UCB Launches Phase 1b Trial Testing UCB0599 for Parkinson’s Disease Treatment

UCB0599 Phase 1b trial

UCB has announced the start of a Phase 1b clinical trial to evaluate the efficacy and safety of its therapeutic candidate UCB0599 for the treatment of Parkinson’s disease.

This multicenter clinical trial will take place across the United States.

Current treatments for Parkinson’s, which include levodopa and dopamine agonists, can help manage early motor symptoms associated with the disease. However, as the disease progresses and neurons continue to degenerate, these therapies ultimately become less effective at treating the symptoms.

Many neurodegenerative diseases, including Parkinson’s, occur due to the accumulation of toxic protein aggregates known as prions.

In the case of Parkinson’s, misfolding and the subsequent aggregation of a protein known as alpha-synuclein results in the formation of Lewy bodies, which are toxic and lead to disease symptoms and progression.

By preventing alpha-synuclein from clumping into Lewy bodies, clearing them out, or stopping their spread from cell to cell, researchers believe they can prevent or slow Parkinson’s progression.

Developed as part of a collaboration between Neuropore Therapies and UCB, UCB0599 is designed to inhibit alpha-synuclein misfolding.

UCB0599 is a small molecule compound that is taken orally and can penetrate the blood-brain barrier, which is a semipermeable membrane that separates the blood from the cerebrospinal fluid and protects the brain from the outside environment. This membrane is an obstacle for the efficient delivery of therapies that need to reach the brain.

“We are pleased to reach the milestone of advancing into Parkinson’s patients for the first time with UCB0599, a therapeutic candidate arising from our collaboration with UCB,” Errol De Souza, president and CEO of Neuropore Therapies, said in a press release. “We believe that inhibition of alpha-synuclein misfolding and oligomerization with an orally active, brain penetrant, small molecule represents a potential advantage over antibody therapeutics that are currently in development.”

In January 2015, Neuropore Therapies granted UCB a license to develop and commercialize therapies that target alpha-synuclein in all indications around the world. It is thought that alpha-synuclein aggregation also plays a role in other neurodegenerative diseases.

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MJFF Awards Casma Therapeutics $370K for Innovative Therapies to Slow PD Progression

Casma Therapeutics grant

The Michael J. Fox Foundation for Parkinson’s Research (MJFF) has awarded Casma Therapeutics $370,000 to advance an innovative class of therapies aimed at slowing disease progression.

The grant will promote the biotechnology company’s investigation into compounds that activate the calcium channel TRPML1 to accelerate autophagy — a natural cellular way of disposing of pathogens and toxic proteins. The hope is that boosting autophagy will protect and rescue damaged neurons. It’s widely believed that Parkinson’s disease (PD) results from neuronal buildup of toxic proteins.

Casma will test its novel TRPML1-activating treatments using human-induced pluripotent stem cell-derived dopaminergic neurons, which model Parkinson’s disease. The neurons will be generated by the National Human Genome Research Institute (NHGRI) from patient samples collected at the National Institutes of Health (NIH). Induced pluripotent stem cells are derived from either skin or blood cells that have been reprogrammed back into a stem cell-like state. This allows for the development of an unlimited source of any type of human cell needed for therapeutic purposes.

The study is in collaboration with co-MJFF grantee Ellen Sidransky, MD, a Parkinson’s expert and top NHGRI researcher.

“Inducing the natural process of autophagy to clear toxic proteins is a promising new approach to treating Parkinson’s,” Daniel Ory, MD, Casma senior vice president, translational medicine, said in a press release. “We share the foundation’s sense of urgency, and we’re eager to move our program forward.”

New discoveries are revealing the fundamental role of autophagy and lysosomal flux in maintaining cellular health, according to a Casma webpage. Lysosomes are special compartments within cells that digest and recycle different types of molecules. Research has shown that inadequate or aberrant autophagy contributes to genetic diseases, including Parkinson’s.

The company believes that restoring cellular balance may arrest or reverse disease progression.

”Funding therapies against emerging targets such as TRPML1 is a crucial plank in our effort to find a cure for Parkinson’s,” said Liliana Menalled, PhD, MJFF senior associate director of research programs. “We are committed to leaving no stone unturned as we pursue therapies that will help the more than 6 million people worldwide living with this disease.”

The Parkinson’s Foundation, which says approximately 60,000 Americans are newly diagnosed each year, puts the global figure even higher, estimating that more than 10 million people live with the disease.

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Vitamin B12 May Protect Nerve Cells From Alpha-synuclein Clumps, Study Suggests

Vitamin B12 effects

Vitamin B12 can prevent the formation of and destroy alpha-synuclein aggregates in the brain, lowering their toxicity and potentially helping to alleviate Parkinson’s disease, according to a study.

The study, “Vitamin B12 inhibits α-synuclein fibrillogenesis and protects against amyloid-induced cytotoxicity,” was published in the journal Food & Function.

When the brain produces an excess of alpha-synuclein, this protein starts to form aggregates and toxic deposits called Lewy bodies. This process is closely associated with the onset and progression of Parkinson’s disease.

As a result, developing new therapies that inhibit alpha-synuclein aggregation is seen “as an attractive therapeutic strategy to ameliorate Parkinson’s disease,” the researchers wrote.

However, developing such therapies is challenging since most of the compounds that inhibit alpha-synuclein aggregation cause adverse side effects such as liver failure, or cannot cross the blood-brain barrier — a semipermeable membrane that protects the brain against the external environment, and is a major obstacle for the efficient delivery of certain therapeutics that need to reach the brain and central nervous system.

“Vitamins are dietary components that are indispensable for life in addition to proteins, carbohydrates, fats and minerals,” the researchers wrote.

Previous studies have shown that vitamins of the B-complex are essential to the development of neurons, the detoxification of the body, and the function of the immune and inflammatory response. Vitamin B12 is widely used as a food supplement, can cross the blood-brain barrier, and has shown positive effects on the cognitive function of animals models and people with dementia.

Here, a team of Chinese researchers used different techniques to assess whether vitamin B12 affected the formation of alpha-synuclein aggregates and whether the vitamin could make alpha-synuclein less toxic to brain nerve cells grown in the lab.

They found that vitamin B12 delayed the formation of clumps of alpha-synuclein, and that the aggregates that formed in the presence of the vitamin were smaller than those created in its absence; these smaller aggregates were less toxic to the nerve cells.

Vitamin B12 was able to do this by directly interacting with alpha-synuclein and preventing it from taking a form that is prone to aggregation. It also destroyed preformed aggregates of alpha-synuclein.

“[Vitamin B12] destabilized and disassembled the preexisting mature [aggregates] into less toxic pieces. In summary, VB12 can efficiently disassemble mature [alpha-synuclein] fibrils and protect [nerve] cells from [alpha-synuclein]-induced toxicity,” the researchers wrote.

“[Vitamin B12] appears to have great potential to develop as an [alpha-synuclein] aggregation inhibitor and functional food ingredient for therapeutic interventions in [Parkinson’s disease],” they added.

These results identify vitamin B12 as a valuable nutrient source that “possesses great potential to be developed as a new functional food ingredient to help alleviate [Parkinson’s disease],” the study concluded.

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When Facing Darkness, We Must Fight to See the Light

scars

There are days when it feels like we are surrounded by darkness. We live with so many unanswered questions about this illness that it can frustrate us. We often are surprised by so many twists and turns. Sometimes we forget that we must endure and do battle with the dark before we can see or enjoy the light.

When we get swallowed up in the dark places of our disease — the despair, the hopelessness, discouragement, and the depression — it is crucial that we take an active role in fighting it. Sometimes we must face that darkness, take control, and do battle until we see the light. And the light is there. However, we need to be facing in the right direction. Sometimes plowing through the darkness first is the only way to reach that light, or at least get us going on the right path.

We often can become lost in our thinking.

We have told ourselves lie after lie that in order to have a happily ever after, we must always be heading west into the perfect sunset and riding upon an unblemished, white stallion. However, more than likely, Parkinson’s disease will not have that happy ending (if lived out to its fullest) that we’ve been taught to dream about. There will not be a white stallion to ride upon as we gallop away. More than likely, we’ll be plopped into a wheelchair, and if we’re lucky, raced around the halls of a nursing home by a caring, but fun, nursing attendant who, hopefully, has enough smarts to buckle us in first.

Grief over the loss created by this disease may be where you are dwelling right now. The loss of freedom or the ability to do what you used to be able to do. The loss of a loved one to this illness. The loss of a dream because of Parkinson’s. The loss of something tangible, real, and of value — the loss of life as you knew it before you found out you had Parkinson’s disease.

You may be experiencing denial or bargaining with God over this whole “mess.” Perhaps you’re in the pit of depression or feel angry about your current condition. Maybe you’re beginning to see some light in the form of acceptance. That acceptance can be something as small as agreeing to take a new pill in hopes of it working better than the old one. Perhaps you’ve been given the go-ahead for deep brain stimulation and decided to go for it. Maybe you’ve just bought a new shirt that you don’t have to fight to button. 

Wherever you’re at, don’t be afraid of the darkness that often seems to follow you and others with this disease. Face it fighting. Face it determined to win and expect to see the light. 

***

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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Plant Chemical Chrysin May Protect Against Parkinson’s-related Changes, Mouse Study Suggests

chrysin, protective effects

Chrysin, a chemical commonly found in plants, may ease behavioral, cognitive, and neurochemical changes in Parkinson’s disease, according to a mouse study.

The study, “Chrysin protects against behavioral, cognitive and neurochemical alterations in a 6-hydroxydopamine model of Parkinson’s disease,” was published in Neuroscience Letters.

Studies have confirmed the involvement of neuroinflammation and oxidative stress in the development of Parkinson’s disease. Oxidative stress is an imbalance between the production of free radicals and the ability of cells to detoxify them, resulting in cellular damage as a consequence of high levels of oxidant molecules.

Both molecular phenomena have been implicated in the degeneration of dopamine-producing neurons — the type of nerve cell that is lost in Parkinson’s disease.

Chrysin is a naturally occurring flavone commonly found in fruits and vegetables. Evidence indicates the plant chemical has anti-allergic, anti-cancer, anti-inflammatory, and antioxidant properties.

A Brazilian team of researchers have now investigated the effects of a 28-day chrysin treatment (10 mg/kg/day, given orally) on a female aged mouse model of Parkinson’s disease.

Researchers first injected a neurotoxin called 6-hydroxydopamine (6-OHDA) into the mice’s right striatum — a brain region involved in voluntary movement control that is severely affected in Parkinson’s. This neurotoxin causes cellular dysfunction and death of dopaminergic neurons, enabling the molecular replication of Parkinson’s disease in a laboratory setting. Injected mice were all 20 months old, which is equivalent to a human age of more than 60 years.

Following the 28-day chrysin treatment protocol, the researchers performed memory, locomotor, and biochemistry tests these animals.

Compared with healthy control animals, chrysin was found to reduce the loss of dopamine and its metabolites (meaning “small products of metabolism”) in the striatum of the Parkinson’s mice, indicating the plant chemical may protect against disease-related dopamine metabolism degradation.

In line with the biological mechanism of Parkinson’s, 6-OHDA administration increased inflammatory responses by elevating levels of proinflammatory cytokines, or small proteins. Chrysin treatment prevented this response, supporting previous research on the compound’s anti-inflammatory properties.

Chrysin was also able to prevent the increase in oxidative stress levels that resulted from 6-OHDA injections. The animals’ antioxidant response also improved following treatment.

In addition, chrysin alleviated disease-related behavioral changes — which in mice manifests as rotational (circling) behavior — and cognitive deterioration including memory and spatial learning abilities. Researchers also noted that “age-related memory decline was partially protected by chrysin at a dose of 1 mg/kg, and normalized at the dose of 10 mg/kg.

“In the present study, chrysin was beneficial against behavioral, cognitive and neurochemical changes in a [Parkinson’s disease] model induced by 6- OHDA in aged female mice. Mechanisms underlying chrysin effects include decrease of oxidative stress and neuroinflammation, which eventually attenuates behavioral and cognitive impairments,” the researchers concluded.

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Alpha-synuclein in Blood Serum May Be Early Parkinson’s Biomarker, Study Suggests

biomarker, alpha-synuclein

Measuring the amount of alpha-synuclein in tiny vesicles collected from blood serum may help diagnose early Parkinson’s and identify patients with different types of this disease.

The study with that finding, “Central Nervous System-Derived Exosomal Alpha-Synuclein in Serum May Be a Biomarker in Parkinson’s Disease,” was published recently in the journal Neuroscience.

As both resting and posture tremor may occur in the early stages of Parkinson’s, patients may be misdiagnosed with essential tremor. Similar to Parkinson’s, essential tremor is a progressive movement disorder, and it predominantly affects hands and arms.

Alpha-synuclein is the main component of Lewy bodies, characteristic protein aggregates that accumulate in brain cells of Parkinson’s patients.

Compared to unaffected individuals, Parkinson’s patients typically have lower levels of alpha-synuclein in their cerebrospinal fluid — the liquid surrounding the brain and spinal cord — which correlates with prognosis. However, measuring alpha-synuclein in the clinic has been precluded by the invasive nature of spinal tap and by the inconsistent results of plasma or serum samples.

Exosomes are tiny vesicles released by neurons and other cells, and have been implicated in the transmission of misfolded proteins, including alpha-synuclein in people with Parkinson’s. As such, researchers hypothesized that exosomes derived from the central nervous system (CNS) could be a peripheral biomarker of Parkinson’s disease.

The scientists recruited 38 newly diagnosed, untreated patients with early Parkinson’s divided into tremor-dominant (TD, 22 patients, mean age 62.7 years) and non-tremor-dominant (NTD, 16 patients, 62.1 years), who were compared to 21 patients with essential tremor (62 years) and 18 healthy controls.

Among the patients with Parkinson’s, those with TD had a shorter disease duration than the people with the NTD subtype (19.2 vs. 35.8 months). The age at disease onset did not differ in these two groups – 61.1 years in TD and 59.1 years in NTS patients.

The results revealed that Parkinson’s patients had lower levels of alpha-synuclein in CNS-derived serum exosomes than those with essential tremor or controls. Importantly, within Parkinson’s patients, those with the NTD type — which has been associated with more frequent depression, lack of motivation and impairment in activities of daily life — had lower amounts than those in the TD subset.

A subsequent analysis found that exosomal alpha-synuclein had a moderate potential to diagnose Parkinson’s disease and a great potential to diagnose non-tremor-dominant patients.

Of note, the amount of CNS-derived alpha-synuclein in exosomes was not significantly associated with disease duration or severity.

Overall, “CNS-derived exosomal [alpha]-synuclein in the serum may be regarded as a biomarker to identify [early Parkinson’s],” the scientists wrote.

Cautioning that studies with larger groups of patients and those with longitudinal monitoring are needed, the team further commented that assessing alpha-synuclein in serum exosomes also may help identify different Parkinson’s types.

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APDA Meets to Discuss Grants, Diversity in Parkinson’s Research, Support, and Care

APDA Grant Research

The American Parkinson Disease Association (APDA) recently hosted two groups of experts who assessed scientific projects vying for funding, and addressed diversity issues in Parkinson’s disease research and care.

The organization met with its scientific advisory board (SAB) to decide which grant projects it will fund for the 2019-2020 academic year. Grants are based on overall significance and field impact, appropriateness of the project’s chief investigator and scientific environment, and feasibility of the project’s proposed budget and end date. Funding decisions will be announced in August.

The APDA also hosted its first-ever Diversity in Parkinson’s Research Conference, which focused on needs surrounding the disease in diverse and under-served communities. Attendees included researchers investigating Parkinson’s in ethnic and minority populations, and clinicians who treat such patients.

Panel discussions included an overview of APDA diversity initiatives, research about biomarkers in diverse populations, disparities in Parkinson’s clinical trial enrollment, and what the field of hypertension can teach Parkinson’s investigators about access to diverse communities.

Currently, most Parkinson’s research focuses on relatively older white men, the APDA said. The organization wants to expand investigations to include more patients of varying ages, genders, races and ethnicities. It also wants more access among these groups for care, programs and services.

”APDA’s mission is to help everyone impacted by Parkinson’s disease live life to the fullest, and we mean everyone,” Leslie A. Chambers, APDA president and CEO, said in a press release.

The organization plans to establish an annual grant to support research focused on closing diversity gaps. For now, it offers an annual $50,000 post-doctoral fellowship, and multiple $75,000 research grants. The three-year $300,000 George C. Cotzias Fellowship supports early-career physician-scientists. In addition, the APDA awards its Centers for Advanced Research $100,000 each year to support PD investigations. (Visit this site for more information on APDA-funded research.)

”It’s so exciting to see the fascinating ideas outlined in the grant submissions,” said Rebecca Gilbert, MD, PhD, APDA vice president and chief scientific officer, of the current crop of proposals. “Proposed research projects included everything from ways of detecting a diagnosis of PD in the blood, to exploring ways that telemedicine can improve the lives of patients with PD. The SAB certainly had their work cut out for them and made some tough choices,” she said.

In addition to deciding who gets new grants, the SAB receives updates during annual meetings about previously funded research. During the May 16 meeting, for example, members were apprised of the latest research at the University of Alabama at Birmingham, where scientists are focused on advances in the role of brain inflammation in Parkinson’s development and progression. The SAB also heard from Washington University School of Medicine researchers studying imaging biomarkers for Parkinson’s.

David Standaert, a leading Parkinson’s researcher at the University of Alabama at Birmingham, also is the SAB’s chairman. He called the Diversity in Research Conference a “fantastic” first step toward finding answers.

”Together, I think we can do great things to make both our research and services more inclusive and accessible,” he said.

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FDA Grants Breakthrough Device Designation to Amprion’s PMCA Early Detection Tool

FDA breakthrough device

The U.S Food and Drug Administration (FDA) has granted a Breakthrough Device designation to Amprion’s proprietary technology, Protein Misfolding Cyclic Amplification (PMCA) — a device that holds the potential to diagnose Parkinson’s disease at a much earlier stage than current diagnostic methods.

If approved by the FDA, Amprion anticipates a market roll-out for PMCA tests as an early detection tool for Parkinson’s within the next 18 months.

There is no effective treatment for Parkinson’s, a progressive nervous system disorder that affects movement, largely due to the fact that there is no sensitive and objective laboratory test that can diagnose the disease at its early stages. Most patients are diagnosed due to clinical symptoms when the disease course is relatively advanced.

Amprion’s PMCA is able to circumvent this problem by tracking specific prion (proteins) biomarkers — in this case alpha-synuclein — in the cerebrospinal fluid (CSF) and blood prior to the onset of clinical symptoms. The CSF is the liquid surrounding the spine and brain.

“Our PMCA test tracks alpha-Synuclein, a protein that misfolds into toxic shapes in the brain and this likely begins decades before disease symptoms. Amprion’s ability to monitor Misfolded Proteins at early stages is both significant and meaningful. This enables us to work with major pharmaceutical companies to develop Prion-targeted drugs to stop or slow the disease,” Claudio Soto, PhD, Amprion’s co-founder and chief scientific officer, and a professor of neurology at McGovern Medical School at UTHealth, said in a press release.

The FDA’s Breakthrough Devices program gives expedited review and assessment to medical devices that have the potential to be an effective treatment or diagnostic tool for life-threatening or irreversibly debilitating diseases. This allows these devices to reach the market faster.

“Prions are proteins gone rogue. This is a small victory in our war against Prions,” said Russ Lebovitz, MD, PhD, and Amprion CEO. “We are honored and look forward to working closely with FDA to fast-track the development and review of our aS [alpha-synuclein] PMCA tests toward final regulatory approval. Early diagnosis of Parkinson’s represents a giant leap for science to crack the code on this disease. Our goal is to stop Parkinson’s on its destructive path.”

In addition to its value as a diagnostic test, the device may significantly contribute to medical research by providing scientists with a tool to study how alpha-synuclein contributes to Parkinson’s development.

The Michael J. Fox Foundation for Parkinson’s Research, National Institutes of Health SBIR/STTR programs, and McGovern Medical School at the University of Texas Health Science Center at Houston were key partners in the development of PMCA.

“Efforts across Parkinson’s research seek to better define, measure and treat alpha-Synuclein pathology. This assay is a valuable tool in that work and we’re proud that The Michael J. Fox Foundation could partner toward its development with funding, samples and consult,” said Samantha Hutten, PhD, the foundation’s senior associate director of research partnerships.

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Patients with Bipolar Disorder at Higher Risk of Developing Parkinson’s, Study Suggests

bipolar disorder

Patients with bipolar disorder appear to have a nearly seven times higher risk of developing Parkinson’s disease later in life, according to a nationwide study in Taiwan.

The study, “Bipolar disorder and risk of Parkinson disease: A nationwide longitudinal study,” was published in the journal Neurology.

An association between major depressive disorder and Parkinson’s disease has been suggested in previous studies. But such an analysis has not been conducted in people with bipolar disorder, which is characterized by unusual shifts in mood, energy, and activity levels.

Data from a hospital registry previously showed that people with manic or depressive episodes — both experienced by those with bipolar disorder — had an increased risk of being diagnosed with Parkinson’s, but the temporal link between these two events had not yet been properly assessed.

To address this lack of knowledge, researchers conducted a longitudinal study using Taiwan’s National Health Insurance Research Database. Clinical records from 56,340 patients with bipolar disorder (mean age 40 years) and 225,360 healthy individuals, collected between 2001 and 2009 and followed until 2011, were evaluated. None of the participants had a history of Parkinson’s or related diseases at the start of the study.

Patients with bipolar disorder developed Parkinson’s significantly more often than those in the control group (0.7% vs, 0.1%). These patients also had a shorter time from enrollment to Parkinson’s disease diagnosis (4.2 vs. 6.5 years), and were younger when Parkinson’s was identified (64.2 vs. 73 years).

Use of antipsychotic agents was found to have no impact on these findings. The prevalence of cerebrovascular diseases, traumatic brain injury, hypertension, dyslipidemia (abnormal levels of lipids), and diabetes did not differ between the two groups.

Further analysis revealed that adult bipolar patients were about 6.78 times more likely to develop Parkinson’s than controls, while bipolar patients older than 65 had a 3.87 times higher risk.

Patients with a high frequency of hospital admission (more than two times per year) for psychiatric episodes were found to have 5.62 times higher risk of Parkinson’s than patients admitted less than once a year. Also, two or more psychiatric admissions for manic/mixed or depressive episodes were associated with a greater likelihood of having Parkinson’s.

“Our population-based longitudinal study found that patients with bipolar disease had an increased risk of developing [Parkinson’s] later in life compared to the controls,” the researchers wrote.

“Additional experiments are required to obtain a deeper understanding of the mechanisms involved” in the development of these two disorders,” they said. In addition, “medical practitioners should be aware that the risk of subsequent [Parkinson’s] should be particularly considered in patients with bipolar disease, especially those with multiple psychiatric admissions for mood episodes.”

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Endurance Exercise May Help Manage Cortisol Levels in Parkinson’s Patients, Study Suggests

cortisol exercise PD

Doing high-intensity endurance exercise reduces morning cortisol levels in patients with Parkinson’s disease, which may have an impact on the progression of non-motor signs and symptoms, a pilot study suggests.

While other studies are needed to confirm if lowering cortisol with physical exercise works for delaying disease worsening, this data supports the further exploration of the role played by the hormone in non-motor symptoms of Parkinson’s.

The study, “Endurance Exercise Reduces Cortisol in Parkinson’s Disease With Mild Cognitive Impairment,” was published in the journal Movement Disorders.

Parkinson’s disease is a complex disorder associated with both motor and non-motor symptoms including sleep problems, depression, and cognitive impairment.

There is evidence that a malfunction of the hypothalamic-pituitary-adrenal axis (HPA) is involved in the progression of non-motor symptoms of Parkinson’s due to an overproduction of the hormone cortisol.

HPA is a system in the body crucial for stress management. It involves a set of complex interactions between two parts of the brain — the hypothalamus and the pituitary glands — and the adrenal glands located at the top of each kidney, which are regulated by different hormones.

After a stressful or threatening event, the HPA axis is activated and several “stress hormones,” primarily cortisol and adrenaline, are released by the adrenal glands into the bloodstream. As the blood levels of cortisol rise, they start to block the release of other hormones from the hypothalamus and the pituitary that, in turn, will induce a drop in cortisol levels.

This type of negative feedback loop is one mechanism by which HPA regulates itself to avoid excessive and sustained production of cortisol.

Beside this natural stress management process, cortisol is also important for a wide range of vital processes, including metabolism and the immune response. There has been a long-standing association between raised or impaired regulation of cortisol levels and a number of psychiatric conditions such as anxiety and depression, even though this is not yet fully understood.

Elevated morning cortisol levels have been reported in Parkinson’s patients. Accordingly, there is evidence that elevated cortisol in Parkinson’s patients is linked to symptoms such as depression and risk behavior.

Physical exercise is associated with a lower production of cortisol in healthy individuals, and there is evidence that it may also reduce the risk and rate of Parkinson’s progression.

Based on this data, the researchers reasoned that doing exercise could lower daytime production of cortisol in Parkinson’s patients, with possible implications for delaying the progression of their non-motor symptoms.

To test this theory, they conducted a small study in which they measured the levels of cortisol in saliva samples collected from eight Parkinson’s patients with mild cognitive impairment (ages 53 to 79). Over six months, participants were asked to perform high-intensity treadmill endurance exercise.

The exercise program included five to 10 minutes of warm-up, 30 minutes of exercise at 80-85% maximum heart rate, followed by five to 10 minutes of cool-down. Participants exercised an average of 2.5 days per week, and over the first eight weeks of training, exercise duration and intensity were gradually increased to target levels.

Saliva samples were collected before and after completing the program, and at specific times immediately after waking up (0, 0.25, 0.50, and 0.75 hours after awakening) and at periods throughout the day (three, six, nine, and 12 hours after awakening).

Overall, cortisol secretion of Parkinson’s patients more closely resembled that of healthy people after they had completed the training program.

Results showed there was an average 19% reduction in cortisol secretion, compared with the pre-training period. In addition, while cortisol reduction was significant during the times immediately after waking up, it was not in the periods later in the day.

“These data support the need for further exploration of HPA axis dysregulation in Parkinson’s disease,” the researchers wrote. “To understand not only its potential role in the mechanisms underlying non-motor symptoms of Parkinson’s, but also its responsiveness to intervention studies such as physical exercise that can improve non-motor symptoms.”

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