All Science News articles summarize a research study and are not an official opinion, endorsement or position of the Parkinson’s Foundation’s.

Insulin resistance (IR) is a precursor to type-2 diabetes (T2D) – a disease that occurs when your blood glucose (blood sugar) is too high. First suggested in the 1960s, a growing number of studies are finding links between Parkinson’s disease (PD) and T2D. And contrary to popular belief, you needn’t be overweight to have IR. In fact, having IR usually has no symptoms – which is why it often goes undetected. While researchers don’t fully understand what causes IR, we do know that left unmanaged, T2D can lead to serious problems such as heart disease, stroke, nerve damage, eye disease, gum disease, foot problems, bladder problems, sexual problems – and, may possibly negatively impact the course of PD. 

A recently published study in the Journal of Parkinson’s Disease titled, “High Prevalence of Undiagnosed Insulin Resistance in Non-Diabetic Subjects with Parkinson’s Disease” (Hogg et al., 2018), sought to determine how common IR was in non-diabetic people with PD. A battery of motor, non-motor, cognitive, and quality of life assessments were conducted. Other information gathered included height, weight, and Body Mass Index (BMI), as well as lab tests for fasting plasma insulin (the amount of insulin in your blood prior to eating a meal), fasting plasma glucose (the amount of glucose in your blood prior to eating a meal) and HbA1c (a measure used to estimate average blood glucose levels over a period of months). The study participants’ HOMA-IR was also calculated. HOMA-IR, which stands for Homeostasis Model Assessment for Insulin Resistance, is a mathematical equation that estimates steady state beta cell function (beta cells store and release insulin) and insulin sensitivity – which takes both fasting plasma insulin and fasting plasma glucose into account.

Results

• Study participants’ IR status (whether they had or didn’t have insulin resistance) did not significantly impact motor, non-motor, cognitive, or quality of life assessments in this study group.
• The HOMA-IR revealed that nearly 60% (90 out of 154 participants) of the non-diabetic study participants may have undiagnosed insulin resistance – despite having normal blood sugar levels.
• Higher BMI (being overweight or obese) was associated with increased IR.
• The HOMA-IR also revealed that a substantially higher percentage (41%) of their lean study participants had IR, as compared to healthy adults without PD.

What Does This Mean?

This study suggests that nearly two thirds of non-diabetic people with PD may be insulin resistant, despite having normal blood sugar, and in some cases, despite being lean. Thus, the big take-away from this study is that people with PD may want to have a more sensitive insulin test conducted, such as the HOMA-IR, to see if they have undiagnosed insulin resistance. There are several other IR tests as well. Which of these tests, or combinations thereof, might be best to evaluate a person’s IR is something to be discussed with one’s health care provider.

Another important take-away (although not specifically addressed in the Hogg et al. (2018) study), is that there are an increasing number of studies suggesting that IR negatively impacts dopamine functioning in the brain. Parkinson's symptoms, including tremors, stiffness, and slowness of movement, are caused by a lack of dopamine in the brain. This is particularly noteworthy for two reasons: One, the cornerstone of therapy for PD is the drug levodopa (also called L-dopa). Levodopa works by converting into dopamine and replenishing the brain's reduced supply; straight dopamine has difficulty crossing the blood/brain barrier. Two, IR is thought to precede the development of T2D by 10 to 15 years. Thus, having advanced notice of possible IR has great value, as IR is usually reversible. And while the jury is still out as to whether – and to what extent – having IR increases one’s risk for developing PD, taking proactive steps to mitigate one’s risk for developing T2D has profound long and short-term health benefits.

Learn More

The Parkinson’s Foundation believes in empowering the Parkinson’s community through education. Learn more about the connection between diabetes and Parkinson’s in the below Parkinson’s Foundation recourses or by calling our free Helpline at 1-800-4PD-INFO (473-4636).

• Substantial Matters: Episode 21: What Other Conditions Are Related to Parkinson's
• Parkinson’s Today: What’s Hot Medication Edition: Exenatide and Gocovri
• Parkinson.org: Diet & Nutrition

All Science News articles summarize a research study and are not an official opinion, endorsement or position of the Parkinson’s Foundation’s.

Usually, the first Parkinson’s disease (PD) symptom that causes people to seek medical attention is resting tremor. Three out of four people in the early Parkinson’s stages experience it. Done without conscious control or choice, a resting tremor is an involuntary, rhythmic muscle contraction that causes shaking/tremor. Most often initially detected in the hand, resting tremor may also begin in the foot or face. While the term “resting tremor” may sound benign, people with PD describe it as a symptom that is impossible to escape, socially isolating, career-ending and a constant reminder that the disease will only get worse.

Standard, first-line treatment for PD resting tremor is the combination therapy of carbidopa and levodopa. Its success rate is variable and with long-term use, commonly leads to abnormal involuntary movements called dyskinesias. Deep brain stimulation (DBS) — which involves surgically implanting small electrodes into specific brain regions — is another treatment for PD tremors. DBS delivers pulses of electricity into the brain and works like a pacemaker to help counteract abnormal brain activity in PD. Traditionally, doctors have reserved DBS for later stages of PD, when medications are no longer working and quality of life is deemed unacceptable. However, that delay in recommending DBS may be changing.

A recently published study in the journal, Neurology, titled, “Effects of deep brain stimulation on rest tremor progression in early-stage Parkinson disease” (Hacker et al., 2018), involved a post hoc analysis (an additional analysis after the study finished that was not part of the original study design) as to whether having DBS in the early stages of PD might specifically improve resting tremor.

A total of 28 people with PD (25 men, 3 women) ranging in age from 50 to 75, and with no history of dyskinesia or motor fluctuations, participated in the two-year study. Patients were randomly assigned to receive either optimal drug therapy alone (ODT), or DBS with drug therapy. A well-accepted, reliable, battery of tests designed to evaluate motor function, called the Unified Parkinson’s Disease Rating Scale–III (UPDRS-III), was conducted at baseline. The UPDRS-III was accessed on medication, and also off medication (after a one-week therapeutic washout). These on and off medication measurements were then repeated every six months for 24 months. Areas evaluated included the limbs, defined as hands, legs, and face. A participation satisfaction survey was also administered.

Results

From baseline to 24 months:

• 86% of medication-only patients developed a resting tremor in previously unaffected limbs, as compared to only 46% of patients receiving DBS and medication.
• While the total UPDRS-III scores off medication did not differ between the groups, rest tremor measured off medication was 3.1 points better for the patients receiving DBS and medication, compared to the patients receiving medication only. Rest tremor was the only measure from the UPDRS-III that showed a statistically significant improvement­ – meaning, these findings are unlikely random or due to chance, but are instead meaningful and potentially causal, i.e., DBS + medication worked better.
• Rest tremor scores measured on medication improved over the two years for the DBS and medication group, while they worsened for the medication only group. At the end of the two years, the difference between the two groups was statistically significant. 
• In the medication-only group, the average number of limbs affected by tremor doubled, whereas it decreased slightly in the DBS and medication group.
• In the patient satisfaction survey, nearly half said the greatest benefit of undergoing DBS was the management of their tremor. Note: DBS is also used for bradykinesia (slowness of movement), and rigidity.

What Does This Mean?

This Hacker et al. (2018) study suggests that having DBS in the early stages of PD may not only improve resting tremor, it may also slow the progression. The possibility of diminishing such a distressing symptom could be a game changer for those who have had to put activities, work, and interests on hold due to their tremor. As with any surgery, DBS is not without risk. This is brain surgery, involving two holes being drilled into one’s head. Serious or permanent complications are rare, but they happen.

This study does have some limitations. It was a small study, involving just 28 people. In addition, some of the analyses done were post hoc, which means they were conducted after seeing the data. In most clinical trials, the primary outcome measure (what the researcher thinks will demonstrate the greatest therapeutic benefit) is decided before the trial ever takes place. While the post hoc analysis showed an interesting relationship between DBS and slowed rest tremor progression, more studies are needed to further test this hypothesis.

Learn More

The Parkinson’s Foundation believes in empowering the Parkinson’s community through education. For more information on medications and deep brain stimulation, read our books Parkinson’s Disease: Medications and A Guide to Deep Brain Stimulation.

For more insights on this topic, listen to our podcast episode “What is Deep Brain Stimulation?”.

This isn’t a solicitation for a financial donation. But I am going to ask for something valuable that is in short supply and critical to getting an approved therapy to slow the progression of Parkinson’s disease (PD), and move us closer to a cure. It is something you can do to improve the lives of people with PD and take an active role in the Parkinson’s community. Only you have the power to do this. 

The discovery that clumping of a misfolded protein in the brain (called alpha-synuclein) causes loss of dopamine neurons and dysfunction in other areas of the brain and nerves that control bodily functions provides opportunities for new Parkinson’s therapies. The research community is excited that preventing this protein clumping process or clearing these toxic clumps may be able to slow or stop the progression of Parkinson’s disease.

However, we still don’t have biomarkers, such as a blood test, that allows us to assess PD progression and test promising therapies in people with PD. Therefore, our best opportunity to test a new potential disease modifying therapy is to see if it can slow progression of PD signs and symptoms in people who were recently diagnosed with early PD and who are not taking symptomatic medications (like levodopa, dopamine agonists, amantadine, or MAO-B inhibitors).

But this poses a difficult challenge! Those diagnosed with early PD based on a combination of bradykinesia (slow and small movement), rigidity (stiffness) and tremor (shaking), can usually only go about six to twelve months before they will want or need medication to relieve symptoms.

Ideally, researchers would like to observe patients in a clinical trial to test a potential disease slowing medication immediately following diagnosis, and for as long as possible. This gives us the best chance of identifying a difference in the rate of progression between those treated with active (“real”) study medication and those treated with placebo. The shorter the testing period, the more difficult it is to identify the beneficial effect of a disease slowing medication. Conversely, the longer the testing period, the more obvious a slowing effect should be.

However, if the proposed time period to test the new medication is too long, many patients will need symptomatic treatment, and researchers will lose their ability to monitor clinical disease progression. Therefore, most trials of potential disease slowing medications in early PD observe patients for about six months to a year.

The key problem is that patients with early PD who are able and willing to enroll in a clinical trial, and whose PD symptoms are mild enough to go up to a year before starting symptom medications are in short supply. To test promising disease slowing therapies, patients with early PD must be identified as early as possible and referred to centers hosting a clinical trial before beginning symptomatic PD medications. Unfortunately, this process fails too often. Patients often wait to seek treatment until their symptoms become troublesome. After all, why see a doctor when you don’t need treatment? However, research-wise it is then too late to participate in an early PD disease slowing trial. Additional unwanted delays may also occur between the time it takes to make an appointment and be seen.

In another disappointing scenario, patients with early PD are diagnosed and immediately placed on symptom medication, even though it’s not immediately required. The doctor may do so instinctively and without considering the lost research opportunity. Of course, immediately beginning medication may be necessary in cases where progression has been swift or if necessary to maintain employment.

The critical time of about one year from an early PD diagnosis until symptom medication is required is called the “Golden Year” for participation in disease slowing clinical trials. It is critical that care providers and patients don’t unknowingly waste this Golden Year.

Therefore, I ask this of care providers and patients:  

Care Providers: When you diagnose early PD, please don’t unnecessarily institute symptomatic therapy. Evaluate whether a clinical trial for early untreated PD patients is being conducted within a reasonable distance and discuss the possibility of participating with your patient. At a minimum, let your patient know that there are early PD disease modifying trials being conducted and they may want to learn more about the trials before beginning therapy. Centers conducting such trials would be delighted to discuss ongoing trials with your patient.

Patients: If you have new onset of tremor or slowness, or if a care provider says you may have PD, don’t wait until your condition worsens to the point that you feel you need treatment. Seek evaluation with a specialist as soon as possible. If you are diagnosed with PD, ask about clinical trials. Search online for open trials you can enroll in by visiting ClinicalTrials.gov and Parkinson.org/ClinicalTrials. In addition, if you are diagnosed with PD and your doctor wants to begin medication immediately, consider seeking a second opinion from a center that conducts clinical trials. If you explain that you were recently diagnosed and interested in learning about clinical trials that center will often quickly provide you with an appointment.

Our ability to test promising new potential disease slowing therapies depends on both patients and health care providers understanding the critical value of the Golden Year in PD. I hope that individuals with early PD will consider participating in clinical trials, and the earlier, the better.

The journey to a cure will likely be incremental. If a medication does not work, we want to find out, discard it, and move on to other promising new therapies. Once we demonstrate that a therapy can slow disease progression, we will want to improve on it or find other therapies that can also slow progression and perhaps use them together.

We also need to ensure that clinical trials are designed to meet the needs and priorities of the PD community. This can only be done by working with people with PD to design and implement clinical trials, such as is done in the Parkinson’s Foundation Parkinson's Advocates in Research program. This model of patient engagement in research is being increasingly mandated by regulatory agencies and study sponsors as critical to the research process. Finally, we must be sure study participants and people with PD involved in research represent the diverse PD population to ensure that new treatments benefit the greater PD community. Once we can slow disease progression sufficiently and can identify patients early enough (even before the onset of slowness, stiffness and tremor), the result will be equal to having a cure. 

This article was written by Robert A. Hauser, MD, MBA, University of South Florida Parkinson's Disease and Movement Disorders Center, a Parkinson’s Foundation Center of Excellence. Dr. Hauser’s primary research interest is in the development of new medical and surgical treatments for Parkinson's, tremor, tardive dyskinesia, dystonia, and restless legs syndrome. 

The microbiome is a hot topic in Parkinson’s disease (PD). The microbiome is the network of microorganisms, along with viruses and bacteria, that help the body stay healthy. In the PD community, when we talk about the microbiome, we’re referring to the bacteria found in the gut. Leading experts have suggested that the microbiome has a potential role in the pathogenesis (way a disease develops) and in the treatment of Parkinson’s. This has sparked the idea that we might be able to improve PD symptoms if we change the microbiome through diet or other ways. In this month’s What’s Hot in Parkinson’s disease, we will explore the not so hidden viruses within the gut.

What is in the human gut microbiome? The microbiome has many living creatures, such as bacteria and fungi. Most people are not aware that viruses live in your gut, which are called bacteriophages. Fun fact: the human gut houses more viruses than bacteria.

George Tetz, MD, and colleagues, in a recent issue of Scientific Reports examined bacteriophages in Parkinson’s disease. Dr. Tetz looked at the gut phagobiota (the combination of all gut bacterias). He and his colleagues analyzed existing data and calculated the phage (virus) to bacteria ratio in early untreated people with PD. The researchers also compared their findings to a group of people without Parkinson’s.

People with Parkinson’s have less of a specific type of bacteria that produces lactic acid. These bacteria play a role in the processes that produce dopamine and affect the intestine’s ability to absorb. According to the study, people with PD did not have less bacteriophages than people without PD, but people with Parkinson’s were found to have an increased number of a specific kind of bacteriophage called the lytic-phase bacteriophage.  

Though there were only 31 people with Parkinson’s in this study, the results were fascinating. If a person received bacteriophages, it would shift the microbiome and change the intestine’s ability to absorb. Another study recently reported that consuming dairy is associated to developing Parkinson’s later in life. Dr. Tetz and his colleagues speculate that dairy impacts bacteriophages and specifically Lactococcus (a type of lactic acid bacteria).

The idea that change in the gut microbiome and bacteria found within may be important to Parkinson’s has gained momentum. We need to be careful in interpreting this study, as study participants with PD had not been exposed to dopamine and the number of participants was small.

We cannot automatically assume that this gut virus study shows a direct link to the cause of Parkinson’s. We also do not yet know if altering the viruses or other components of the microbiome will improve treatment or alter PD progression. However, we are hopeful that more research will lead to better diets, novel treatment approaches and may even help current medications work more effectively. Considering there are more viruses in the human gut than bacteria, these viruses are now more visible to clinicians and future researchers than ever.

References

1. Tetz G et al. Parkinson’s disease and bacteriophages as its overlooked contributors. Sci Rep 2018 Jul 17; 8:10812.
2. Okun MS. Bacteriophages, the Microbiome, and Parkinson Disease: Possible Treatment Implications. Journal Watch Neurology, 2018.

You can find out more about our National Medical Advisor, Dr. Michael S. Okun, by also visiting the Center of Excellence, University of Florida Health Center for Movement Disorders and Neurorestoration. Dr. Okun is also the author of the Amazon #1 Parkinson's Best Seller 10 Secrets to a Happier Life and 10 Breakthrough Therapies for Parkinson's Disease.

All Science News articles summarize a research study and are not an official opinion, endorsement or position of the Parkinson’s Foundation’s.

In 10 to 15 percent of people with Parkinson's disease (PD), the disease is familial (tied to genetics), while the rest are nonfamilial. Mutations in the LRRK2 gene are the most common cause of familial PD. In fact, researchers have identified more than 100 LRRK2 gene mutations in families with PD. 

It’s important to understand that all human beings, regardless of their PD status, have the LRRK2 gene. LRRK2 serves a variety of important functions. It is active in the brain and is also found in many other organs and tissues throughout our bodies. This matters because new findings suggest LRRK2 may play a key role in all forms of Parkinson’s, even in people that do not have a LRRK2 genetic mutation. This may be the linchpin scientists have been seeking for treating all people with PD.

A recently published research article in Science Translational Medicine titled “LRRK2 activation in idiopathic Parkinson’s disease” (Di Maio et al., 2018) sought to investigate whether the wild-type (normal, as opposed to mutated) LRRK2 plays a role in idiopathic PD. What they found is stunning. By developing two new tests to determine the activation state of LRRK2 under different conditions, the research scientists revealed a series of connections that may lead to breakthrough PD therapies. In short, there might be a new way to help treat all people with PD.

Results

The research scientists:

• Developed a genetically engineered detection technology that could identify whether the LRRK2 was active or inactive (on or off), with better resolution than other available tests.  
• Validated their tests in human embryonic kidney cells that had either normal LRRK2, mutated LRRK2 or no LRRK2 at all.

From this test, scientists learned:

• LRRK2 is activated in both dopamine neurons and in immune cells in the brain (microglia) in post-mortem brain tissue from people with idiopathic PD but not in normal, healthy brain tissue.
• LRRK2 activation occurs in dopamine cells in two different rat models of PD. In one model, rats were given a mitochondrial toxin (called rotenone) that causes oxidative damage. In the other model, rats were engineered to make too much alpha-synuclein  — the protein known to accumulate in PD brains, which leads to Lewy body formation. In both cases, LRRK2 was activated even though the rats had normal LRRK2.
• LRRK2 activation occurs early and before any brain cells have died, is triggered by oxidative damage, plays a role in alpha-synuclein accumulation in the brain, and has downstream effects on waste management in cells (tested in the rotenone rat model).

What Does This Mean?

To understand why this study places LRRK2 at such a pivotal point in PD, here’s the essential background information you need to know:

In a normal, healthy cell, LRRK2 is inactive. However, in a cell where there is oxidative damage, LRRK2 becomes activated, then:

• Activated LRRK2 inactivates other proteins that are important to the cells’ waste management process, leading to the build-up of alpha-synuclein.
• Clumps of alpha-synuclein interfere with mitochondrial function, which results in oxidative stress.
• Oxidative stress activates even more LRRK2, forming a vicious cycle.
• Ultimately, this results in large clumps of alpha-synuclein, called Lewy bodies, which are the hallmark of PD.

This new study developed tests so we can now see the evidence of activated LRRK2, which we couldn’t see before, as well as where LRRK2 is located, e.g., in dopamine neurons and microglia. Previous detection technologies could not specifically identify LRRK2 activation in idiopathic PD and/or the images were not helpful.

Taken together, this data suggests that LRRK2 activation may play a central role — not only in familial PD with LRRK2 mutations — but also, in nearly all cases of PD. Further, this study shows evidence that LRRK2 kinase inhibitors, which are currently in development by several pharmaceutical companies, can break the vicious circle of LRRK2 activation, suggesting a new avenue of PD therapy development.

Learn More

The Parkinson’s Foundation believes in empowering the Parkinson’s community through education. Learn more about LRRK2 by visiting the Parkinson’s Foundation resources below or by calling our free Helpline at 1-800-4PD-INFO (473-4636) for answers to all your Parkinson’s questions.

• Genetics and Parkinson's
• PD GENEration: Mapping the Future of Parkinson's
• Podcast Episode: Genetics and PD: What do we know so far?

Many people with Parkinson’s disease (PD) struggle with gastrointestinal issues. More specifically, the movements of the digestive system (known as gastrointestinal motility).

Evidence from recent studies has strongly suggested a link between the gastrointestinal system and Parkinson’s. An important next step for the field is to examine potential gastrointestinal treatments. In this month’s What’s Hot we will examine a recent randomized study of a medication that assists with moving things along in the stomach and intestines (known as a promotility drug) administered to people with Parkinson’s.

First, let’s review recent Parkinson’s-related gastrointestinal studies. Pathological studies by Braak and colleagues raised the idea that pre-motor Parkinson’s may start in the intestines. Recently, several researchers observed alpha synuclein containing Lewy bodies in the gut of people with Parkinson’s.

Currently, the only Food and Drug Administration (FDA) approved drug for gastric motility issues is metoclopramide (Reglan). Metoclopramide blocks dopamine and unfortunately makes Parkinson’s symptoms worse. We tell Parkinson’s patients to avoid metoclopramide. Another alternative is domperidone (Motilium). However, domperidone is not FDA approved or available in the U.S. It blocks dopamine, but does not enter the brain and is considered safe for people with Parkinson’s. Domperidone is available in most countries.

Another researcher, Marrinan and colleagues, recently published a randomized double-blind placebo controlled trial (this type of trial is known as the “gold standard” of clinical research) of a new gastric promotility medication called camicinal (GSK962040). Camicinal works in the gut as a motilin agonist (a drug that attaches to the same receptor as a natural chemical and causes the same effect).

Motilin is a hormone that stimulates the intestines. It is produced from cells in the small intestine. Motilin drugs stimulate the motilin receptor and lead to release of the hormone.

Researchers recently hypothesized that the new medication camicinal could improve delayed stomach emptying and help the body absorb PD medications. Thirty-eight people with Parkinson’s enrolled in the study. A randomized group received 50 mg of camicinal each day, while others received a placebo. The study was conducted over seven to nine days. The study found that medication “off” time was improved by more than two hours in the camicinal group that also experienced faster absorption. When compared to the placebo group, the camicinal group also saw an improvement according to the MDS-UPDRS (a scale used to measure the multiple aspects of PD).

Though this study was small and of short duration, its results highlight the potential for a new approach to gastrointestinal issues common in Parkinson’s. Camicinal has recently completed a trial for diabetic gastroparesis (ClinicalTrials.gov) and the results should help inform the research for people with Parkinson’s who have similar issues.

Other gastrointestinal therapies that people with Parkinson’s should keep an eye on include the 5-HT₄ receptor agonists (e.g. velusetrag) and ghrelin agonists (e.g. relamorelin). Please keep in mind that camicinal is not FDA approved. However, we should remain hopeful that a larger and more in-depth study of camicinal (and similar compounds) could potentially bring great benefit to the Parkinson’s community.

Selected Reference:

Marrinan SL, Otiker T, Vasist LS, Gibson RA, Sarai BK, Barton ME, Richards DB, Hellström PM, Nyholm D, Dukes GE, Burn DJ. A randomized, double-blind, placebo-controlled trial of camicinal in Parkinson's disease. Mov Disord. 2017 Dec 26. doi: 10.1002/mds.27259. [Epub ahead of print] PubMed PMID: 29278279.

Barboza JL, Okun MS, Moshiree B. The treatment of gastroparesis, constipation and small intestinal bacterial overgrowth syndrome in patients with Parkinson's disease. Expert Opin Pharmacother. 2015;16(16):2449-64. doi: 10.1517/14656566.2015.1086747. Epub 2015 Sep 16. Review. PubMed PMID: 26374094.

You can find out more about our National Medical Director Dr. Michael S. Okun by visiting the Center of Excellence University of Florida Health Center for Movement Disorders and Neurorestoration. Dr. Okun is also the author of the Amazon #1 Parkinson's Best Seller 10 Secrets to a Happier Life.

Parkinson’s disease (PD) specialists have long debated the potential value of Parkinson’s-specific physical therapy. All great medical debates are usually settled by two factors: time and data. In this month’s What’s Hot, we review a paper recently published in Lancet Neurology (Ypinga 2018) that provides insight and data for whether people with Parkinson’s should begin or continue specialized physiotherapy.

Ypinga and colleagues performed an observational study which analyzed data from a Dutch health insurance claims database. Only people with Parkinson’s who received physiotherapy were included. The researchers reviewed patients with three years of follow-up and divided the groups into those receiving specialized Parkinson’s physiotherapy or those receiving usual physiotherapy.

Performance and results were compared. Researchers were interested in Parkinson’s-related health issues, such as being admitted to a hospital because of a fracture, orthopedic injury or pneumonia.  

The study had 2,129 people with Parkinson’s in the specialized physiotherapy group and 2,252 people with Parkinson’s who received usual physiotherapy. Results showed that 17 percent of the specialized physiotherapy group had complications, compared to 21 percent in the regular physical therapy group. Interestingly, the specialized therapy group required fewer treatment sessions and had cheaper direct and total healthcare costs.

Should every person with Parkinson’s seek a Parkinson’s-specific specialized physical therapist?  Not so fast. This study was conducted in the Netherlands where NetPD has created an integrated network of well-trained and highly Parkinson’s disease educated physical therapists. The therapists within this Dutch network share a similar philosophy and access to a common educational curriculum. We cannot therefore generalize the findings to every specialized Parkinson’s physical therapist in the world.

We can however follow Ypinga and colleagues and carefully study the potential benefit for any proposed Parkinson’s-specific specialized physical therapy. Data and time will ultimately tell us what is or is not effective — and whether there is an associated cost savings. Though this study found no difference in mortality among the two groups, the data was convincing for those living in the Netherlands to seek a specialized physiotherapist.

References:

1.Ypinga JHL, de Vries NM, Boonen LHHM, Koolman X, Munneke M, Zwinderman AH, Bloem BR. Effectiveness and costs of specialised physiotherapy given via ParkinsonNet: a retrospective analysis of medical claims data. Lancet Neurol. 2017 Dec 12. pii: S1474-4422(17)30406-4. doi: 10.1016/S1474-4422(17)30406-4. [Epub ahead of print] PubMed PMID: 29246470.

2.Okun MS. Is Specialized Physiotherapy for Parkinson’s Disease Better? NEJM Journal Watch, 2018.

You can find out more about our National Medical Director Dr. Michael S. Okun by visiting the Center of Excellence University of Florida Health Center for Movement Disorders and Neurorestoration. Dr. Okun is also the author of the Amazon #1 Parkinson's Best Seller 10 Secrets to a Happier Life.

Most people associate Parkinson’s disease (PD) with tremors, a motor symptom. However, non-motor symptoms are common and can be more troublesome and disabling than motor symptoms. They can include cognitive changes, mood and sleep disorders, autonomic symptoms or weight loss. Rush University Medical Center, a Parkinson’s Foundation Center of Excellence, is not only on the front lines of PD-related cognitive research, but is actively hosting life-changing programs targeting these non-motor, and in particular, cognitive and behavioral symptoms.

Jennifer G. Goldman, MD, MS, is unique in the Parkinson’s field. She is a fellowship-trained movement disorder specialist with additional background in behavioral neurology and neuropsychiatry — an uncommon combination that provides her with a unique skillset to treat Parkinson’s non-motor symptoms.

In between seeing patients, Dr. Goldman conducts research studies to better understand what causes a person with PD to experience neuropsychiatric symptoms (such as memory loss or cognitive changes, anxiety, depression, psychosis and hallucinations). She utilizes MRI (magnetic resonance imaging) brain scans and clinical assessments to evaluate cognitive and behavioral effects. More broadly, Dr. Goldman’s research tries to find the mechanisms of the brain and biomarkers (measurable substances that attribute to the onset and progression of a disease) that contribute to Parkinson’s-related non-motor symptoms.

Research, like Dr. Goldman’s, plays a vital role in developing treatments to stop non-motor issues from progressing. “We have very good medicines, therapies and surgical treatments that can help motor symptoms, but we are far behind on being able to treat or stop any of the neuropsychiatric symptoms — particularly cognitive decline and dementia — that take a toll on quality of life for patients and care partners,” said Dr. Goldman.

Dr. Goldman and her team set out to do more. Funded through a Parkinson’s Foundation Moving Day grant, the center created a dedicated program to address the unmet needs of people with PD experiencing cognitive, behavioral and emotional symptoms of Parkinson’s.

“The Integrated Cognitive Behavioral Movement Disorder Program” includes a multidisciplinary and comprehensive clinic and offers an educational series to support people with PD and care partners who need to treat and cope with non-motor symptoms.

Roughly nine million people living with Parkinson’s in the world are not being treated by a specialist.  Through funding, the Parkinson’s Foundation supports Rush’s efforts to host an open clinic to reach as many people as possible who are most likely not receiving expert care.

While addressing cognitive and behavioral issues can be daunting for patient and doctor alike, Dr. Goldman knows that there is still a social stigma attached to mental health. She regularly sees patients who are afraid to be labeled as having a cognitive or behavioral issue in addition to their PD. Terms like dementia and psychosis can be incredibly scary for anyone coping with Parkinson’s.

“It is a well-known problem that many doctors do not have enough time during an appointment to truly explain and talk through mental health issues,”

-Dr. Goldman

This is one reason the Rush team welcomes the conversation and helps people advocate for their mental health through their clinic.

A Day at the Integrated Cognitive Behavioral Movement Disorder Clinic

On clinic day, people with any stage of Parkinson’s, from anywhere in the country are seen by the center team. Upon arriving they are:

1. Provided a comprehensive assessment by the center’s allied health team, which includes a physical therapist, occupational therapist, speech therapist, nutritionist, neuropsychologist, social worker, nurse, physician assistant and movement disorder specialist.
2. Together, the team determines a personalized treatment strategy, keeping in mind the patient’s symptoms — motor and non-motor.
3. If the patient lives in another city or state, the team will provide their assessment and treatment recommendation and refer the patient to a clinic and doctor closer to their home for future visits. If a patient is referred to the clinic and can commute for care, they can choose to receive care at Rush moving forward.  

Care doesn’t stop with the patient. “One of our program goals is to also spend time with the care partner,” Dr. Goldman said. “Most of the time, clinic appointments are not really about the care partner, but we often find that caregivers need to be addressed as well.”

To educate and aid even more people the clinic hosted an educational series. Dr. Goldman, the clinic team and invited guest speakers addressed a different neuropsychiatric topic, such as depression and hallucinations, in each of the eight sessions held. Fifty-two attendees attended the first session in July 2017. After the presentation, the session transitions into moderated support groups — one for people with PD and one for caregivers. Each can share stories about the topic addressed and ask the speakers questions. Participants are encouraged to take available resources, such as Parkinson’s Foundation books. Future series will address apathy, depression and anxiety and will include an online webinar component with virtual chats to allow people to participate from home.

“We felt there was a great need to have a forum where we could educate the Parkinson’s community about the neuropsychiatric symptoms because there is a lot of misinformation, fear and stigma surrounding these issues,” said Dr. Goldman.

Between the clinic and its sessions, the center hopes to see even more people with PD advocate for themselves. The dream remains to ultimately prevent Parkinson’s non-motor symptoms altogether, but for now, programs like the Rush Cognitive Behavioral clinic exist to make life better for people with Parkinson’s, on a physical and emotional level.

The Rush University Medical Center is located in Chicago, IL. Learn more about your nearest Center of Excellence.

The Parkinson’s Foundation, in collaboration with the Brain Donor Project, is working to shed light on the critical need for brain donation to advance Parkinson’s disease (PD) research. According to the National Institutes of Health (NIH), there are vastly inadequate brain donations to meet the research demand of several disorders, in particular Parkinson’s.

“Because Parkinson’s is exclusively a human disease, we are entirely dependent on brain donation to help us truly understand how Parkinson’s affects the human brain,” said James Beck, PhD, Parkinson's Foundation’s Chief Scientific Officer.

As suggested in a JAMA Neurology article, the aging population is poised to see a global spike in the number of people diagnosed with Parkinson's.  Authors Ray Dorsey, MD, University of Rochester Medical Center, and Bastiaan R. Bloem, MD, PhD, Radboud University Medical Center, both Parkinson’s Foundation Centers of Excellence, liken this surge to a pandemic requiring immediate action. Expert care and research remain our only chance to fight this disease in time to help future generations.

Since one brain can provide tissue for up to hundreds of research studies, an individual brain donation is a highly valuable gift that almost anyone can make.

What are the steps of brain donation?

1. Decide whether this is the right option for you.
2. Register to become a brain donor through the Brain Donor Project.
3. Match with a brain bank in the NIH NeuroBioBank network. Receive forms and additional information needed to finalize your registration. 
4. Let your family know of your decision so they can ensure your wishes are carried out. Consider using the NIH NeuroBioBank brochure for reference.
5. Provide designated family members with the brain bank contact information. Your family will not incur any expense for the donation.
6. Help hundreds of researchers further their Parkinson’s research.

Timing is everything — in the last 20 years, neuroscientists have learned more about the human brain than at any other point in recorded history. Your donation to The NIH NeuroBioBank will ensure that scientists continue to advance PD research. According to the NIH, increasing the amount of brain tissue available for research allows scientists to better understand how to prevent, diagnose, treat and cure brain disorders, like Parkinson’s.

Through a coordinated network of brain banks in the United States, the NIH NeuroBioBank arranges for donated brain tissue to be evaluated and made available to researchers while following the highest standards for research and providing brain tissue to the greatest number of scientists possible. With just one brain, multiple researchers can further their studies.

“From the discovery of levodopa, the first true therapy for PD, to the next generation of therapies in clinical trials today, each critical advance has been made because of the generosity of people contributing their brains to help solve Parkinson’s,” said Dr. Beck.

According to the Brain Donor Project, many donors and their families share a mutual feeling of satisfaction knowing that they are contributing to the health and well-being of future generations. Brain donation makes it possible to advance science and work toward cures for neurological diseases.

In this blog, Angie Hott discusses her work as a Parkinson’s advocate and her participation in the upcoming 2018 Parkinson’s Policy Forum, co-sponsored this year by the Parkinson’s Foundation and The Michael J. Fox Foundation. The event will take place March 19 to 21 in Washington, D.C. You can view a live stream of the Forum’s educational panels on March 19 and 20 by visiting the Parkinson's Foundation's Facebook page.

Forum attendees will conduct a full day of meetings on Capitol Hill on Wednesday, March 21. At the same time, Parkinson’s advocates across the country will take part in Parkinson’s Advocacy Day. Be sure to check your email and visit our Facebook page on March 21 for instructions on how to easily email your lawmakers and make your voice heard.

The 2018 Parkinson’s Policy Forum is just around the corner, and advocates from across the country will travel to Washington, D.C. to meet with their members of Congress and educate them on the ways public policy impacts Parkinson’s disease (PD) research and care.

Two of those advocates are Angie Hott and her husband Dan.

Diagnosed in 2008 when he was 50, Dan Hott is an Air Force veteran who, with Angie, has four children — Caity (28), Violet (18), Isaac (14) and Levi (13) — and lives in Berkeley Springs, West Virginia. For the Hotts, advocacy and innovation have become cornerstones of their family life.

“When one person in the family has Parkinson’s disease we all have Parkinson’s disease, in a sense,” said Angie. “We have to use our voices for those who need us, and for the greater purpose of finding a cure,” she added.

In Angie’s public school STEAM (science, technology, engineering, the arts and mathematics) and character education work, she talks about Parkinson’s disease and encourages the kids to pursue a career in science or medicine. In fact, earlier this year, when she was teaching that it is positive to be curious and learn new things, she challenged students to “create something new that will help others.” A group of 8-year-old students she was working with used their engineering know-how and a big box of Legos to devise ways Dan could be more mobile. Science and medicine is a big interest at home, too, as the Hotts’ daughter Violet will attend Columbia University in the fall to study neuroscience.

“We will never be able to financially offer much, but we sure can encourage the younger generation to care and to pursue work to better understand the brain and find a cure for PD,” said Angie.

At this year’s Parkinson’s Policy Forum, Dan and Angie Hott look forward to meeting other advocates, sharing their story, and encouraging their members of Congress to support policies that further research funding and increase access to care for people living with Parkinson’s.

“Last year was our first Forum and I’m really looking forward to this year — I think I’ll be less nervous and better equipped to talk about our family and what Parkinson’s means to us,” she added.

Angie’s advocacy efforts aren’t limited to the Forum in Washington, D.C. She and her extended family and friends regularly reach out to their senators and representative on issues that matter to the PD community. 

The Hotts also pursue state and local public policy work. In February, Angie wrote an email encouraging West Virginia Governor Jim Justice to declare April 2018 Parkinson’s Awareness Month, and she was successful in her efforts. Governor Justice will issue the proclamation, which will be another opportunity in April for the Hotts to raise awareness about PD and why our voices matter.