Low-level Exposure to Pesticides Damages Cells in Ways That Might Lead to Parkinson’s, Study Reports

pesticides

Even low-level exposure to certain pesticides disrupts cells in a way that mimics the effects of mutations linked Parkinson’s disease — raising a likelihood of the disease developing in people predisposed to it, a new study reports.

These findings may also explain why people living near agricultural areas are seen to be at greater risk of developing Parkinson’s, leading the study’s researchers to suggest that current standards of safety regarding agrochemicals might need to be reconsidered.

The study, “Nitration of microtubules blocks axonal mitochondrial transport in a human pluripotent stem cell model of Parkinson’s disease,” was published in The FASEB Journal.

Prior research has reported a link between exposure to herbicides or pesticides used in agriculture — paraquat, maneb and rotenone — and the development of Parkinson’s disease.

These compounds are toxic to mitochondria — the powerhouses of a cell — leading to the death of dopamine-producing neurons in the substantia nigra, a brain area specifically involved in Parkinson’s disease.

“People exposed to these chemicals are at about a 250-percent higher risk of developing Parkinson’s disease than the rest of the population,” Scott Ryan, the study’s senior author, said in a press release.

A research team at the University of Guelph, in Ontario, Canada, explored the mechanisms underlying this risk.

Researchers used stem cells from Parkinson’s patients who had a specific mutation in the alpha-synuclein gene — associated with an increased risk of Parkinson’s — as well as normal embryonic stem cells in which this mutation was introduced by gene editing.

One point of importance in this study was the use of  human cells, Ryan noted. “Until now, the link between pesticides and Parkinson’s was based primarily on animal studies as well as epidemiological research that demonstrated an increased risk among farmers and others exposed to agricultural chemicals,” he said. “We are one of the first to investigate what is happening inside human cells.”

The team generated dopamine-producing neurons from the stem cells, and then exposed them to rotenone and paraquat or maneb. According to the release, paraquat is used on crops as they grow, and maneb after they are harvested to prevent spoiling.

Researchers found that exposure to the toxins prevented mitochondria from moving within cells as necessary, depriving neurons of energy.

Importantly, these toxic effects — seen in both patients’ cells and cells with the genetic risk factor introduced — occurred at doses below the U.S. Environmental Protection Agency’s threshold for lowest observed effect. Higher doses would likely be necessary to affect normal neurons, or those without the Parkinson’s risk mutation.

“People with a predisposition for Parkinson’s disease are more affected by these low level exposures to agrochemicals and therefore more likely to develop the disease,” Ryan said. “This is one of the reasons why some people living near agricultural areas are at a higher risk.”

“Our results are the first to demonstrate a gene by environment interaction in [Parkinson’s], whereby agrochemical exposure selectively triggers a deficit in mitochondrial transport,” the researchers wrote.

Ryan further noted that the results underscore the need to re-evaluate current acceptable levels for these agrochemicals. “This study shows that everyone is not equal, and these safety standards need to be updated in order to protect those who are more susceptible and may not even know it.”

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Certain Genetic Variants Linked to Risk of Compulsive Behaviors in Parkinson’s Patients, Study Reports

compulsive disorders and PD

Mutations in four specific genes may help to identify those Parkinson’s patients at risk of developing the addictive behaviors known as impulse control disorders, researchers report.

Their study, “Dopaminergic and Opioid Pathways Associated with Impulse Control Disorders in Parkinson’s Disease,” was published in Frontiers in Neurology.

People with Parkinson’s are more likely than others — at a threefold higher risk, in fact — of developing such disorders, and the compulsive behaviors related to a lack of control over activities that range from gambling and sexual activity to eating, shopping and hobbies.

Patients with impulse control disorders may also show an addiction-like pattern of dopaminergic medication use, the study reports.

Treatment with dopaminergic replacement therapies, such as Mirapex (pramipexole) and Requip (ropinirole), are considered a risk factor for impulse control disorders in this patient population.

But not all patients using these therapies develop compulsive behaviors, indicating that some are more susceptible than others.

Previous studies have suggested that genetics plays a role in this risk, with specific genes proposed to be linked to disorder susceptibility.

Indeed, research estimates that common genetic variants could account for about 57% of the variability reported in the incidence of compulsive behaviors among Parkinson’s patients.

Researchers in Norway analyzed genetic data on 119 Parkinson’s patients who met study requirements and were enrolled in the Norwegian ParkWest study — a population-based study of incident Parkinson’s in newly diagnosed patients and healthy controls.

Among patients, 29.4% had at least one impulse control disorder and 63% were taking dopamine agonist medications, whose use was linked to a 4.5 higher risk of an impulse control disorder.

A total of 16 genes were analyzed, all known to be involved in nerve cell communication and signaling pathways, as well as in mechanisms linked to impulse control disorders and related behaviors.

Eleven genetic variants — or changes in a gene’s DNA — evident in these genes were significantly associated with impulse control disorders. In particular, an alteration in the DRD1 gene (which encodes the dopamine receptor D1) was associated with 2.9 times higher risk of developing  such disorders.

Other genetic variants, such as those in the OPRK1 gene (which encodes the kappa-opioid receptor 1), were found to have a protective role.

Adding the genetic status of four genes — DRD1, OPRK1, OPRM1 and COMT — to patients’ age and dopamine agonist use further improved (by 13%) the research team’s ability to identify those at risk of developing impulse control disorders.

“These results confirm and expand existing knowledge about the genetic architecture of impulse control disorders in Parkinson’s disease,” the researchers wrote.

“Our findings demonstrate that a genetic panel [based on DRD1, OPRK1, OPRM1, and COMT] can provide valuable information with regard to the clinical differentiation between Parkinson’s patients at risk of impulse control disorders and patients without risk,” they added.

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Facing My Fear of Death with Hope

hope, death

Sherri Journeying Through

Necrophobia: The fear of death or dead things. Thanatophobia: The fear of dying.

Everyone, at some point in their lives, thinks about death and gets a little nervous, if not downright scared.

It may not be death that people fear so much as the prologue of suffering they may have to endure. For example, I don’t fear the actual moment of death itself, because I believe that the next moment — or soon thereafter — I will be in a far better place. I have, however, feared the process.

How will I go? Will I fade quietly as I snore my last snore? Or will I gasp for my last breath? Will I be joking around to the end, then close my eyes and happily drift off into eternal sleep? Will I suffer from pain or be pain-free? There are endless scenarios, and I am hoping for pain-free and quick. And I’m hoping that it’s in God’s agenda, too.

However, what if it isn’t God’s agenda? What if His agenda involves years of pain, years of disintegrating into an unrecognizable, immobile, sickly shell? What if that?

That thought freaked me out the other day. What if that? What if I can’t control my movements, what if I speak funny, I drool all over my shirt, I choke when I eat while someone else feeds me?

What if all that and I am alone in a nursing home where those I have loved have stopped coming to visit because they “can’t bear to see Mama like that anymore?”

What if the only attention I get is the stares of the curious grandchildren who visit their grandmother once a week, the woman in the room next to mine?

What if?

But, what if NOT?

Necrophobia. Thanatophobia. Names for fear of death or dying, or of things that are dead.

J.K. Rowling wrote in the Harry Potter series, “It is the unknown we fear when we look upon death and darkness, nothing more.” And it is there, in the middle of the book, “Harry Potter and the Half-Blood Prince,” that I find the words to explain my thoughts. It is the unknown that I fear.

Will there be gasping? Drooling? Choking? Children seeing a disease and not a person? It is the unknown we fear.

If there is a fear of dying, then there must be an opposite. I call this opposite, courage for the future. While courage is not necessarily a state of being, as fear can be, it is an action, a response. A response to act courageously (even in the midst of fear itself).

You may still be afraid, but now you’re facing that fear with hope. Hope does not disappoint because with it comes peace, and in peace, fear cannot survive. The kind of pure peace that surpasses all human understanding.

So, what then can I confidently say to fear?

“I know no such thing,” she said to herself as the children walked by her door in her room at the nursing home. And then she stuck out her tongue at them, causing them to giggle. Her expressionless face, molded into stone by her disease, began to crumble with her fear and she did the only logical thing she could think to do. She smiled.

***

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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Patients with IBD at Increased Risk of Parkinson’s, ‘Real Life’ Study Suggests

IBD and Parkinson's

Patients with inflammatory bowel disease (IBD) are at an increased risk of developing Parkinson’s disease, a new study suggests.

The research, “Inflammatory bowel disease increases the risk of Parkinson’s disease: a Danish nationwide cohort study 1977–2014,” was published in the journal Gut.

Inflammation plays a key role in the development of Parkinson’s and multiple system atrophy (MSA), two conditions that belong to the “parkinsonism” group of disorders and cause motor problems such as tremors, slow movement and stiffness.

Both Parkinson’s and MSA patients have aggregates of the protein alpha-synuclein in the brain.

IBD is a chronic condition mainly characterized by inflammation of the gut. In fact, chronic inflammatory immune activity is increasingly being recognized as a fundamental element of neurodegenerative disorders, and in Parkinson’s, inflammation in the intestine may reflect the earliest symptom of the disease.

This may occur due to the so-called “gut-brain axis”, a system that incorporates two-way communication between the nervous and endocrine (hormonal) systems and regulates immune responses in the gut and brain. All aspects of this system appear to be heavily influenced by the activity of intestinal microbes.

Previous research has indicated that the LRKK2 gene, the greatest genetic contributor to Parkinson’s disease and a regulator of inflammation and alpha-synuclein clearance, also is associated with Crohn’s disease, one of the two most common forms of IBD.

To provide “real-life” evidence of the link between IBD and the risk of Parkinson’s and MSA, Danish researchers conducted a nationwide study involving all 76,477 patients diagnosed with IBD in Denmark from 1977 to 2014.

A total of 7.5 million non-IBD individuals from the general population were used as controls.

Individuals were followed from IBD diagnosis to the occurrence of Parkinson’s or MSA, using data from the Danish National Patient Register. This was the first epidemiological study assessing the risk of parkinsonism in a nationwide group of IBD patients with long-term follow-up, researchers noted.

Over the study duration, 335 IBD patients (0.4%) and 39,784 non-IBD individuals (0.5%) were diagnosed with Parkinson’s, while MSA was detected in 13 patients with IBD (0.02%) and 866 controls (0.01%).

Importantly, the results showed that patients with IBD had a 22% higher risk of developing Parkinson’s in comparison with non-IBD individuals, independent of age at IBD diagnosis, gender, or length of follow-up.

Although the incidence of MSA was low, results also showed a tendency toward higher risk in IBD patients compared to controls.

Specifically, the risk of developing Parkinson’s or MSA was 35% higher in patients with ulcerative colitis —  another main type of IBD — but not in those with Crohn’s disease.

“The study suggests that clinicians should be aware of symptoms of parkinsonism in patients with IBD,” researchers wrote. They also underscored the need to further study the role of gut inflammation and the brain-gut axis in the development of Parkinson’s-related disorders.

As for potential treatment advances, the authors said that “the identification of risk factors associated with [early] phases of Parkinson’s disease may allow for early intervention studies that could modify or slow down disease progress.”

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Dual-Target Compounds Could Lead to Single and More Effective Therapy for Parkinson’s, Study Reports

dual-target compounds

Pharmacologic compounds that can act on two target molecules show promise as potential therapies for Parkinson’s disease, according to a study that details a new way of finding such compounds.

The study, “Docking screens for dual inhibitors of disparate drug targets for Parkinson’s disease,” was published in the Journal of Medicinal Chemistry.

Neurodegenerative diseases such as Parkinson’s are complex and affect multiple molecules, and treating them often requires modulating several targets.

Developing a single therapy that can act on several biological targets is, for this reason, a major goal in treating these disorders, because such a therapy is of greater efficacy  compared to single-target therapies, and more likely to avoid the side effects associated with a combination therapy.

A frequently used method to design compounds that specifically bind to target molecules is known as structure-based drug design or molecular docking. The method uses a three-dimensional structure of a target molecule to predict the “best-fit” orientation of a compound that stably binds to its target.

However, the rational design of compounds that interact with several targets is very challenging, and the vast majority of known multi-target drugs has been discovered by serendipity and mainly involve targets that are either closely related or recognize similar molecules.

Now, researchers used structure-based virtual screening to find potential therapeutic compounds that would simultaneously target and suppress two unrelated molecules associated with Parkinson’s disease — A2A adenosine receptor (A2AAR) and monoamine oxidase B enzyme (MAO-B).

A compound that could target both A2AAR and MAO-B would potentially improve motor function and better protect nerve cells (related to A2AAR suppression), and increase dopamine levels – a key chemical messenger found in reduced levels in Parkinson’s patients — due to MAO-B suppression.

Virtual screening of a commercial chemical library containing 5.4 million compounds spotted 24 compounds with elevated binding potential to both A2AAR and MAO-B.

Experiments showed that 14 of these compounds bound to at least one of the molecules, and four compounds targeted both molecules. Two of them were considered to have the best profile for the dual binding, and functional tests confirmed they could suppress both A2AAR and MAO-B.

The two compounds were able to induce protective effects in dopamine-producing nerve cells grown in the lab, which are used as a Parkinson’s model.

These compounds “provide excellent starting points for development of dual-target A2AAR/MAO-B leads that could be evaluated in vivo for antiparkinson activity,” the researchers wrote.

Despite the structural differences between A2AAR and MAO-B, structure-based virtual screening was still able to identify effective dual-target compounds, supporting its use as a tool for identifying multi-target compounds for disparate targets.

“Our results demonstrate that molecular docking screening can guide discovery of ligands with specific polypharmacological profiles [that act on multiple targets], which can contribute to development of drugs against complex diseases with improved efficacy and less side effects,” the researchers concluded.

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Mutation Common to Familial Parkinson’s and Tuberculosis May Lead to Ways of Treating Both Diseases

macrophages

A mutation common to familial Parkinson’s was seen in a study focused on tuberculosis to prevent immune cells of the brain from working properly, allowing protein to accumulate in nerve cells — and, potentially, to this specific disease’s development.

The study, “LRRK2 is a negative regulator of Mycobacterium tuberculosis phagosome maturation in macrophages,” appeared in The EMBO Journal.

Mutations in the LRRK2 gene are the most common genetic cause of Parkinson’s disease. As these alterations result in excessive activation of the protein LRRK2 kinase, researchers are focused on developing treatments that might block LRRK2. But exactly how LRRK2 causes Parkinson’s and why its blockers work is not well understood. (About 15 percent of Parkinson’s patients have a family history of the disease and identifiable mutations.)

Besides Parkinson’s, mutations in the LRRK2 gene are associated with chronic inflammation and bacterial infections. Again, however, the gene’s precise role in immunity is unclear.

When bacteria, or any unwanted microorganism, enters the body, immune cells called macrophages kick into action. Macrophages are responsible for recognizing and engulfing the bacteria in small compartments called phagosomes. Another cellular structure, called the lysosome, then fuses with the phagosome to destroy the bacteria trapped inside the phagosomes.

Using a combination of experimental strategies, researchers found that LRRK2 prevented phagosomes and lysosomes from fusing as they should in both human and mouse macrophage cells infected with Mycobacterium tuberculosis (Mtb) — the pathogenic bacteria that causes tuberculosis. Importantly, treating these cells with an LRRK2 blocker significantly reduced Mtb levels.

Mice genetically modified to lack the LRRK2 protein had an quicker  immune response against Mtb, and lower levels of this bacteria in their lungs up to two weeks after infection compared to normal mice.

“Importantly, these data uncover LRRK2 as a regulator of the early clearance of Mtb,” the researchers wrote.

“We think that this mechanism might also be at play in Parkinson’s disease, where abnormal masses of protein called ‘Lewy bodies’ build up in neurons in the brain and cause damage,”  Susanne Herbst, PhD, with The Francis Crick Institute and the study’s co-first author, said in a press release.

LRRK2 may prevent immune cells in the brain from properly breaking down debris, leading to a protein build-up in neurons that disrupts their function.

“By studying TB, we have found a possible explanation for why LRRK2 mutations are a genetic risk factor for Parkinson’s,” Herbst said.

Patrick Lewis, a study’s co-author and a professor at the University of Reading, noted that while research in Parkinson’s has focused on neurons and why they degenerate, the potential key role of other cells, particularly those involved in the immune response, is increasingly appreciated.

“This study reinforces why we should think more broadly about the events that cause neurodegeneration, and that some of the answers to Parkinson’s disease might come from immunology,” Lewis said.

The scientists’ work may also lead to new TB treatments, taken from work in Parkinson’s. “LRRK2 inhibiting drugs are already being developed to treat Parkinson’s disease and we’re trying to see if we can repurpose them as a potential new TB therapy,” said Max Gutierrez, the study’s senior author. “This should be relatively straightforward because TB infects the lungs, so the LRRK2 inhibitors wouldn’t need to cross the blood-brain barrier like they do in Parkinson’s disease.”

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Alkahest Awarded Grant to Support Development of ALK4290 for Parkinson’s

Alkahest

The Michael J. Fox Foundation for Parkinson’s Research (MJFF) recently awarded Alkahest a grant to support the development of ALK4290 as a new therapy for Parkinson’s disease.

The immune system plays an important role in the development and progression of Parkinson’s disease. New therapies targeting the recruitment of immune cells, or inhibiting brain inflammation, could be effective in treating the disease.

ALK4290 is an oral, small molecule medicine that acts as a key modulator of inflammation, with potential effects on multiple symptoms associated with Parkinson’s disease.

The investigational compound has been well-tolerated in previous clinical studies and is currently being studied in wet age-related macular degeneration (wAMD), a medical condition that frequently leads to vision loss in the center of the visual field.

Both studies (ALK4290-201 and ALK4290-202) are open-label Phase 2 clinical trials evaluating the therapeutic effects and safety of a six-week oral treatment regimen of ALK4290 in patients with either newly diagnosed wAMD or refractory wAMD. Both studies will be conducted in Europe (Hungary and Poland).

The MJFF grant will test whether ALK4290 can be used to treat Parkinson’s disease. Researchers will evaluate the effect of ALK4290 in two pre-clinical models relevant to Parkinson’s disease biology and will assess whether ALK4290 reverses deficits in motor function and loss of neurons through inhibition of inflammation in these animal models.

This project will attempt to determine the mechanisms underlying immune cell involvement in Parkinson’s disease, providing further support for the link between neuroinflammation and disease progression. If the study proves successful, the compound will rapidly enter clinical testing to evaluate its potential benefits for Parkinson’s patients.

“Parkinson’s disease is a condition with significant impact on patients whose needs are still unmet. We are excited about the prospects of evaluating ALK4290 as a novel therapeutic in this indication and continuing our commitment to developing innovative treatments for age-related disorders,” Steven Braithwaite, Alkahest’s chief scientific officer, said in a press release.

“Our Foundation funds novel approaches to slow or stop Parkinson’s progression, the greatest unmet need for the millions living with this disease,” added Liliana Menalled, PhD, MJFF senior associate director of research programs. “The ALK4290 molecule shows strong data to support additional evaluation as a potential Parkinson’s therapy, and we look forward to seeing the results of Alkahest’s experiments.”

The grant, “Development of ALK4290 as a novel PD therapeutic,” will be coordinated by S. Sakura Minami, PhD, who has 15 years of research experience in the field of neuroscience. She leads her research group at Alkahest, Inc., a biotech company located in the San Francisco Bay area, to better understand the mechanisms underlying aging and to develop therapies for age-related diseases.

ALK4290 was acquired by Alkahest from Boehringer Ingelheim with exclusive rights for its development and commercialization worldwide.

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Obesity, Sedentary Behavior Not Linked to Parkinson’s Disease Risk, Study Shows

Obesity and Parkinson's

Increased body mass and sedentary behavior do not increase the risk of having Parkinson’s disease, a study shows.

To date it is still not fully understood what causes Parkinson’s disease, but several environmental and lifestyle factors have been suggested as contributors to this disease.

In the study, “Body mass index, sitting time, and risk of Parkinson disease,” which was published in the journal Neurology, researchers from the Karolinska Institutet in Sweden focused on the potential of body mass index (BMI) — a measure indicative of obesity — and sitting time to contribute for Parkinson’s disease development and progression.

The team already had reported that more physical activity around the house and commuting lowered Parkinson’s risk. “Regardless of time spent on physical activity, sedentary behavior characterized by sitting extended periods of time has been associated with increased general morbidity and mortality,” the researchers wrote. “Thus, sedentary behavior may affect PD pathogenesis through mechanisms other than physical activity.”

Clinical records of 41,638 individuals who completed a comprehensive questionnaire with extensive assessment of lifestyle factors at a national fund-raising event in September 1997 (The Swedish National March Cohort) were analyzed.

During the study period (13 years) 286 participants were diagnosed with Parkinson’s disease.

Participants who spent six or more hours seated per day had a 6 percent higher risk. Also, those with body max index of 30 or higher had a 13 percent increased risk compared to leaner patients. These results were not found to be influenced by age, sex, or smoking status.

Although some differences were found, these data do not show a significant correlation between baseline body mass and sitting time with the risk of developing Parkinson’s, which is in accordance with previous studies.

However, researchers highlighted that all the analysis was based in data collected at the beginning of the study, and some measures could have changed during follow-up. “If such changes are related to the outcome, this could lead to misclassification and an over- or underestimation of any true association,” they wrote.

Still, it is widely accepted that the underlying mechanisms of Parkinson’s start many years before symptom onset. So, any factor that might contribute to development of this disease may occur in an “exposure window of interest closer to the baseline exposure assessment,” they said.

“Future studies should focus on environmental factors other than obesity and sedentary time in efforts to disentangle the complex causation of Parkinson’s disease,” the authors suggested.

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Non-Motor Symptoms Different Among Men and Women, Study Shows

non-motor symptoms

Non-motor symptoms (NMS) in Parkinson’s disease are significantly more frequent and differ between men and women, a new study shows.

The study, “Frequency of non-motor symptoms in Parkinson’s disease presenting to tertiary care centre in Pakistan: an observational, cross-sectional study,” was published in the journal BMJ Open.

Parkinson’s NMS include anxiety, depression, dementia, psychosis, sleep impairment, pain, fatigue, constipation, and sexual dysfunction.

Although NMS are common and most of them treatable, some, such as bowel incontinence or sexual dysfunction, may be under-reported due to embarrassment or lack of awareness that they may be associated with Parkinson’s. Prior research in the U.S. has indicated that phsysicians failed to recognize anxiety, depression and fatigue in more than half of encounters with patients.

To determine the frequency of non-motor symptoms in Parkinson’s patients, researchers used the 30-item NMS questionnaire, which is intended to empower patients and caregivers to report relevant NMS not otherwise discussed in routine clinical visits.

This questionnaire has been independently validated and is recommended by the U.K.’s Department of Health for use in clinical practice.

The study included 85 adult Parkinson’s patients who came to a movement disorder clinic at a tertiary care center in Lahore, Pakistan. The team evaluated NMS’ pattern and analyzed potential differences between men and women.

Results revealed a mean of nearly seven different NMS per patient. Constipation (56%) and nocturia (frequent urination at night, 49%) were the most common NMS, while 35% of patients reported urinary urgency.

As for neuropsychiatric complications, 47% of patients reported low mood and sadness, while 36% reported anxiety/panic, and 45% short-term memory impairment.

Light-headedness and dizziness were reported by 40%, sexual dysfuntion by 30%, difficulty falling asleep by 29%, pain unrelated to the musculoskeletal system by 30%, and loss or change in the ability to taste or smell by 29%. All other NMS, including daytime sleepiness, were under 25% in frequency.

Regarding sex differences, feeling sad or blue, light-headededness and dizziness, unexplained pain, unpleasant sensations in the legs while at rest, difficulty in swallowing, and faecal incontinence were the most frequently reported NMS in women; men reported constipation, nocturia, and problems with memory more often.

Male patients reported sexual dysfunction more frequently than women, which the authors attribute to women in Pakistan being uncomfortable with discussing intimate issues.

Among the study’s limitations, the scientists mentioned the low number of women (15), which they hypothesize may be due to men seeking medical care more often.

“In this study we have shown the high frequency of NMS in patients with [Parkinson’s] in Pakistan … Certain NMS are more common in women as compared with men,” researchers wrote, adding that the findings warrant large-scale study to assess the sex-specific incidence of NMS in Parkinson’s patients.

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Brain Training Decreases Severity of Parkinson’s Freezing of Gait, Study Reports

brain training

Brain training reduces the severity and duration of freezing of gait and improves cognition and daytime sleepiness in Parkinson’s patients, a study shows.

The study, “Cognitive training for freezing of gait in Parkinson’s disease: a randomized controlled trial,” appeared in the journal npj Parkinson’s Disease.

Freezing of gait is a symptom of Parkinson’s disease and occurs when patients temporarily feel as if their feet are glued to the floor and hesitate before stepping forward. This often leads to falls and lower quality of life. Studies have shown a connection between freezing of gait and impaired attention and cognitive control.

Researchers in Australia conducted a double-blind trial with Parkinson’s patients who self-reported freezing of gait and had no signs of dementia. Patients were randomly assigned to either cognitive training intervention (20 patients) or an “active control” (18 patients).

Cognitive training consisted of exercises where participants were asked to get up from a chair and walk to a spot marked with a box 5 meters away. Conditions in which patients completed different tasks involving the box were evaluated. Two trials of each condition were completed, one with a left turn and one to the right.

The conditions included: one in which participants walked to the box, turned 180 degrees, and returned to their chair; one where they completed a 540-degree turn in the box before returning to the chair; one in which they shuffled around the box, keeping their inside foot to the outside of the box; and a dual task, where they did the same exercise as the first 180-degree condition, but also completed a cognitive task as they walked, either naming aloud the months backwards or multiples of nine or seven.

Study interventions were conducted twice weekly for seven weeks. Each session took two hours.

The initial 30-45 minutes were common to both groups and included education about a number of topics related to Parkinson’s. Patients undergoing cognitive training then conducted computer tasks targeting processes such as attention, working memory, and brain processing speed. Patients in the active control group completed nonspecific computer tasks.

Investigators primarily evaluated the percentage of time spent frozen during cognitive training, which was analyzed while subjects were both on and off dopaminergic medications. Researchers also assessed several other measures, including mood, well-being, anxiety and depression, sleep quality, and quality of life.

For patients on dopaminergic medication, results showed that those on cognitive training had a significant decrease in the severity of their freezing of gait compared with patients in the active control group. Cognitive training also led to improvements in processing speed and reduced daytime sleepiness.

In contrast, no differences were found when comparing patients not taking regular dopaminergic treatment.

“These results add to the growing body of evidence showing that [cognitive training] is a useful therapeutic technique worthy of continued exploration in [Parkinson’s],” the researchers wrote in the study.

“We believe there is reason to be hopeful for the use of these trials in the future,” Simon Lewis, MD, the study’s senior author and a professor of cognitive neuroscience at the University of Sydney’s Brain and Mind Centre, said in a press release.

He also emphasized the positive feedback from participants and family members, and added that “the results of this pilot study highlight positive trends, and the importance of nonpharmacological trials involving cognitive training has become increasingly clear.”

The researchers also noted the importance of their finding that improvements only occur in patients on dopaminergic medication, “the normal day-day state for patients with Parkinson’s,” said Courtney Walton, PhD, the study’s lead author, who is now at the University of Queensland.

“While more research is needed to better understand and establish these findings, it’s likely that participants in the off- dopaminergic state were too impaired to benefit from any of the potential changes initiated through cognitive training,” Walton said.

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