Subtle Alterations in Postural Behavior May Help Diagnose Parkinson’s Earlier

Postural behavior

People with Parkinson’s have postural adjustments even at early stages of the disease when clinical symptoms of postural instability are not evident and despite the use of antiparkinsonian medications, a recent study shows.

Researchers believe these findings suggest that postural behavior may be used as an early indicator to diagnose the disease.

The study, “Postural Behavior in Medicated Parkinson Disease Patients: A Preliminary Study Searching for Indicators to Track Progress,” was published in the Journal of Central Nervous System Disease.

Parkinson’s disease usually is diagnosed based on the presence of classic  motor symptoms. But other signs of the disease are present sometimes years before motor symptoms are evident, though still insufficient to make a definite diagnosis.

Identifying patients in this earlier phase would ensure they receive treatment early, before their disease progresses to more advanced stages and significantly affects daily activities.

Generally, Parkinson’s patients with early disease are classified as not having postural instability. But modern technologies are more sensitive to subtle impairments in balance, and potentially may identify changes in postural behavior that take place even in earlier stages of disease.

To clarify the presence of postural changes in early Parkinson’s disease, and whether these changes can be used to diagnose the disease before motor symptoms are evident, researchers at the Western Michigan University and collaborators at the Federal University of Piauí, Brazil, investigated two groups of Parkinson’s patients, and compared them to a group of healthy controls.

Participants included nine patients with early disease — defined as a Hoehn and Yahr Stage rating scale up to 2, which means their balance was not yet affected — and nine patients with mid- to advanced disease (a Hoehn and Yahr Stage of 2.5 or higher, whose balance was already compromised).

These patients were all taking antiparkisonian medication, allowing researchers to account for the effects of medication on balance, which the team believes is a clear limitation of prior studies that lacked a standardization on this parameter. Controls included nine healthy subjects matched by age, who had no history of sensory, muscular, or neurological disorder.

Participants were asked to perform two simple postural tasks: stand quietly on a force platform with arms crossed, with eyes open or closed. Each task took 120 seconds. During that time, the platform collected information regarding participants’ center of pressure, including body sway trajectory (how the center of pressure moved), sway amplitude (how far in each direction it went), sway velocity (how fast it moved), and sway jerkiness (how shakier body sway was).

The team found that most measures were similar across patients and controls when they did the test with their eyes open. But Parkinson’s patients already showed greater sway velocity and jerkiness compared to controls in this task. Late-stage patients also had more overall sway movement and greater sway amplitude.

When the task was done with eyes closed, patients also had higher sway jerkiness — though sway was only laterally shakier — compared to controls, but not higher sway velocity. Those with advanced disease also had greater sway amplitude.

No significant differences were seen between groups of Parkinson’s patients in either task. Also, while controls and early-stage patients swayed more, faster, and shakier when they stood still with their eyes closed, no differences were seen in advanced patients with eyes open and closed.

The findings show that Parkinson’s patients have alterations in postural behavior starting in early stages of disease, and despite the use of dopaminergic medication. “This finding indicates that balance control is affected even before clinical signs surface,” the researchers wrote.

“Therefore, postural markers used in this study are [of] great importance to improve early diagnosis of postural instability in PD [Parkinson’s disease], record progress of balance control, and assess fall risk. They should also be implemented in clinical trials of pharmacotherapy and balance training protocols specific to populations diagnosed with PD,” they concluded.

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Study to Test MRI Technique for Possible Early Parkinson’s Diagnosis

MRI and diagnosis

A clinical study will test the potential of a specific magnetic resonance imaging (MRI) technique to diagnose Parkinson’s disease at early stages.

The 18-month project, supported by a grant from the Center for Clinical and Translational Science in the U.K., will take place at the University of Kentucky’s College of Medicine under the leadership of George Quintero, PhD, and Zain Guduru, MD. It is expected to open this year.

Parkinson’s disease is characterized by progressive loss of coordination and movement, and includes tremors, stiffness and slowing of movement. Currently, a person is diagnosed when those symptoms appear.

However, the brain undergoes alterations that precede symptom onset. Detecting these changes earlier would allow a quicker start of treatments for these symptoms, and possibly to slow disease progression.

Previous research by the same team showed that apomorphine, an FDA-approved Parkinson’s therapy, activates brain areas commonly affected by the disease. Brain activity was measured using a blood oxygenation level dependent (BOLD) magnetic resonance imaging (MRI), an imaging technique that assesses changes in oxygen in the blood.

Apomorphine stimulates the production of dopamine in the brain, a messenger molecule (called a neurotransmitter) that is produced by dopaminergic neurons. Dopaminergic neurons die in Parkinson’s, leading to the characteristic deterioration of motor and cognitive skills observed during this disease’s course.

In this new study, researchers will assess responses in the brain before and after taking apomorphine in Parkinson’s patients and in people with essential tremor, a similar movement disorder. These changes will be measured using BOLD-MRI.

The idea is to test whether this technique can accurately discriminate between the two different patient populations upon apomorphine treatment. Since essential tremor is not caused by inadequate dopamine production, only Parkinson’s patients, in theory, should show specific brain alterations in response to apomorphine.

Should results be favorable, BOLD-MRI could be a way of identifying Parkinson’s early and distinguishing it from similar disorders.

“If apomorphine causes a different brain response in the two groups of patients, it could be a promising method for earlier detection of Parkinson’s,” Quintero said in a press release. “And this leads to earlier interventions that can benefit patients.”

Test results may also inform how the disease progresses, and whether subgroups of Parkinson’s disease patients respond differently to treatment.

“This is truly a translational project. We often want to make that transition between basic science research to human research,” Quintero said. “CCTS provided the opportunity to continue this research.”

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Michael J. Fox Foundation Funds Search for Parkinson’s Urine Biomarkers

urine biomarkers, Parkinson's

The Michael J. Fox Foundation for Parkinson’s Research (MJFF) is funding work at Tymora Analytical Operations that screens for protein biomarkers in urine to help detect the neurodegenerative disease earlier.

Tymora, a research and development laboratory company affiliated with Purdue University, uses the EVtrap approach, or Extracellular Vesicles Total Recovery and Purification. This approach analyzes urine samples to find disease biomarkers such as proteins and their versions known as phosphoproteins — proteins that have phosphate groups attached.

More than 100 samples provided by MJFF will be analyzed to look for phosphoproteins found in people with Parkinson’s.

“This award will support our analysis work to find new urine biomarkers, which can lead to early Parkinson’s disease diagnoses and treatments,” Anton Iliuk, PhD, Tymora’s chief technology officer, said in a press release written by Chris Adam.

Iliuk noted that the lack of specific tests to identify Parkinson’s often leads to reviews of medical histories and to neurological and physical tests that can be inconclusive. “Our approach,” he said, “uses a simple urine test, often already performed during regular exams.”

Parkinson’s is typically diagnosed at late stages, when patients are already experiencing symptoms. That reduces treatment effectiveness.

“Diagnosing Parkinson’s at an early stage with our method would give doctors a greater opportunity to successfully treat the condition,” Iliuk said.

According to Tymora, the technology enables the identification of more than 1,200 unique proteins from only 0.2mL of urine. It also allows the identification of up to 1,000 unique phosphoproteins from 10mL of urine, as described in a 2018 study. The team at Tymora previously had demonstrated the feasibility of high-throughput identification of phosphoproteins in tiny vesicles — called exosomes — found in plasma, which contain unique cargo if released by diseased cells.

EVtrap, says Tymora, is the optimal technique to develop urine-derived exosome phosphoproteins for more accurate disease profiling and better treatments.

Most of the company’s technology was developed at Purdue by W. Andy Tao, PhD, Tymora’s chief scientific officer. Tao is a professor of biochemistry at Purdue’s College of Agriculture and received the 2017 Outstanding Commercialization Award for Purdue faculty.

The EVtrap technology aligns with the university’s Giant Leaps celebration of its global advancements in health, which is part of Purdue’s 150th anniversary.

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New MRI Technique Can Visualize Brain Molecular Composition, Study Shows

MRI molecular composition

A new magnetic resonance imaging (MRI) technique allows for the visualization of molecular changes in the brain, a study reports.

This technique will allow researchers to further understand how the brain works and how it changes with ageing or during the onset of neurodegenerative diseases like Parkinson’s.

Moreover, in the future, clinicians may use the brain’s “molecular signature” for early diagnoses — allowing patients to get access to treatment at early stages of disease and increasing their likelihood for better outcomes.

The study, “Disentangling molecular alterations from water-content changes in the aging human brain using quantitative MRI,” was published in the journal Nature Communications.

An MRI scan is obtained using magnetic fields and powerful detectors that track water compositions in tissues. However, brain function depends vastly on molecular interactions within the brain that current MRI scans fail to detect.

“When we take a blood test, it shows us the exact number of white blood cells [key cells of the immune system] in our body and whether that number is higher than normal due to illness,” Shir Filo, a PhD student and the study’s first author, said in a press release.

“MRI scans provide images of the brain but don’t show changes in the composition of the human brain, changes that could potentially differentiate normal aging from the beginnings of Alzheimer’s or Parkinson’s,” Filo added.

Now, researchers found a way to “see” the brain composition at the molecular level. The technique, called quantitative MRI, is able to detect changes in the molecular composition of lipid (fat) molecules within the brain.

The research was led by Aviv Mezer and his team at the Hebrew University of Jerusalem (HUJI)’s Edmond and Lily Safra Center for Brain Sciences.

“Instead of images, our quantitative MRI model provides molecular information about the brain tissue we’re studying. This could allow doctors to compare brain scans taken over time from the same patient, and to differentiate between healthy and diseased brain tissue, without resorting to invasive or dangerous procedures, such as brain tissue biopsies,” Mezer said.

Researchers started by testing their new MRI technique in synthetic, or lab-made complex fat mixtures to validate whether the MRI scans were sensitive enough to detect changes at the molecular level.

The results revealed their technique was able to distinguish between different lipids with high sensitivity. Because the brain is rich in lipids — such as phosphatidylcholine, sphingomyelin or phosphatidylcholine-cholesterol — the team used a measurement called macromolecular tissue volume (MTV) that provides quantitative information about these molecules in a sample.

Quantitative MRI scans of human brains revealed that MTV measures changed depending on the brain region analyzed, demonstrating that this technique works like a detailed map of the living brain.

Importantly, using post-mortem (after death) brain samples, the team found that the variability of certain MTV parameters between human brain regions also correlated with specific gene-expression profiles. Gene expression is the process by which information in a gene is synthesized to create a working product, like a protein.

Next, the researchers investigated whether the molecular composition of the brain varied according to age, specifically young versus old. They scanned 23 young adults (mean age 27 years) and 18 older adults (mean age 67 years).

Researchers focused their analysis on the brain’s white and gray matter. White matter is made up of nerve cell projections, known as axons or fibers, that connect distinct parts of gray matter. The length and condition of the fibers influence the way the brain processes information. Gray matter includes neuronal cell bodies as well as synapses, or the junctions between nerve cells that allow them to communicate with each other.

The results showed not only evident changes in the brain’s size, but also tiny and region-specific molecular changes in various brain regions related to aging. Even in the absence of age-related reductions in brain size, molecular changes were detected using the new MRI technique.

Overall, this supports the potential of this new type of MRI method to better understand how our brains age.

“[W]hen we scanned young and old patients’ brains, we saw that different brain areas ages differently. For example, in some white-matter areas, there is a decrease in brain tissue volume, whereas in the gray-matter, tissue volume remains constant. However, we saw major changes in the molecular makeup of the gray matter in younger versus older subjects,” Mezer said.

Researchers hope that, in the future, they can apply this new MRI technique to provide an early diagnosis of diseases like Parkinson’s. That could allow access to treatment that may delay or even halt disease progression.

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SIRT2 Protein May Be Blood Marker of Parkinson’s That Differs from Atypical Parkinsonian Syndromes, Study Says

SIRT2 and blood biomarkers

High levels of a protein called SIRT2 in the blood may serve as a diagnostic biomarker to differentiate between Parkinson’s patients and those with atypical Parkinson syndromes, a study finds.

Levels of this marker also may aid in diagnosing Parkinson’s at early stages.

The study, “Elevated Serum SIRT 2 May Differentiate Parkinson’s Disease From Atypical Parkinsonian Syndromes,” was published in the journal Frontiers in Molecular Science.

Patients with Parkinson’s typically show toxic clumps of the alpha-synuclein protein in the brain, which is thought to play a significant role in the disease’s development and progression.

Previous studies have shown an association between alpha-synuclein and a protein called SIRT2 in the context of Parkinson’s. In particular, SIRT2 seems to promote neurodegeneration by helping the buildup of alpha-synuclein plaques.

Atypical Parkinson syndromes are very similar to Parkinson’s and often have overlapping symptoms, including tremor, muscle stiffness and balance problems. These similarities make it hard to distinguish between the two, particularly early in the disease course.

A significant need for laboratory tests that can help doctors differentiate between these two exists. One strategy often used for diagnostic purposes and that can help differentiate in cases of similar diseases is looking at differences in the level of protein expression.

As SIRT2 is known to play a role in Parkinson’s, researchers studied whether levels of SIRT2 protein expression in the serum (a blood component) of Parkinson’s patients were different from those with atypical Parkinson syndromes and healthy elderly people serving as controls.

Serum SIRT2 protein levels were analyzed in 68 Parkinson’s patients, 34 people with atypical Parkinson syndromes, and 68 elderly controls. SIRT2 expression was correlated with alpha-synuclein levels in Parkinson’s and elderly controls.

Results showed SIRT2 expressed at significantly higher levels in people with Parkinson’s compared to those with atypical Parkinson syndromes or elderly controls. Importantly, SIRT2 levels could differentiate between Parkinson’s and atypical Parkinson syndromes patients with good sensitivity and specificity, as well as between people with atypical Parkinson syndromes and elderly controls.

In people with early stage Parkinson’s, a significant positive link was also seen between SIRT2 levels and a higher score on the Unified Parkinson’s Disease Rating Scale (UPDRS) part III motor score (which measures disease progression), the Hoehn & Yahr stage (which also measures disease activity and progression), and disease duration. In other words, higher SIRT2 levels correlate with disease activity and disease duration.

For the entire group of Parkinson’s patients evaluated, the link between SIRT2 levels and high UPDRS and Hoehn & Yahr scores did not hold.

This early stage finding is important because most Parkinson’s disease (PD) patients “are diagnosed at a late stage when vulnerable dopaminergic neurons in the substantia nigra [a midbrain area important to movement] have already been lost, and it is nearly impossible to detect PD by any screening test before the appearance of motor symptoms,” the researchers wrote.

“The present study is the first to report elevated serum SIRT2 in PD. The study also provided a simple test to distinguish PD from APS [atypical Parkinson syndromes] and may have translational utility for diagnosis,” they concluded.

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

epigenetics, Parkinson's

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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Changes in Gait, Cognition May Be Early Signs of Idiopathic Parkinson’s, Research Suggests

gait and Parkinson's

Changes in gait and cognition precede a diagnosis of idiopathic (without known cause) Parkinson’s disease, and may occur earlier than typical non-motor symptoms, a study has found.

The study, “Prediagnostic markers of idiopathic Parkinson’s disease: Gait, visuospatial ability and executive function,” was published in Gait & Posture.

Motor symptoms in idiopathic Parkinson’s disease (IPD) are identified relatively late in the disease course, reducing the odds of neuroprotective benefit from available treatment options. Identifying individuals during the prodromal (early) period that precedes motor symptoms could be of great use for clinical studies seeking new therapies to prevent or delay disease progression.

A team of French researchers sought to determine the existence of any subtle gait disorders or other signs that precede the diagnosis of IPD, based on data from a long-standing study of human aging across the adult lifespan: the Baltimore Longitudinal Study of Aging (BLSA).

Conducted by the National Institute on Aging (NIA) Intramural Research Program, the BLSA continuously enrolls healthy volunteers age 20 and older who are followed throughout their life independently of the development of age-related diseases.

Ten pre-diagnosed IPD patients (eight men and two women) and 30 healthy control subjects were chosen for this study.

Subjects were assessed for the disease approximately 2.6 years before diagnosis. Clinical examination included gait speed, spatio-temporal gait parameters, balance, upper-limb motor skills, neuropsychological profile, and non-motor symptoms.

In comparison to the control group, IPD patients had shorter step length and reduced gait speed in a usual gait speed testing condition. Despite also having shorter step length when testing maximum gait speed, no differences between the IPD and control samples were found in walking speed.

Moreover, patients had worse mental rotation ability (the ability to rotate mental representations of two-dimensional and three-dimensional objects, which is related to the brain’s capacity for visual representation), and impaired ability to name different examples that could be inserted into a category (for instance, naming all types of flowers one can think of in one minute).

Compared to control subjects, IPD patients had no changes in upper-limb motor function, no depression, no sleep disturbances, no urinary symptoms, and no orthostatic hypotension (when blood pressure suddenly drops when standing up quickly).

Researchers concluded that the observed “changes might serve as markers to improve the early detection of IPD patients, who could then benefit from pharmacological neuroprotection trials and/or prevention trials of lifestyle-related interventions in order to delay, or even prevent, clinical manifestations.”

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Simple Breath Test May Aid in Early Diagnosis of Parkinson’s, Study Reports

breath test

A new device that uses just a breath sample might, in the future, help diagnose early-stage Parkinson’s patients or identify those who may be at risk, according to researchers.  

The innovative technology, developed by researchers at the Israel Institute of Technology, was able to detect alterations in the breath of newly diagnosed Parkinson’s patients, even before they begin medication.

Although the device and collection method still needs to be perfected to reach the sensitivity of other diagnostic approaches such as brain ultrasound scans, researchers believe the tool shows promise.

Findings were reported in the study, “Sensor Array for Detection of Early Stage Parkinson’s Disease before Medication, published in the journal ACS Chemical Neuroscience.

The team had already tested its device in the past, and were able to detect differences in the exhaled breath of people already being treated for Parkinson’s disease and healthy controls.

Now they wanted to see if the device could detect differences in the breath of patients with early-stage Parkinson’s who were not yet on any medications.

The device consists of an array of 40 cross-reactive sensors based on gold nanoparticles or single-walled carbon nanotubes, attached to different chemical ligands. Each of these ligands can bind certain airy or volatile molecules in the breath that change the electrical signals of the sensor.

They tested the device on 29 patients who had recently been diagnosed with idiopathic Parkinson’s disease — with no known cause — and were not yet on medication, and 19 healthy individuals of similar ages, used as controls.

The device’s performance was also compared with other currently used diagnosed tests, namely brain ultrasonography and smell detection.

The sensor was able to distinguish Parkinson’s patients from controls with a sensitivity of 79%, a specificity of 84%, and accuracy of 81%, better than smell detection tests, which have 62% sensitivity, 89% specificity and 73% accuracy, and almost as good as brain ultrasound scans, at 93% sensitivity, 90% specificity, and 92% accuracy.

“[O]ur studies provide additional confirmation of the ability of our sensors array to detect altered breath VOC [volatile organic compounds] composition characteristic of PD [Parkinson’s disease],” the researchers wrote.

Early diagnosis of Parkinson’s can help patients begin neuroprotective therapies sooner, before extensive loss of dopamine-producing nerve cells — those affected in Parkinson’s disease — has occurred in the brain. However, to date, diagnosis is still subject to considerable errors.

So far, studies on early Parkinson’s diagnosis using volatile biomarkers have only been done in patients who are already being treated and medicated. “There is a great need to evaluate untreated patients for establishing a real world screening and diagnostic technology,” the authors said.

Further improvements, as well as more testing in patients, are still necessary for the device to reach the sensitivity of other diagnostic methods like brain ultrasound scans.

“Future development of the sensors array technique has the potential to produce a small, portable system with the advantage of unbiased determination which could be used in initial screening of at-risk subjects without the need for experienced clinical personnel,” the researchers concluded.

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New Brain PET Scanner Shows Promise for Earlier and Less Expensive Diagnosis of Parkinson’s

PET scanner

A new brain scanner, which is 10 times less expensive and much smaller than current models, has the potential to significantly improve the diagnosis of dementia linked to neurodegenerative diseases, such as Parkinson’s disease, Alzheimer’s, and amyotrophic lateral sclerosis (ALS).

The scanner, which uses Positron Emission Tomography (PET) imaging, is being developed by two particle physicists, Jannis Fischer and Max Ahnen, PhDs, at ETH Zurich in Switzerland. Their work was recently recognized by Forbes magazinewhich included the duo in its “30 Under 30 Europe” list for 2018, in the category of Science and Healthcare.

PET scanning is an imaging technique commonly used to diagnose cancer, but it recently has also been used for neurological and cardiovascular diseases.

After a patient is injected intravenously with a tracing substance — called radioisotopes — the PET tracer travels through the blood vessels allowing clinicians to see its distribution over time to determine the health status of the brain.

While PET scanners can help diagnose certain neurological diseases 10 to 20 years before the development of the first symptoms, its practical use is limited because of the scanners’ high cost and large size — a conventional scanner requires 15 square meters of floor space and costs between US$1.5 and $5.5 million.

Ahnen and Fischer’s work, being conducted at ETH Zurich’s Institute for Particle Physics and Astrophysics, follows seminal work by researchers and doctors at the University of Zurich and the University Hospital of Zurich.

The new brain scanner, called Brain PET, will be a fraction of the cost of conventional scanners now found in hospitals and will take up less than 2 square meters.

“It looks a bit like a hair salon chair with an integrated hairdryer hood,” Ahnen said in a university news release. Its  compact size makes it much more mobile and useful for smaller clinical facilities.

Brain PET is also much cheaper to use. PET scanners now are at the top of hospital expenses, and many facilities are unable to afford them. The affordability of the new scanner will make it available for a broader range of patients.

“We will be able to reach much wider sections of the population than in the past,” Fischer said.

A prototype of Brain PET is expected to be completed by September 2018, after the project won ETH’s Pioneer Fellowship, a grant fostering the development of highly innovative products for the benefit of society.

The two physicists are setting up their new company, Positrigo, and hope Brain PET will be on the market in 2021, a goal both “optimistic, but also realistic,” they said.

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Source: Parkinson's News Today