Tag: Parkinson's Disease

Categories : Medical Research & Technology Neurodegenerative DiseasesTags :

Soft Robotic Garments Help Parkinson’s Patients to Walk More Freely

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Freezing is one of the most common and debilitating symptoms of Parkinson’s disease, when they suddenly lose the ability to move their feet, often mid-stride, resulting in a series of staccato stutter steps that get shorter until the person stops altogether. These episodes are one of the biggest contributors to falls among people living with Parkinson’s disease. 

Today, freezing is treated with a range of pharmacological, surgical or behavioural therapies, none of which are particularly effective. What if there was a way to stop freezing altogether?

In a Nature Medicine report, researchers used a soft, wearable robot to help a person living with Parkinson’s walk without freezing. The robotic garment, worn around the hips and thighs, gives a gentle push to the hips as the leg swings, helping the patient achieve a longer stride. The device completely eliminated the participant’s freezing while walking indoors, allowing them to walk faster and further. 

The soft robotic apparel was developed by researchers from the Harvard John A. Paulson School of Engineering and Applied Sciences (SEAS) and the Boston University Sargent College of Health & Rehabilitation Sciences.

“We found that just a small amount of mechanical assistance from our soft robotic apparel delivered instantaneous effects and consistently improved walking across a range of conditions for the individual in our study,” said Conor Walsh, professor at SEAS and co-corresponding author of the study. 

For over a decade, Walsh’s Biodesign Lab at SEAS has been developing assistive and rehabilitative robotic technologies to improve mobility for individuals’ post-stroke and those living with ALS or other diseases that impact mobility. Some of that technology, specifically an exosuit for post-stroke gait retraining, received support to develop and commercialise the technology.

“Leveraging soft wearable robots to prevent freezing of gait in patients with Parkinson’s required a collaboration between engineers, rehabilitation scientists, physical therapists, biomechanists and apparel designers,” said Walsh, whose team collaborated closely with that of Terry Ellis,  Professor and Physical Therapy Department Chair and Director of the Center for Neurorehabilitation at Boston University.

The team spent six months working with a 73-year-old man with Parkinson’s disease, who, despite using both surgical and pharmacologic treatments, endured substantial and incapacitating freezing episodes more than 10 times a day, causing him to fall frequently. These episodes prevented him from walking around his community and forced him to rely on a scooter to get around outside.

In previous research, Walsh and his team leveraged human-in-the-loop optimization to demonstrate that a soft, wearable device could be used to augment hip flexion and assist in swinging the leg forward to provide an efficient approach to reduce energy expenditure during walking in healthy individuals.

Here, the researchers used the same approach but to address freezing. The wearable device uses cable-driven actuators and sensors worn around the waist and thighs. Using motion data collected by the sensors, algorithms estimate the phase of the gait and generate assistive forces in tandem with muscle movement.

The effect was instantaneous. Without any special training, the patient was able to walk without any freezing indoors and with only occasional episodes outdoors. He was also able to walk and talk without freezing, a rarity without the device.

“Our team was really excited to see the impact of the technology on the participant’s walking,” said Jinsoo Kim, former PhD student at SEAS and co-lead author on the study.

During the study visits, the participant told researchers: “The suit helps me take longer steps and when it is not active, I notice I drag my feet much more. It has really helped me, and I feel it is a positive step forward. It could help me to walk longer and maintain the quality of my life.”

“Our study participants who volunteer their time are real partners,” said Walsh. “Because mobility is difficult, it was a real challenge for this individual to even come into the lab, but we benefited so much from his perspective and feedback.”

The device could also be used to better understand the mechanisms of gait freezing, which is poorly understood.

“Because we don’t really understand freezing, we don’t really know why this approach works so well,” said Ellis. “But this work suggests the potential benefits of a ‘bottom-up’ rather than ‘top-down’ solution to treating gait freezing. We see that restoring almost-normal biomechanics alters the peripheral dynamics of gait and may influence the central processing of gait control.”

Source: Harvard John A. Paulson School of Engineering and Applied Sciences

Categories : Neurodegenerative Diseases New Compounds and TreatmentsTags :

Nanoparticles from Coffee Grounds could Stall Neurodegenerative Disease Development

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Researchers may potentially have found a preventive solution for neurodegenerative disorders in the most unlikely of sources: used coffee grounds. The researchers found caffeic-acid based Carbon Quantum Dots (CACQDs) have the potential to protect brain cells from the damage caused by several neurodegenerative diseases – if the condition is triggered by factors such as obesity, age and exposure to pesticides and other toxic environmental chemicals.

Carbon Quantum Dots are essentially simple nanoparticles made of carbon that have found a growing number of applications, including bioimaging thanks to its fluorescent properties and as photochemical catalysts. Their active surfaces can be doped with different elements for desired effects, are biocompatible and can be produced simply from a range of organic substances such as lemon juice and used tea leaves.

The University of Texas at El Paso team behind the study was led by Jyotish Kumar, a doctoral student in the Department of Chemistry and Biochemistry, and overseen by Mahesh Narayan, PhD, a professor and Fellow of the Royal Society of Chemistry in the same department. Their work is described in the journal Environmental Research.

“Caffeic-acid based Carbon Quantum Dots have the potential to be transformative in the treatment of neurodegenerative disorders,” Kumar said.

“This is because none of the current treatments resolve the diseases; they only help manage the symptoms. Our aim is to find a cure by addressing the atomic and molecular underpinnings that drive these conditions.”

Neurodegenerative diseases, when they are in their early stages and are caused by lifestyle or environmental factors, share several traits.

These include elevated levels of free radicals in the brain, and the aggregation of fragments of amyloid-forming proteins that can lead to plaques or fibrils in the brain.

Kumar and his colleagues found that CACQDs were neuroprotective across test tube experiments, cell lines and other models of Parkinson’s disease when the disorder was caused by a pesticide called paraquat.

The CACQDs, the team observed, were able to remove free radicals or prevent them from causing damage and inhibited the aggregation of amyloid protein fragments without causing any significant side effects.

The team hypothesises that in humans, in the very early stage of a condition such as Alzheimer’s or Parkinson’s, a treatment based on CACQDs can be effective in preventing full-on disease.

“It is critical to address these disorders before they reach the clinical stage,” Narayan said.

“At that point, it is likely too late. Any current treatments that can address advanced symptoms of neurodegenerative disease are simply beyond the means of most people. Our aim is to come up with a solution that can prevent most cases of these conditions at a cost that is manageable for as many patients as possible.”

Caffeic acid belongs to a family of compounds called polyphenols, which are plant-based compounds known for their antioxidant, or free radical-scavenging properties. Caffeic acid is unique because it can penetrate the blood-brain barrier and is thus able to exert its effects upon the cells inside the brain, Narayan said.

In the simple one-step ‘green chemistry’ method, the team ‘cooked’ caffeic acid at 230°C for two hours to reorient the caffeic acid’s carbon structure and form CACQDs. The CACQDs were then extracted according to a molecular weight cutoff of 1kDa.

The sheer abundance of coffee grounds is what makes the process both economical and sustainable, Narayan said.

Source: University of Texas at El Paso

Categories : Environmental Effects Neurodegenerative DiseasesTags :

Nanoplastics Promote Conditions for the Development of Parkinson’s

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Tiny fragments of plastic known as nanoplastics interact with a particular protein that is naturally found in the brain, creating changes linked to Parkinson’s disease and some types of dementia, according to a Duke University-led study.

In Science Advances, the researchers report that the findings create a foundation for a new area of investigation, fuelled by the timely impact of environmental factors on human biology.

“Parkinson’s disease has been called the fastest growing neurological disorder in the world,” said principal investigator, Andrew West, PhD, professor at Duke University School of Medicine.

“Numerous lines of data suggest environmental factors might play a prominent role in Parkinson’s disease, but such factors have for the most part not been identified.”

Improperly disposed plastics have been shown to break into very small pieces and accumulate in water and food supplies, and were found in the blood of most adults in a recent study.

“Our study suggests that the emergence of micro and nanoplastics in the environment might represent a new toxin challenge with respect to Parkinson’s disease risk and progression,” West said.

“This is especially concerning given the predicted increase in concentrations of these contaminants in our water and food supplies.”

West and colleagues in Duke’s Nicholas School of the Environment and the Department of Chemistry at Trinity College of Arts and Sciences found that nanoparticles of the plastic polystyrene — typically found in single use items such as disposable drinking cups and cutlery — attract the accumulation of the protein known as alpha-synuclein.

West said the study’s most surprising findings are the tight bonds formed between the plastic and the protein within the area of the neuron where these accumulations are congregating, the lysosome.

Researchers said the plastic-protein accumulations happened across three different models performed in the study – in test tubes, cultured neurons, and mouse models of Parkinson’s disease.

West said that questions remain about how such interactions might be happening within humans and whether the type of plastic might play a role.

“While microplastic and nanoplastic contaminants are being closely evaluated for their potential impact in cancer and autoimmune diseases, the striking nature of the interactions we could observe in our models suggest a need for evaluating increasing nanoplastic contaminants on Parkinson’s disease and dementia risk and progression,” West said.

“The technology needed to monitor nanoplastics is still at the earliest possible stages and not ready yet to answer all the questions we have,” he said.

Source: Duke University Medical Center

Categories : Neurodegenerative DiseasesTags :

Finding the Right Treatment for Controlling Parkinson’s Symptoms

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Finding the right medication regimen to treat Parkinson’s disease (PD) is a complex healthcare challenge. Wearable health trackers provide detailed information on patients’ symptoms, but this complex data is difficult to turn into useful treatment insights. Now, new research in the INFORMS journal Management Science shows that combining wearable health tracker data with state-of-the-art algorithms results in promising treatment strategies that could improve PD patients’ outcomes.

“Our model identified a Parkinson’s disease medication strategy: Frequent dosing of a slow-release medication formulation that would benefit almost all patients,” says Matt Baucum of Florida State University, one of the study authors.

“In fact, our model uses wearable sensors to predict that patients would spend almost twice as long each day (82% longer) with well-managed symptoms under our recommended medication strategy, compared with their existing medication regimens.”

The paper suggests the resulting models can offer novel clinical insights and medication strategies that can potentially democratise access to improved care.

“Our research suggests that combining rich data from wearable health trackers with the pattern-discovery capabilities of machine learning can uncover treatment strategies that otherwise might have gone underutilized,” says Anahita Khojandi, study co-author from the University of Tennessee, Knoxville.

“The algorithms we developed can even be used to predict patients who might benefit from more advanced PD therapies, which really highlights their ability to extract the maximum value from wearable data.”

Baucum and Khojandi, alongside fellow authors Dr Rama Vasudevan of Oak Ridge National Laboratory and Dr Ritesh Ramdhani a neurologist at Hofstra/ Northwell, emphasise that this work is ground-breaking for PD patients who may experience improved symptom control through continuous sensor monitoring and a novel AI approach.

Source: Institute for Operations Research and the Management Sciences

Categories : Neurodegenerative DiseasesTags :

Non-invasive Transcranial Stimulation Improves Walking in Parkinson’s Disease

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Altered gait is common in patients with Parkinson’s disease (PD), and the usefulness of treatments is limited. Researchers in Japan have developed a novel transcranial stimulation method using external electrodes, the team demonstrated significant gait improvements in PD patients. The results, which also showed improvements for other neurological disorders, are published in the Journal of Neurology, Neurosurgery & Psychiatry.

Motor function declines characterises PD, particularly in relation to gait disorders, manifesting as decreased step length, reduced arm swing, slow movements, rigidity, and postural instability, which are prevalent among patients with PD. While non-pharmacological approaches like transcranial direct current stimulation show promise in improving motor function, recent research focuses on gait-combined closed-loop stimulation, which synchronises brain stimulation with the individual’s gait rhythm.  proposes a novel intervention for gait improvement, thus creating new hope for patients with PD.

“We recently developed a novel neuromodulation approach using gait-combined closed-loop transcranial electrical stimulation (tES) and demonstrated promising gait improvements in patients who are post-stroke. Here, we tested the efficacy of this intervention in patients with Parkinsonian gait disturbances,” explains lead author Ippei Nojima from Shinshu University and Nagoya City University, Japan.

To this end, the clinical researchers from Japan recruited 23 patients with PD or Parkinson’s syndrome. All study participants were randomly assigned to receive either the active treatment or sham treatment.

During the course of the trial, a low-current electrode (up to 2mA) was externally affixed to the occipital region of the head. A reference electrode was then placed in the neck region to establish a stable electrical reference point and to complete the electrical circuit. The treatment included performing tES on the cerebellum in a non-invasive manner. The brain side showing severe impact was specifically targeted during the electrotherapy.

“Gait disturbance lowers activities of daily living in patients with PD and related disorders. However, the effectiveness of pharmacological, surgical, and rehabilitative treatments is limited. Our novel intervention might be able to improve physical function for not just patients with PD but also for those with other disabilities,” comments senior author Yoshino Ueki from the Department of Rehabilitation Medicine at Nagoya City University.

The cerebellum plays a key role in gate control, so electrical stimulation of this region is likely to exert therapeutic benefits. The therapy showed encouraging results after just ten repetitions. The treatment group showed a significant improvement in gait parameters including speed, gait symmetry, and stride length.

Professor Nojima said, “These findings showed that gait-combined closed-loop tES over the cerebellum improved Parkinsonian gait disturbances, possibly through the modulation of brain networks generating gait rhythms.”

Interestingly, no patient dropped out during the study. Moreover, patients from both the groups (treatment and sham) showed good and comparable compliance. Side effects such as skin irritation, vertigo, or odd sensations/perceptions were also not observed in any of the volunteering patients. This study has special significance, considering the fact that Japan is witnessing a sharp rise in its elderly population.

Source: Shinshu University

Categories : Exercise NeurologyTags :

Dopamine’s Role in Exercise Feeling ‘Hard’ or ‘Easy’

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Dopamine, long associated with pleasure, motivation and reward-seeking, also appears to play an important role in why exercise and other physical efforts feel ‘easy’ to some people and exhausting to others. These are the findings of of a study of people with Parkinson’s disease, which is published in NPG Parkinson’s Disease. Parkinson’s disease is marked by a loss of dopamine-producing cells in the brain over time.

According to the researchers, the findings might eventually lead to more effective ways to help people establish and stick with exercise regimens, new treatments for fatigue associated with depression and many other conditions, and a better understanding of Parkinson’s disease.

“Researchers have long been trying to understand why some people find physical effort easier than others,” says study leader Vikram Chib, Ph.D., associate professor in the Department of Biomedical Engineering at the Johns Hopkins University School of Medicine and research scientist at the Kennedy Krieger Institute. “This study’s results suggest that the amount of dopamine availability in the brain is a key factor.”

Chib explains that after a bout of physical activity, people’s perception and self-reports of the effort they expended varies, and also guides their decisions about undertaking future exertions. Previous studies have shown that people with increased dopamine are more willing to exert physical effort for rewards, but the current study focuses on dopamine’s role in people’s self-assessment of effort needed for a physical task, without the promise of a reward.

For the study, Chib and his colleagues from Johns Hopkins Medicine and the Kennedy Krieger Institute recruited 19 adults diagnosed with Parkinson’s disease, a condition in which neurons in the brain that produce dopamine gradually die off, causing unintended and uncontrollable movements such as tremors, fatigue, stiffness and trouble with balance or coordination.

In Chib’s lab, 10 male volunteers and nine female volunteers with an average age of 67 were asked to perform the same physical task, that of squeezing a hand grip equipped with a sensor, on two different days within four weeks of each other. On one of the days, the patients were asked to take their standard, daily synthetic dopamine medication as they normally would. On the other, they were asked not to take their medication for at least 12 hours prior to performing the squeeze test.

On both days, the patients were initially taught to squeeze a grip sensor at various levels of defined effort, and then were asked to squeeze and report how many units of effort they put forth.

When the participants had taken their regular synthetic dopamine medication, their self-assessments of units of effort expended were more accurate than when they hadn’t taken the drug. They also had less variability in their efforts, showing accurate squeezes when the researchers cued them to squeeze at different levels of effort.

In contrast, when the patients hadn’t taken the medication, they consistently over-reported their efforts, meaning they perceived the task to be physically harder, and had significantly more variability among grips after being cued.

In another experiment, the patients were given a choice between a sure option of squeezing with a relatively low amount of effort on the grip sensor or flipping a coin and taking a chance on having to perform either no effort or a very high level of effort. When these volunteers had taken their medication, they were more willing to take a chance on having to perform a higher amount of effort than when they didn’t take their medication.

A third experiment offered participants the choice between getting a small amount of guaranteed money or, getting either nothing or a higher amount of money on a coin flip. Results showed no difference in the subjects on days when they took their medication and when they did not. This result, researchers say, suggests that dopamine’s influence on risk-taking preferences is specific to physical effort-based decision-making.

Together, Chib says, these findings suggest that dopamine level is a critical factor in helping people accurately assess how much effort a physical task requires, which can significantly affect how much effort they’re willing to put forth for future tasks. For example, if someone perceives that a physical task will take an extraordinary amount of effort, they may be less motivated to do it.

Understanding more about the chemistry and biology of motivation could advance ways to motivate exercise and physical therapy regimens, Chib says. In addition, inefficient dopamine signalling could help explain the pervasive fatigue present in conditions such as depression and long COVID, and during cancer treatments. Currently, he and his colleagues are studying dopamine’s role in clinical fatigue.

Source: John Hopkins Medicine

Categories : Lab Tests and Imaging Neurodegenerative DiseasesTags :

A Stool Sample Could Detect Some Parkinson’s Cases Early

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One early indicator of Parkinson’s disease (PD) is isolated REM-sleep behaviour disorder. Researchers have shown that a greater concentration of α-synuclein aggregates can be detected in the stool samples of patients. In the scientific journal npj Parkinson’s Disease, they now present a method for detecting these aggregates.

There are two forms of PD. In 70% of cases, it originates in the central nervous system. However, in around 30% of cases it originates in the nervous system of the intestine (“enteric nervous system”). The latter form is referred to as “body-first Parkinson’s disease” (for short: body-first PD) and the characteristic deposits of aggregates of the body’s own α-synuclein protein are formed in the neurons in the intestine.

A preliminary form of body-first PD is the so-called isolated REM-sleep behaviour disorder (for short: iBRD). It causes in part complex movements during REM-sleep insofar as the patient experiences vivid and disturbing dreams. These movements can endanger the sufferer themselves or others.

A research team headed by Professor Erdem Gültekin Tamgüney from the Institute of Physical Biology at HHU now reports that it is possible to detect an elevated level of α-synuclein aggregates in the stool samples of patients. To achieve this, the team used a new surface-based fluorescence intensity distribution analysis (sFIDA) to detect and quantify individual particles of α-synuclein aggregates.

Professor Tamgüney: “We are the first to prove the presence of α-synuclein aggregates in stool samples. Our results show a significantly higher level of α-synuclein aggregates in iRBD patients compared with healthy individuals or patients with Parkinson’s. These findings could lead to a non-invasive diagnostic tool for prodromal synucleinopathies — including Parkinson’s — which could in turn enable therapies to be initiated at an early stage before symptoms occur.” However, more research is required before the process can find its way into clinical practice, for example investigation into why the level is lower in Parkinson’s patients.

The study was conducted in a collaboration to establish a biobank with stool samples from patients and control subjects, and to develop the test procedure and conduct the tests on the samples, and to eventually commercialise the technique.

Background

In body-first PD, the deposits of fibrils of the body’s own α-synuclein protein, which are characteristic of Parkinson’s, are first formed in the neurons of the enteric nervous system, which serves the gastrointestinal tract. The aggregates then spread to the central nervous system in a way similar to prions, i.e. an existing aggregate combines individual α-synuclein proteins in its vicinity into further aggregates in a nucleation process; these aggregates then spread further through the body.

The influence of what happens in the gastrointestinal tract on the brain is referred to as the “gut-brain axis.” The gastrointestinal tract is exposed to the environment and it is possible that harmful substances such as chemicals, bacteria or viruses ingested directly with food or via interaction with the microbiome of the gastrointestinal tract may trigger the pathological formation of α-synuclein aggregates.

Source: Heinrich-Heine University Duesseldorf

Categories : Injury & TraumaTags :

Head Injury Doubles Long-term Mortality Risk

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Adults who suffered any head injury during a 30-year study period had two times the rate of mortality than those who did not have any head injury, and mortality rates among those with moderate or severe head injuries were nearly three times higher, according to new research published in JAMA Neurology.

Head injury can be attributed to a number of causes, from motor vehicle crashes, unintentional falls, or sports injuries. Furthermore, head injury has been linked with a number of long-term health conditions, including disability, late-onset epilepsy, dementia, and stroke.

Previous studies have shown increased short-term mortality among hospitalised patients with head injuries. This longitudinal study evaluated 30 years of data from over 13 000 community-dwelling participants (ie not hospitalised or in nursing homes) to determine if head injury has an impact on mortality rates in adults over the long term. Of these, 18.4% reported one or more head injuries during the study period, and of those who suffered a head injury, 12.4% were recorded as moderate or severe. The median period of time between a head injury and death was 4.7 years.

Death from all causes was recorded in 64.6% of those individuals who suffered a head injury, and in 54.6% of those without any head injury. Accounting for participant characteristics, investigators found that the mortality rate from all-causes among participants with a head injury was 2.21 times the mortality rate among those with no head injury. Further, the mortality rate among those with more severe head injuries was 2.87 times the mortality rate among those with no head injury.

“Our data reveals that head injury is associated with increased mortality rates even long-term. This is particularly the case for individuals with multiple or severe head injuries,” explained the study’s lead author, Holly Elser, MD, PhD, MPH a Neurology resident at Penn. “This highlights the importance of safety measures, like wearing helmets and seatbelts, to prevent head injuries.”

Investigators also evaluated the data for specific causes of death among all participants. Overall, the most common causes of death were cancers, cardiovascular disease, and neurologic disorders (which include dementia, epilepsy, and stroke). Among individuals with head injuries, deaths caused by neurologic disorders and unintentional injury or trauma (like falls) occurred more frequently.

When investigators evaluated specific neurologic causes of death among participants with head injury, they found that nearly two-thirds of neurologic causes of death were attributed to neurodegenerative diseases, like Alzheimer’s and Parkinson’s disease. These diseases composed a greater proportion of overall deaths among individuals with head injury (14.2%) versus those without (6.6%). Further research into this association is recommended.

Source: University of Pennsylvania School of Medicine

Categories : Neurodegenerative DiseasesTags : 1 Comment

Serious Infections Increase Alzheimer’s and Parkinson’s Risk

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Old man
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Infections needing hospitalisal treatment in early- and mid-life are associated with an increased subsequent risk of Alzheimer’s and Parkinson’s diseases, according to a population-based, case control study by published in PLOS Medicine. No such increase was seen for amyotrophic lateral sclerosis (ALS), however.

The study used Swedish data on individuals diagnosed with Alzheimer’s disease, Parkinson’s disease or ALS, from 1970–2016, as well as five matched controls per case. The analysis included more than 290 000 Alzheimer’s disease cases, 100 000 Parkinson’s disease cases and 10 000 ALS cases.

The results show that a hospital-treated infection five or more years before diagnosis was associated with a 16% increased risk of Alzheimer’s disease and a 4% higher risk of Parkinson’s disease. The associations only applied to individuals diagnosed before the age of 60, whereas no association was found for those diagnosed later in life.

Individuals with multiple hospital treatments for infections before age 40 was associated with the highest risk of disease, with more than doubled risk of Alzheimer’s disease and more than 40% increase in the risk of Parkinson’s disease.

No association was observed for ALS, regardless of age at diagnosis. Due to the observational nature of the study, no causal link could be established.

“These findings suggest that infectious events may be a trigger or amplifier of a pre-existing disease process, leading to clinical onset of neurodegenerative disease at a relatively early age,” said Jiangwei Sun, the study’s first author and postdoctoral researcher at Karolinska Institutet.

Source: Karolinska Institutet

Categories : Cardiovascular Disease Neurodegenerative DiseasesTags :

Heart Attack Survivors at Lower Risk of Parkinson’s

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Credit: American Heart Association

Heart attack survivors may be slightly less likely to develop Parkinson’s disease later in life, according to new research published in the Journal of the American Heart Association.

Parkinson’s disease (PD) is a common neurodegenerative disorder. While a number of non-motor manifestations arise, the typical clinical features involve a movement disorder consisting of bradykinesia, resting tremor, and rigidity, with postural instability occurring at a later stage. The cause of PD is not known, but a number of genetic risk factors have now been characterised, as well as several genes which cause rare familial forms of PD. Secondary parkinsonism, which has symptoms similar to Parkinson’s disease, may be caused by stroke, psychiatric or cardiovascular medications, or other illness.

“We have previously found that following a heart attack, the risk of neurovascular complications such as ischaemic stroke or vascular dementia is markedly increased, so the finding of a lower risk of Parkinson’s disease was somewhat surprising,” said lead study author Jens Sundbøll, MD, PhD. “These findings indicate that the risk of Parkinson’s disease is at least not increased following a heart attack and should not be a worry for patients or a preventive focus for clinicians at follow-up.

“It is not known whether this inverse relationship with risk of Parkinson’s disease extends to people who have had a heart attack. Therefore, we examined the long-term risk of Parkinson’s disease and secondary parkinsonism among heart attack survivors,” Dr Sundbøll said.

Drawing on Danish National Health Service data, the researchers compared the risk of PD and secondary parkinsonism among roughly 182 000 patients who had a first-time heart attack between 1995 and 2016 (average age 71 years old; 62% male) and more than 909 000 matched controls. 

Over a maximum continual follow-up of 21 years, after adjusting for a wide range of potential confounding factors, the analysis found that, when compared to the control group:

  • there was a 20% lower risk of PD among people who had a heart attack; and
  • a 28% lower risk of secondary parkinsonism among those who had a heart attack.

“For physicians treating patients following a heart attack, these results indicate that cardiac rehabilitation should be focused on preventing ischaemic stroke, vascular dementia and other cardiovascular diseases such as a new heart attack and heart failure, since the risk of Parkinson’s appears to be decreased in these patients, in comparison to the general population,” Dr Sundbøll said.

Certain risk factors are common to both heart attack and PD, with higher risk found among elderly men and lower risk among people who drink more coffee and are more physically active. Interestingly, however, some classic heart attack risk factors – such as smoking, high cholesterol, hypertension and Type 2 diabetes – are associated with a reduced risk of PD.

In general, more heart attack patients smoke and have high cholesterol, either of which may explain the slightly reduced risk of PD among heart attack survivors.

“There are very few diseases in this world in which smoking decreases risk: Parkinson’s disease is one, and ulcerative colitis is another. Smoking increases the risk of the most common diseases including cancer, cardiovascular disease and pulmonary disease and is definitely not good for your health,” Dr Sundbøll noted.

One limitation of the study is that there was not enough information about smoking and high cholesterol levels among the participants, which may have influenced the findings. The study participants were almost entirely white, limiting the generalisability to other ethnic groups.

Source: American Heart Association