As My Losses from Parkinson’s Accelerate, It’s Time to Fight Back


Don’t forget you’re human. It’s OK to have a meltdown, just don’t unpack and live there. Cry it out and then refocus on where you are headed.” —Unknown

I tend to have meltdowns more frequently these days.

Why is this happening?

My losses from this disease seem to be accelerating. Following are some examples:

  • In boxing class, I sometimes struggle with the punching choreography and can’t seem to coordinate my hands to do the actions required.
  • When reaching to place items on a high shelf, I lose my balance and fall backward.
  • My speed bag workouts are slowing down, and I lose my rhythm more often.
  • I am clumsier and tend to knock things over.
  • Typing on a computer keyboard is an exercise in futility. Sometimes my finger holds pressure on a key too much, and at other times, not enough. I can’t tell anymore.

I suspect that you can relate to my experiences only if you also have Parkinson’s disease (PD). While these setbacks may seem inconsequential, when they occur with increased frequency, it becomes frightening and overwhelming.

I must be mindful of what I do now more than ever. Falling and injuring myself a few weeks ago shocked me to the reality and seriousness of this disease. I find myself cursing at PD and yelling expletives at the top of my lungs in my house when my body fails me. My pet bunny doesn’t know what to make of this. I think the poor guy thinks I am yelling at him.

When my body does not move the way my mind is telling it to, my frustration levels accelerate. This may also be a harbinger of things to come.

Fighting back. (Photo by Michelle Del Giorno)

Running on empty

Some research indicates that over 50 percent (and as much as 60-70 percent) of dopamine-producing neurons are dead by the time Parkinson’s symptoms first appear. I have no doubt that the disease is aging me before my time. A 90-year-old friend is starting to experience symptoms that are due to aging — the same signs that I have at age 66 because of PD.

My neurologist has suggested that sometimes I need to take a step back, refocus, and not be too hard on myself. He knows me well.

I must fight back — and not give in!

At any given moment, you have the power to say: This is not how the story is going to end.” Christine Mason Miller


Note: Parkinson’s News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The opinions expressed in this column are not those of Parkinson’s News Today or its parent company, BioNews Services, and are intended to spark discussion about issues pertaining to Parkinson’s disease.

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ISCO’s Phase 1 Trial Testing Neural Stem Cell Therapy Completes Patient Enrollment

ISC-hpNSC neural stem cells trial

Patient enrollment and dosing is now complete for International Stem Cell Corporation’s (ISCO) Phase 1 trial testing its ISC-hpNSC neural stem cells — a cellular therapy that offers a new approach for treating Parkinson’s disease.

“We are excited to announce the completion of enrollment of the world’s first approved human pluripotent stem cell-based clinical trial for the treatment of Parkinson’s disease. This is a major milestone for the Company and we expect to announce complete clinical results of this phase 1 clinical trial in the first half of 2020,” Andrey Semechkin, PhD, ISCO’s co-chairman and CEO, said in a press release.

ISC-hpNSC, which stands for human parthenogenetic stem cell-derived neural stem cells, is a cellular therapeutic that can not only differentiate into dopaminergic neurons, but can also release brain-protecting agents, offering a new approach for Parkinson’s treatment.

A one-time transplant of ISC-hpNSC into the brains of Parkinson’s patients can replace the dead and dying dopaminergic neurons and can offer protection to the remaining neurons, reducing disease symptoms and preventing further deterioration, according to the company.

The open-label, single center, Phase 1 trial (NCT02452723) — ongoing at The Royal Melbourne Hospital in Australia — is evaluating the safety, tolerability and preliminary effectiveness of transplanting ISC-hpNSC into Parkinson’s patients over a 12-month period, with a five-year, long-term follow-up.

A total of 12 patients are divided into three groups, each injected with 30 million, 50 million, or 70 million ISC-hpNSC. The stem cells are injected directly into the striatum and substantia nigra regions of the brain, which are directly affected in Parkinson’s disease.

The 12th and final trial participant recently received the transplant, with the highest dose of ISC-hpNSC.  Eight participants are already in the five-year follow-up phase.

The trial’s interim results will be presented at the 2019 American Academy of Neurology 71st Annual Meeting, taking place in Philadelphia May 4-11.

At six and 12 months after the cell transplants, patients undergo a positron emission tomography (PET) scan, a non-invasive imaging technique that allows clinicians to visualize the metabolic processes in the body.

Researchers also will compare the participants’ clinical response before and one year after receiving ISC-hpNSC, using the Unified Parkinson Disease Rating Scale (UPDRS), which measures the course of disease; the Parkinson’s Disease Quality of Life Questionnair-39, which assesses difficulties in daily living; and patient motor diaries.

Results from a six-month analysis after cell transplants revealed the therapy was safe, with no serious adverse events. The company called this “a very significant achievement due to the invasive nature of the transplantation procedure.”

The analysis also showed a 25% reduction in patients’ off time — the period when levodopa therapy begins to fail and Parkinson’s symptoms return.

“[N]ow that we have completed the most expensive stage of the phase 1 clinical trial, ISCO will have more resources available to invest in growing and developing its commercial business, where we have recently made significant progress,” Semechkin said.

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Lack of Tissue Oxygenation from Sleep Apnea Linked to Parkinson’s, Study Suggests

obstructive sleep apnea

Lack of tissue oxygenation associated with episodes of upper airway obstruction in patients with obstructive sleep apnea syndrome (OSAS) may increase the levels of alpha-synuclein in the blood and may contribute to the development of Parkinson’s disease, a study says.

The study, “Plasma α‐synuclein levels are increased in patients with obstructive sleep apnea syndrome,” was published in the Annals of Clinical and Translational Neurology.

Parkinson’s disease mainly results from the gradual loss of dopaminergic neurons in the substantia nigra, a region of the brain responsible for controlling movement.

The disease also seems to be associated with overproduction of the protein alpha-synuclein in nerve cells of the brain. When this protein clumps together, it gives rise to small toxic deposits inside brain cells, called Lewy bodies, inflicting damage and eventually killing them.

Of note, alpha-synuclein phosphorylation — a chemical modification in which a phosphate group is added to the protein — is known to occur in Parkinson’s disease, and is thought to be a critical step in disease progression as it enhances alpha-synuclein’s toxicity, possibly by increasing the formation of alpha synuclein aggregates.

“Recent studies found that [obstructive sleep apnea] was a risk factor for PD [Parkinson’s disease] onset, and hypoxia [lack of oxygen] may have contributed to it. [In addition,] previous studies both in vitro and in vivo revealed that hypoxia is able to induce overexpression of alpha‐synuclein (…). However, the detail mechanism remains to be further investigated,” the researchers wrote.

In this study, a group of Chinese scientists investigated the relationship between lack of tissue oxygenation caused by episodes of upper airway obstruction during sleep, and the levels of alpha-synuclein in patients with OSAS.

OSAS occurs when the throat muscles intermittently relax and block upper airways during sleep.

The study enrolled 42 patients who had been diagnosed with OSAS (eight with mild, 16 with moderate and 18 with severe OSAS) and 46 age- and sex-matched individuals with simple snoring (controls). The levels of total and phosphorylated alpha-synuclein in the patients’ blood plasma were measured by Enzyme-Linked Immunosorbent Assay (ELISA), a technique that allows researchers to measure the amount of a specific protein of interest using an enzymatic reaction).

Results showed that patients with OSAS had significantly higher levels of both total (37.68 ng/ml vs 21.08 ng/ml) and phosphorylated (26.87 ng/ml vs 14.61 ng/ml) alpha-synuclein in the plasma compared to controls.

Moreover, correlation analyses revealed the levels of both total and phosphorylated alpha-synuclein were positively correlated with the apnea–hypopnea index (an index that measures the severity of sleep apnea) and the oxygen desaturation index (an index that measures the number of times oxygen levels dip below a given threshold during sleep).

Conversely, the levels of both total and phosphorylated alpha-synuclein in the plasma were negatively correlated with the lowest and mean oxyhemoglobin saturations — the fraction of hemoglobin (red blood cells) bound to oxygen relative to the total hemoglobin found in the blood.

“In summary, the present study found that increased alpha-synuclein levels in the plasma are correlated with the degree of hypoxia in OSAS, indicating that chronic hypoxia caused by OSAS may be involved in the pathogenesis [disease manifestations]” of Parkinson’s, the scientists concluded.

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Rock Steady Boxing Saved Me from the Great Lakes


I will never again underestimate the strength of a McDonald’s paper cup — or my Rock Steady Boxing class.

The other day, I took my grandson to his favorite playground: McDonald’s. A friend was meeting us there with her grandson. By the time she arrived, the place was packed. There was only one spot available with a good view of the playing area: a table near the back windows that was covered with a gigantic puddle of sticky soda.

Someone had a massive spill and didn’t bother to report it. By the time we got there, it had formed a smaller version of the Great Lakes. Soda was all over and spilling onto the floor, creating a pool at least 2 feet wide by 5 feet long.

With a root beer in my right hand and a box of apple juice in the other, I turned to set the drinks on the table and lost my footing. I was facing the windows when my feet suddenly began sliding into the middle of the Great Lakes. I couldn’t grab onto anything to steady myself and slammed my shoulder into the top of the chair. In an attempt to stop sliding, I banged the root beer cup onto the window ledge, and with all of the strength I could muster I pushed my weight against it and tried to pull myself up. 

It sounds crazy, but that large paper cup filled with root beer gave me the leverage I needed to get upright.

The entire time I was pushing against that cup, I was wondering when it would give way and leave me crashing to the floor. But then I realized my left arm and hand pushing against the windowsill were holding me up.

Six months ago, I couldn’t have held myself up like that.

I would have tumbled to the floor, ended up in the middle of the Great Lakes, and needed to be rescued from drowning in my embarrassment. But the muscles in my arms are stronger now. Other muscles throughout my body are more powerful, too. I can thank my Rock Steady Boxing class for that, and the encouragement of the coaches and the friends I’ve made there. Without the classes, I would have landed on my backside on the cement floor of the play area at the local McDonald’s, otherwise known, for the sake of this column, as the Great Lakes.


Note: Parkinson’s News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The opinions expressed in this column are not those of Parkinson’s News Today or its parent company, BioNews Services, and are intended to spark discussion about issues pertaining to Parkinson’s disease.

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Globin Protein Levels May Help Assess Efficacy of Dopamine Agonists in Parkinson’s Patients, Study Shows

globin dopamine therapy

Evaluation of two specific proteins circulating in the blood, called alpha- and beta-globin, may help monitor treatment efficacy and risk of side effects among patients with Parkinson’s disease, a study suggests.

The study, “2D-DIGE as a strategy to identify serum protein biomarkers to monitor pharmacological efficacy in dopamine-dictated states of Parkinson’s disease and schizophrenia,” was published in Neuropsychiatric Disease and Treatment.

Parkinson’s disease is triggered by the death of dopamine-producing neurons in the midbrain, which control movement. Lack of dopamine — a crucial chemical messenger that allows nerve cells to communicate — causes impaired body control and induces the motor symptoms that are commonly associated with this disease, such as tremors, gait, and balance problems.

Given the underlying mechanisms of Parkinson’s disease, patients are commonly prescribed dopamine agonists to overcome dopamine loss and manage symptoms. However, the use of these therapeutic compounds is linked to several adverse effects including hallucinations, which are due to increased activity of dopamine in the brain.

Despite research efforts, no tests are currently available to help recognize if a treatment is effective or if a treated patient is reaching a point of dopamine over-activity and increased risk of side effects. As such, clinicians still rely almost completely on patients’ compliance and symptoms to assess therapeutic efficacy.

Therefore, researchers in the study explored whether a simple blood test could identify patients’ at risk of experiencing treatment-related adverse reactions. The team recruited five patients with Parkinson’s disease and five patients with schizophrenia who had never been treated with dopamine-related therapies.

The psychotic symptoms of schizophrenia are known to be caused by overactivity of dopamine in the brain — similar to what occurs as a side effect of dopamine-agonist use in Parkinson’s patients.

Comparing the different proteins in the participants’ blood samples revealed that alpha- and beta-globin proteins were consistently present in Parkinson’s patients but absent in schizophrenia patients.

To better understand if these two proteins could be used as biomarkers of dopamine status, the team further analyzed them in a group of 100 individuals

The cohort included six Parkinson’s patients who had not received any therapy, 44 patients who had received treatment, and five patients who had undergone treatment with different dopamine agonists and had experienced treatment-related adverse effects such as visual or auditory hallucinations.

The remaining participants had been diagnosed with schizophrenia, among whom five had not received prior treatment (treatment-naïve), 36 were treated with dopamine inhibitors, and four were treated and experienced Parkinson’s-like symptoms.

The levels of alpha- and beta-globin were three-fold higher in treatment-naïve Parkinson’s patients compared with treatment-naïve schizophrenic patients. In addition, the expressions of both proteins were significantly higher in patients treated for Parkinson’s disease than in those treated for schizophrenia.

Overall, the amount of these two proteins circulating in the blood was found to be inversely correlated with mid-brain dopamine concentrations. This means that schizophrenic untreated patients (who have the highest dopamine activity) had the lowest levels of alpha- and beta-globin proteins, while Parkinson’s untreated patients (who have the lowest dopamine activity) had the highest levels of both proteins.

Disease scoring, gender, and age had no impact on the levels of the two proteins.

“The inverse relationship between globin expression and dopamine concentration in the brain holds value as a translational tool in the therapeutics of Parkinson’s disease,” the researchers wrote.

Moni­toring the levels of alpha- and beta-globin proteins could be a useful “tool for clinicians to efficiently and effectively treat Parkinson’s disease and schizophrenia,” they said.

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Natural Variant of Vitamin B12 Can Prevent Neurodegeneration in Parkinson’s Preclinical Models

vitamin B12 AdoCbl 5’-deoxyadenosylcobalamin

An active form of vitamin B12 can reduce the effects of dopamine loss in Parkinson’s disease caused by genetic mutations in the LRRK2 gene, a study suggests.

These finding means that this form of vitamin B12 could be used as the basis for developing new therapies for treating Parkinson’s.

The study, “Vitamin B12 modulates Parkinson’s disease LRRK2 kinase activity through allosteric regulation and confers neuroprotection,” was published in Cell Research.

Several studies have shown that overactivation of the LRRK2 enzyme, due to genetic mutations in the LRRK2 gene, is associated with the development of a hereditary form of Parkinson’s disease. But increasing evidence has suggested that this enzyme also may contribute to the progression of sporadic cases of Parkinson’s — ones caused by environmental factors.

Increased activity of the LRRK2 enzyme contributes to the accumulation of toxic alpha-synuclein fibers in dopamine-producing neurons of the substantia nigra — a brain region involved in the control of voluntary movements, and one of the most affected in Parkinson’s disease.

Given its important role, researchers have focused on finding ways to prevent the activity of this enzyme as a strategy for treating this neurodegenerative disorder.

Now, an international team of researchers has found that one natural variant of vitamin B12, called AdoCbl (5’-deoxyadenosylcobalamin), can effectively regulate the activity of the LRRK2 enzyme. AdoCbl is approved by the U.S. Food and Drug Administration.

When tested in experimental cell line models, the team found that AdoCbl could significantly reduce the enzyme’s activity, even when it was genetically modified to carry the G2019S mutation — the most common LRRK2 variant linked to Parkinson’s.

Further analysis confirmed that AdoCbl had the ability to directly bind to LRRK2, changing its three-dimensional structure, and preventing its normal function. This allows AdoCbl to work as a strong inhibitor of the enzyme.

“AdoCbl represents a starting point for the development of a new class of LRRK2 activity modulators for the much-needed treatment of LRRK2-linked pathological conditions such as Parkinson’s disease,” the researchers said.

To explore AdoCbl’s therapeutic potential, the team next administrated it in worms carrying the G2019S mutation. The experiments revealed that AdoCbl treatment could prevent the death of dopamine-producing nerve cells and prevent the manifestation of symptoms associated with neurodegeneration.

Additional analysis also revealed that AdoCbl could prevent neurotoxicity and dopamine deficits in fly and mouse models carrying different LRRK2 mutations associated with Parkinson’s.

Identification of vitamin B12 as a modulator of LRRK2 activity “constitutes a huge step forward because it is a neuroprotective vitamin in animal models and has a mechanism unlike that of currently existing inhibitors,” Iban Ubarretxena, director of the Biofisika Institute and co-author of the study, said in a press release.  Biofisika is  a joint research center of the University of the Basque Country (Universidad del País Vasco/Euskal Herriko Unibertsitatea).

“[This active form of vitamin B12] could be used as a basis to develop new therapies to combat hereditary Parkinson’s associated with pathogenic variants of the LRRK2 enzyme,” he added.

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How Did Life Get Crazy Busy? I’m Overwhelmed!

Dr. C's

I thought that when I retired, I would have more time, not less. How did life get so busy? There are not enough hours in the week to finish all the things I want to. If I push myself harder and longer, then I get fatigued and overwhelmed, but then I need more rest, which results in less time. That thwarts the desired outcome.

I have a long to-do list, and I feel oppressed just looking at it, particularly when I am already worn out. I have been fighting this battle for the past five years, and there are a few things that make it a little easier for me.

To give you some idea of what my seven-day week looks like, here is my to-do list, with the average number of hours spent on each task:

Table of tasks and hours

A seven-day week has 168 available hours. I am already overbooked, and I haven’t included several projects that are on my waiting-to-do list. These include finishing/publishing three manuscripts, finishing/publishing my graphic novel, and a blog that hasn’t had a new post in over a year.

There is “Santa,” an important part of my identity, which will consume most of my time in December. Finally, there are requests for my professional services, such as a paper or a presentation. When these requests come in, something on the above list must change, and it can be too much.

The emotional confusion of being overwhelmed puts a halt to effective project engagement. The way out of being so damn busy and feeling weighed down is to put into place some form of a time management system. The first thing is to realize how much time your chronic disease consumes each week. There are lots of ways this happens, and flexibility is crucial to coping.

The second thing is to set aside the time needed for things that add to your well-being, like sleep, exercise, meals, and family. If you are like me, with lots of irons in the fire, you have a full list of things that require your time. It comes down to making choices, setting priorities. Sometimes, we have to say no to people.

Time is a resource that can be thought of like money. There is a limited “time budget” to spend, and I want to allocate that time in the best way possible in order to get the most out of this life with a chronic disease. I spend time in concentrated blocks of three to four hours. This helps to avoid distractions. Also, these blocks can be reallocated when something unexpected comes up — something always does!

Delegation, when appropriate, is a good time-management strategy. My partner has taken on the email, social networking, and the appointment calendar, which frees up time.

There are resources to help with time management skills. Here are a few:
1. A time management skills book that looks at multiple life demands on our time
2. A 30-minute audiobook talk with clear tips on time management
3. A TED Talk on time management
4. Columnists who offer time-management tips and time-management apps

What issues do you face with not having enough time in the week to get everything done?


Note: Parkinson’s News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The opinions expressed in this column are not those of Parkinson’s News Today or its parent company, BioNews Services, and are intended to spark discussion about issues pertaining to Parkinson’s disease.

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Studying Epigenetic Changes May Help Diagnose Parkinson’s Disease Earlier, Researchers Say

epigenetics, Parkinson's

Understanding and identifying epigenetic changes may become a potential strategy for early Parkinson’s diagnosis, when patients still lack the characteristic symptoms of the disease, according to a recent study.

The study, “DNA methylation changes associated with Parkinson’s disease progression: outcomes from the first longitudinal genome-wide methylation analysis in blood,” was published in Epigenetics.

Parkinson’s disease patients carry a unique profile of certain epigenetic marks — modifications that sit on top of DNA and control which genes can become activated or not — that change as disease progresses.

“Using this [epigenetics] approach, you could put patients at risk for PD [Parkinson’s disease] on certain therapies before symptoms arise,” Travis Dunckley, assistant research professor at the Arizona State University’s (ASU)-Banner Neurodegenerative Disease Research Center, said in an ASU news release written by Gabrielle Hirneise.

Parkinson’s disease is characterized by the progressive loss of coordination and movement. These symptoms are currently the basis for Parkinson’s clinical diagnosis. However, they appear when the disease is in an advanced phase, a time during which current therapies are much less effective.

“One of the biggest issues with neurodegenerative diseases like Parkinson’s disease or Alzheimer’s disease is that diagnosis is mostly clinically based, and it comes late in the disease — the brain is already degenerated, and it is extremely difficult to restore brain function at that stage,” Dunckley said.

To increase the likelihood of response to available therapies, identifying the disease during its early stages — before the onset of symptoms — is key.

“When physicians treat PD [Parkinson’s disease] patients, it is usually too late to change the trajectory of the disease. I am interested in early diagnostics to try to identify people prone to the disease before they get it,” Dunckley added.

While there is a genetic component to Parkinson’s disease — estimated to contribute to 40% of disease risk — environmental factors play a key role in the disease, namely by interacting with the genome (our complete set of genes).

Parkinson’s is “about 60% environmental — it’s much less genetic than many other neurodegenerative diseases,” Dunckley said.

One way that the environment interacts with the genome is through epigenetic changes — external chemical modifications to DNA that can turn genes on or off but that do not change the actual DNA sequence.

One type of epigenetic mark is the addition of chemical methyl groups that sit on top of genes and work as “switch off” or “switch on” signals. However, unravelling the role of these epigenetic marks in Parkinson’s disease is challenging.

“It is hard to link them without confounding variables in that there are a lot of environmental factors,” Dunckley said. “It’s difficult to say whether epigenetic changes are based on disease, environmental factors or a combination of disease and environmental factors.”

Dunckley and collaborators at the University California, San Diego(UCSD), Texas A&M University, Harvard University and The Translational Genomics Research Institute (TGen), aimed to characterize the epigenetic landscape, specifically the changes in DNA methylation patterns (called methylome), over time in a group of Parkinson’s patients.

In the largest epigenetics study to date in Parkinson’s research, the scientists profiled the methylome of 189 patients and compared it to that of 191 healthy controls. After two years, the same analysis was performed to assess how the DNA methylation patterns changed in Parkinson’s patients versus controls.

The researchers found that the sites in the DNA that are methylated vary between Parkinson’s and healthy individuals, and that these methylation patterns change over time.

Patients receiving dopamine replacement therapy also had a different methylation pattern compared with untreated patients, with the patterns changing more in the untreated group — further supporting the link between epigenetic changes and Parkinson’s progression.

“The main findings are that one, the epigenome does change as the disease progresses. The second finding is that the PD medications themselves alter the epigenome,” Dunckley said. 

If researchers are able to identify a methylation pattern that is specific to Parkinson’s patients, clinical diagnosis can be made earlier and allow patients to receive treatment before irreversible changes occur in the brain.

The researchers are expanding these early findings by performing the same type of analysis in a new subset of patients but for longer period of time.

“The next study we are doing is a replication and extension of this one to validate the findings and extend the observation period to five years,” Dunckley said.

“We are also including patients that are very early in PD [Parkinson’s disease] progression, patients who have symptoms that are highly predictive of future PD. The ultimate goal is to identify changes in these earliest stages of disease that can be predictive of future PD onset,” he added.

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Parkinson’s Foundation Grants $1.5 Million to Programs in 38 States

Parkinson's Foundation grants

In support of local health, wellness and educational programs, the Parkinson’s Foundation is granting $1.5 million to Parkinson’s community programs in 38 states.

Grants range from $5,000 to $25,000, and focus on programs that either help underserved Parkinson’s disease communities, target newly diagnosed patients, or advocate for clinical trial education and participation.

“We are proud to announce these community grants and expand programs and resources in Parkinson’s communities across the entire nation,” said John L. Lehr, Parkinson’s Foundation president and CEO. “These grant recipients share our passion and commitment to making life better for people with Parkinson’s.”

In the past eight years, the organization has funded some 338 community-based programs that seek to meet unfulfilled patient needs.

A full roster of this year’s community grant awardees can be viewed here.

One of those recipients explained how the grant will benefit Parkinson’s patients in her community.

“We are deeply honored to have been awarded a Parkinson’s Foundation grant and are very excited at the opportunity to join current recipients in improving the everyday life of individuals with Parkinson’s,” Karen Weisinger of the Calvin Chin’s Martial Arts Academy in Newton, Massachusetts, said in a press release.

“Thanks to the Parkinson’s Foundation, we look forward to bringing this unique tai chi program to people with newly diagnosed PD,” she said.

Tai chi is an internal exercise system that combines breathing with slow, gentle movements to improve the flow of energy (chi) through the body, to quiet and calm the mind and emotions and improve overall health and well-being.

Tai chi has been found to be effective in reducing falls, which could be of extreme importance for those with Parkinson’s, who many times see their balance deteriorate as their condition progresses.

The Parkinson’s Foundation seeks to enhance life for patients by improving care and driving investigations toward a cure.

All funded programs are designed to help Parkinson’s patients live better-quality lives. They include education, wellness, dance, art, boxing, cycling, yoga, nutrition, caregiver support, and music therapy.

Researchers have found that Parkinson’s patients who exercise at least two-and-a-half hours a week also experience a slower decline in their quality of life. Specifically, more recent studies have focused on the concept of intense “forced” exercise, such as boxing, suggesting that certain types of exercise may be neuroprotective by actually slowing disease progression.

Yoga focused on mindfulness — a mental exercise focused on accepting oneself in the present — also has been found to lower anxiety, depression and motor impairment in people with mild-to-moderate Parkinson’s disease.


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Approved Blood Pressure Medication Also May Treat Parkinson’s Disease, Animal Study Suggests

Felodipine for Parkinson's

Felodipine, an approved therapy for high blood pressure, is able to promote the clearance of toxic protein aggregates in mouse models of neurodegenerative diseases, including Parkinson’s, according to a study.

The study, “Felodipine induces autophagy in mouse brains with pharmacokinetics amenable to repurposing,” was published in the journal Nature Communications.

A common feature of most neurodegenerative diseases, such as Alzheimer’s, Parkinson’s, and Huntington’s diseases, is the accumulation of toxic protein aggregates within neurons, or brain cells. Buildup of these proteins damages the cells and leads to neurodegeneration in these disorders.

Toxic material is normally cleared from the body through a mechanism called autophagy, which refers to the process by which cells degrade and purge unwanted material, such as harmful protein clusters.

Because autophagy often is impaired in neurodegenerative diseases, researchers are interested in identifying chemical compounds that can stimulate this process and potentially improve the clearance of toxic aggregates and reduce disease symptoms. However, no such treatment exists yet.

One possibility is to identify an existing medication that can be used for this purpose. Therapeutic compounds frequently have multiple targets, which means the same therapy often can treat different conditions. It is typically easier and faster to repurpose existing therapies because they already have gone through clinical trials and been found safe for human use.

To try to find one of these medications that might induce autophagy and be suitable for treating neurodegenerative diseases, researchers at the UK Dementia Research Institute and the University of Cambridge screened several different therapies that were approved for other indications.

They previously had identified an approved medication for high blood pressure and angina known as verapamil (sold under the brand names Calan, Covera, and Verelan, among others) as a powerful inducer of autophagy. However, it does not cross the blood-brain barrier (a thin membrane that protects the central nervous system, including the brain) and is therefore not appropriate for the treatment of neurodegenerative diseases.

The researchers then screened a panel of similar therapies to identify any that actually would penetrate the blood-brain barrier and have strong autophagy-inducing effects. This led them to felodipine as the most suitable candidate.

Felodipine (sold under the brand name Plendil) is approved by the U.S. Food and Drug Administration for the treatment of hypertension (high blood pressure). Laboratory studies indicated that felodipine promotes autophagy and clears a variety of toxic protein aggregates found in neurodegenerative diseases.

To further investigate felodipine, researchers tested the effects of the compound in animal models of Huntington’s and Parkinson’s diseases.

They performed a pharmacokinetic analysis to determine the optimal treatment regimen in mice that would mimic the concentration the therapy reaches in humans at currently prescribed doses. (Pharmacokinetics refers to how a compound is absorbed, distributed, metabolized, and excreted in the body.)

Results indicated that felodipine was effective at reducing the buildup of aggregates in mice with the Huntington’s and Parkinson’s disease mutations, as well as in a zebrafish model of dementia. Furthermore, long-term treatment with felodipine was associated with a decrease in signs of the diseases.

Notably, these effects were observed at concentrations of felodipine that would be safe for humans.

“These data suggest that this drug may have efficacy in humans with appropriate neurodegenerative diseases that may be ameliorated by autophagy induction,” the authors wrote.

“This is the first time that we’re aware of that a study has shown that an approved drug can slow the build-up of harmful proteins in the brains of mice using doses aiming to mimic the concentrations of the drug seen in humans,” David Rubinsztein, PhD, said in a press release. Rubinsztein, a professor of molecular neurogenetics at Cambridge, led the study. “As a result, the drug was able to slow down progression of these potentially devastating conditions and so we believe it should be trialled in patients.

“This is only the first stage, though. The drug will need to be tested in patients to see if it has the same effects in humans as it does in mice. We need to be cautious, but I would like to say we can be cautiously optimistic,” he said.

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