oxidase. Should not be taken in patients receiving levodopa, may increase blood pressure, fever, or agitation
	Amoxapine	Generics®	Block dopamine receptors in the brain, worsening PD symptoms

Note: There may be additional brand names for each medication. This is not intended to be a complete list.

* The package insert for Haldol® (haloperidol) lists use in patients with Parkinson’s disease as a contraindication 

Medications that should not be taken with

Selegiline hcL (eldepryl, deprenyl, Zelapar) and rasagiline (Azilect) 

Medication	Chemical Name	Brand Name
Narcotic/Analgesic	Meperidine Tramadol Methadone Propoxyphene	Demerol® Ultram® Dolophine® Darvon®
Antidepressants	Mirtazapine St. John’s Wort	Remeron® Several Brands
Muscle Relaxants	Cyclobenzaprine	Flexeril®
Cough Suppressant	Dextromethorphan	Numerous Brands
Decongestants/ Appetite Suppressants (found in cough, cold, allergy, and sinus medicines)	Pseudophedrine Phenylephrine Ephedrine	Sudafed® Sudafed PE®

Note: There may be additional brand names for each medication. This is not intended to be a complete list. Using these agents with selegiline or rasagiline increases the risk of one or more of the following: high blood pressure, increased heart rate, respiratory depression, seizures, tremors, fever, confusion, or behavior changes. 

Medication classes that should be discussed with doctor or pharmacist 

Newer Antipsychotics:

Clozapine (Clozaril) and quetiapine (Seroquel) have the least risk of worsening Parkinson symptoms and are the treatments of choice for drug induced hallucinations and psychosis. 

Antidepressants: 

Some agents within this class may worsen PD symptoms, increase confusion, or interact with some of your PD medi­ cations. 

Antihistamines: 

These are found in cough, cold, allergy, and sleep medica­ tions. When taking these medications, the elderly are at an increased risk of the following side effects: blurred vision, confusion, constipation, urinary retention, and dry mouth. The newer antihistamines loratadine (Claritin®) and deslor­ atadine (Clarinex®) may have less side effects than older antihistamines. Cetirizine (Zyrtec®) may or may not have less risk. Topical eye or nose sprays/drops have the least risk of these side effects. 

Non-prescription medications and supplements: 

Some of these agents may interact with PD medications. They may not be contraindicated; however, an adjustment in the timing of the medication may be needed. For example, iron supplements may decrease the absorption of levodopa and these medications should be spaced as far as possible.

The above tables were compiled by Maria Tan, Pharm .D. candidate and Mary Wagner, Pharm.D., MS Ernest Mario School of Pharmacy at Rutgers, the State University of New Jersey. 

The information contained in this supplement is solely for the infor-

mation of the reader. It should not be used for treatment purposes, but rather for discussion with the patient’s own physician. 

For additional free copies of this supplement, please call or visit the website :

AMERICAN PARKINSON DISEASE ASSOCIATION (800) 223-2732 • www.apdaparkinson.org 

Marine Corps Marathon, D.C. SUNDAY, OCTOBER 28, 2018 Washington, D.C. Fundraising Commitment: $1,500

September 12, 2018

Marine Corps Marathon, D.C.

SUNDAY, OCTOBER 28, 2018

Washington, D.C.

Fundraising Commitment: $1,500

The Marine Corps Marathon, known as 'the best marathon for beginners,' is the largest marathon in the world that doesn't offer prize money, earning its nickname, “The People's Marathon.”  You’ll tackle 26.2 miles starting in Arlington, VA and tour downtown DC past the Lincoln Memorial, Tidal Basin, and multiple national museums to finish at the Marine Corps War Memorial.  When you run with Parkinson's Champions you will be running through our nation’s capital to achieve a personal goal. But for the 1 million Americans living with Parkinson's disease, your run means so much more.

Parkinson's Champions Runners receive:

• Guaranteed race entry
• Parkinson's Champions running singlet for race day
• Personalized online fundraising page
• Invitation to race weekend events including pre-race pasta party for you and a guest
• One-on-one fundraising support

Register as an individual or grab friends, family and colleagues to form a team to train and fundraise together!

Want to register as a team? Teams of 3 – 5 are eligible for our team fundraising challenge. Work together to hit your goal. Contact champions@parkinson.org for more details!

To participate with Parkinson's Champions in the 2018 Marine Corps Marathon, fill out the application at:

http://parkinson.org/get-involved/Parkinsons-Champions/Marine-Corps-Marathon-DC 

If you have questions, send an email to champions@parkinson.org. For more information, visit the Marine Corps Marathon site:  http://www.marinemarathon.com

http://parkinson.org/get-involved/Parkinsons-Champions/Marine-Corps-Marathon-DC