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Taste, Smell Impairments May Help Identify People at Risk for Parkinson’s, Study Suggests

taste and smell impairment

Impaired sense of smell or taste can raise a person’s risk of developing Parkinson’s disease 2.5 times, a study suggests.

The study, “Incidence of Parkinson’s disease in a large patient cohort with idiopathic smell and taste loss,” was published in the Journal of Neurology.

Currently, Parkinson’s disease is diagnosed mainly on the assessment of patients’ motor symptoms and their severity. However, evaluation scales can be subjective and might fail to detect small changes.

Non-motor symptoms have gained increased attention because of their potential to anticipate Parkinson’s-related motor manifestations. Approximately 90% of Parkinson’s patients have altered smell sensitivity during the disease’s initial and moderate stages, thought to be partly because of brain connectivity changes.

To explore the incidence and diagnostic potential of smell and taste disorders in Parkinson’s disease, researchers reviewed the clinical records of 474 people who had been diagnosed with smell and taste loss of unknown cause.

Patients diagnosed and followed over a period of 15 years at the Smell and Taste Clinic in Dresden, Germany, were interviewed by phone using a standardized questionnaire to record their condition and clinical history.

At the time of the first assessment at the clinic, patients had already experienced reduced or lost  odor and taste sensitivity for a mean period of 4.6 years. Onset of olfactory (smell) disturbances was in general noticed at a mean age of 57.9 years; gustatory (taste) disorders, 59.3 years.

Of the 474 participants, 14.3% had a normal sense of smell, 40.5% had reduced, and 45.1% had complete loss of smell. Regarding taste, 90.1% of the participants had normal sensation, 9.5% had reduced, and 0.4% had complete loss of taste.

Collectively, 242 people were diagnosed with a qualitative olfactory or gustatory disorder, of whom 21.1% had parosmia (distortions of the sense of smell), 32.9% had phantosmia (olfactory hallucinations), and 7.6% had parageusia (distortions of the sense of taste).

Participants’ clinical reports revealed that 45 (9.5%) had developed Parkinson’s disease after the initial idiopathic smell and/or taste loss diagnosis.

Six of the Parkinson’s patients had combined olfactory and gustatory disorders at the time of diagnosis, whereas 38 had pure olfactory disorders and one patient had a pure gustatory disorder.

The frequency of taste disorders was similar between those with and without Parkinson’s. In contrast, Parkinson’s patients had a higher prevalence of initial complete loss of smell compared to those without the disease.

The team did not find a significant association between taste or smell loss and the development of the disease. Still, patients who developed Parkinson’s reported a decrease in olfactory and gustatory function more frequently than non-Parkinson’s patients.

Researchers found that “patients with a decrease in olfactory or gustatory function developed Parkinson’s with a significantly higher rate compared to patients with a stable smell or taste function.” Overall, impaired smell or taste sense increased the risk of developing Parkinson’s disease 2.47 times.

“Risk stratification might be considerably improved by correct diagnostic allocation of smell and taste loss, the use of both olfactory and gustatory testing, and subsequent long-term monitoring of these functions,” researchers said.

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Analysis of Tiny Vesicles Released by Red Blood Cells May Help Identify Parkinson’s Patients, Study Shows

extracellular vesicles

A new blood-based analysis that evaluates the levels and content of tiny vesicles released by red blood cells may help diagnose patients with Parkinson’s disease according to disease stage, researchers suggest.

The new method was described in the study, “Portrait of blood-derived extracellular vesicles in patients with Parkinson’s disease,” published in Neurobiology of Disease.

Parkinson’s disease is linked to a broad spectrum of clinical manifestations and several molecular mechanisms.

This represents a challenge for the development and identification of useful biomarkers for diagnosis and disease progression, as well as to track the effectiveness of new treatments.

All human cells produce tiny vesicles containing fatty molecules, proteins, and genetic information, which they release to the surrounding environment. These so-called extracellular vesicles are produced both in healthy and disease conditions, and are used by cells to communicate among themselves.

Given the major role these extracellular vesicles may have, researchers hypothesized that their cargo could hold useful information on the biological state of the body, representing a possible new diagnostic tool.

To this end, Canadian researchers developed a new method of isolating extracellular vesicles from blood samples that would preserve their integrity, while still removing any potential contaminants.

Using flow cytometry, a technique that allows the visualization and sorting of cells and small particles according to their size and shape, the team could identify not only extracellular vesicles but also which cells originated them. After the vesicles were isolated, the team could analyze their content.

Following the assay’s optimization, the team analyzed blood samples collected from 60 Parkinson’s patients and 37 age- and sex-matched healthy volunteers.

They found that Parkinson’s patients had about 1.8 times more extracellular vesicles released by red blood cells than healthy controls. However, upon further analysis, the team found that only five patients were responsible for this significant difference, implying that the number of extracellular vesicles could not be used to differentiate between Parkinson’s patients and healthy controls.

The quantity of extracellular vesicles released by other blood cell types was similar between groups.

When researchers analyzed vesicle numbers in regards to patients’ disease severity status — measured by total scores on the Unified Parkinson Disease Rating Scale (UPDRS) — they found that at least 87% of the variation in the total number of red blood cell-derived vesicles was due to a variation in UPDRS scores.

To validate their results, the team used the same analysis approach in a new set of blood samples collected from 42 Parkinson’s patients. Once more, they found they could use the number of red blood cell-derived extracellular vesicles to distinguish between patients according to their UPDRS scores.

Analysis of the content of the isolated vesicles revealed a total of 818 proteins, eight of which were found in significantly different amounts between controls and patients, allowing researchers to group individuals according to stages of disease (control, mild Parkinson’s, and moderate Parkinson’s).

“Our study shed light on a potential biomarker indicative of disease stage, which is derived from 2 measures: the number of [red blood cells-derived extracellular vesicles] and the expression of 8 different proteins,” the researchers wrote.

Although the analysis and isolation of extracellular vesicles through flow cytometry may not be accessible to all laboratories, “identification of specific proteins that match clinical stages of Parkinson’s” could be performed using simple and less expensive techniques, according to the researchers.

“The ability to develop a biomarker that not only works as a diagnostic tool but a predictor of disease stages/course would represent a major breakthrough in the field, opening up to new therapeutic opportunities,” they concluded.

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15 CSF Proteins Seen as Possible Biomarkers of Early Parkinson’s Fail at That Task, Study Reports

Parkinson's and biomarkers

Proteins in the cerebrospinal fluid that were seen as possible diagnostic biomarkers of Parkinson’s disease cannot serve in this role, because they lack robustness and reproducibility in earlier stages of the disease, a study has found.

The study, “Evaluation of cerebrospinal fluid proteins as potential biomarkers for early stage Parkinson’s disease diagnosis,” was published in PLOS One.

Parkinson’s is a chronic and progressive neurodegenerative disorder, mainly caused by the gradual loss of dopaminergic neurons in the substantia nigra, a region of the brain responsible for movement control. It is typically diagnosed based on the presence of motor symptoms, but these can be difficult to determine as disease-causing in Parkinson’s earlier stages.

Previous studies have suggested that specific proteins in the cerebrospinal fluid (CSF) —  which circulates in the brain and spinal cord — could work as early signals, or biomarkers, of disease to assist in a diagnosis. But CSF proteins have never been fully validated as Parkinson’s biomarkers in a clinical setting.

Researchers in Belgium, Germany, and the U.K. tested the suitability of 15 CSF proteins proposed as potential biomarkers for an early stage Parkinson’s diagnosis.

The panel of proteins explored were beta-amyloid (Aβ40 and Aβ42), alpha-synuclein (α-syn), tau (p-Tau and t-Tau),  neurofilament light chain (NFL), interleukin 6 (IL-6), protein deglycase (DJ-1), S100β (a calcium-binding protein), osteopontin (OPN), high-mobility group box 1 (HMGB1), ubiquitin carboxyl-terminal esterase L1 (UCHL1), Fms-related tyrosine kinase 3 ligand (FLT3LG), matrix metalloproteinase 2 (MMP2) and apolipoprotein A-I (ApoA1).

Researchers began by measuring the levels of these CSF proteins in a group of 80 patients with early stage disease and 80 healthy people serving as controls. Out of the 15 CSF proteins tested, six — α-syn, DJ-1, Aβ42, S100β, p-Tau and t-Tau — were significantly dysregulated among patients.

“Aβ42, t-Tau, p-Tau, α-syn and DJ-1 were decreased in early clinical PD [Parkinson’s disease] patients compared to the controls, whereas S100β levels was increased in early clinical PD patients,” the researchers wrote.

To confirm these candidates, researchers next performed this same test in an independent group of 30 Parkinson’s patients with advanced disease and 30 healthy controls. Here, a type of beta-amyloid, Aβ42, was the only CSF protein whose levels were significantly different — significantly lower — in Parkinson’s patients compared to controls.

“Decreased Aβ42 levels in CSF samples from PD patients had been reported recently, suggesting it may be a reliable candidate. However, in this study … analysis showed that this potential marker was not suitable for diagnostic purposes,” the researchers wrote.

Finally, to assess whether a combination of these markers could distinguish early Parkinson’s patients from healthy individuals, they used a machine learning approach based on an algorithm to identify markers that might improve disease diagnosis. Based on this model, a set of markers comprising α-syn, S100β, and UCHL1 were identified as promising candidates.

“[T]his model aligned with findings published in the literature, where α-syn is characterized as the hallmark protein of PD, closely involved in the progression of neuronal degeneration and subsequent motor impairments, while S100β has been considered a possible marker for the accompanying neurodegeneration,” the researchers wrote. However, “the decision tree could not be confirmed” in the second group of patients and controls.

“[C]urrently proposed protein CSF markers for PD diagnosis, as identified in late stage PD cohorts, lack robustness and reproducibility when applied in the early clinical stages of (…) PD,” they added.

The researchers believe that further efforts, including the EU-BIOMARKAPD project that is exploring alternative approaches to biomarker identification, may support the development of potential protein CSF biomarkers for clinical diagnosis or disease monitoring in early stage Parkinson’s disease.

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The ABCs of Parkinson’s: ‘F’ Is for ‘Fear’

fear

Sherri Journeying Through

Editor’s note: A continuation of the “ABCs of Parkinson’s” series.

“You have Parkinson’s disease.”

“What exactly does that mean?” I asked.

While I waited for a response to my question, my thoughts covered a multitude of fears in a minimal amount of time. I sat and listened to my doctor’s explanation, which began sounding like background noise. I answered no to the question of whether I had any questions, when in fact I had multitudes but didn’t want to hear the answers for fear of what they might be. I was loaded with a sample starter of Mirapex (pramipexole) and something else I can’t remember for lack of paying attention. Then, I said thank you, scheduled the next visit, and left. 

“It’s gonna be OK,” my husband tried reassuring me later at home. But, how did he know what OK looked like and if I was going to like the picture?

I know as well as the next person that fears are normal. They can be both healthy and destructive. I know fear is common among people with Parkinson’s disease. As I began learning more about PD and acquiring information about the disease, I saw that fear was not only a real part of Parkinson’s but something that was rarely ever mentioned, let alone discussed. Were we supposed to be brave on the outside while we were shaking like crazy on the inside?

I had a professor in college who said it’s not that we fear the dark but that we fear the things we cannot see in the dark. I suppose you could then say — as a person with a chronic disease — that we often find it easy to “live in the dark,” as this disease manifests itself with things we can’t see. Things we didn’t know would be coming. We aren’t so much afraid of Parkinson’s disease or having it. It is safer to say that we fear what Parkinson’s could, can, and will do to us. 

My edition of Merriam-Webster defines fear as “a reason for dread … taking the form of terror, horror, panic, alarm, dismay, consternation, and trepidation.” Yep. I’d say those terms fit. 

Fear can be my greatest enemy in this journey with Parkinson’s disease. It can cause anxiety at every level. Honestly, dread, terror, panic, dismay, and consternation have all had their heyday with my mind when it comes to this disease.

At times in my life, I have felt powerless because of this disease. I have experienced moments of terror when an intense, overpowering fear has swept over me and consumed my thoughts with the what ifs. Panic has seized me in the most unexpected moments: seeing a person in a wheelchair, a woman who shuffles into the store in front of me, an older man who drops his coffee mug because his hand is shaking. There are reminders all around that cause me to panic and be reminded that this could be me in five months, or two years, or six days, or …

I have been dismayed and at times have lacked the courage and the power to fight this monster. I have felt paralyzed by the confusion of what to do next, helpless in this new battle I was chosen for, and afraid that I may not know how to fight well, or may not have the necessary weapons.

What do you do with that feeling of helplessness and dread? What do you do when panic consumes your life and leaves you exhausted and powerless?

I can’t accomplish much of anything when I’m feeling overwhelmed, and my mind is confused and cluttered. Eventually in my struggle, I remember and believe that the God who made me will not allow this trial to consume me, nor will He leave me defenseless to fight it alone. Some say that religion or God is for those who are weak. You can call me weak.

There is comfort in knowing that I don’t face the battles of this disease alone. The unknowns. The what ifs. If I truly believe what I write, then I can step out and do what often seems impossible to do in the darkest valleys: face my fears. What makes that possible is faith. And it is faith that gives us hope.

***

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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Enjoying the Journey Despite Parkinson’s Disease

journey

Sherri Journeying Through

I recently received an email from someone concerned that he may have early signs of Parkinson’s disease. I have met others who have PD, but not someone in the throes of wondering if the symptoms he is are experiencing are, in fact, PD.

I can’t stop thinking about him. I think it’s because it takes me back to my diagnosis, to my days of wondering what was going on. I can relate and understand all too well.

He is scared, wondering if he does have PD. I can look back and see myself where he is now — scared, uncertain, and desperate. I can see now that, although the future is still uncertain, I have been blessed with a wonderful doctor and the support of friends and family, and I’ve been given the opportunity to encourage others. I couldn’t see those things then; all I had was the fear that my future was being taken away and a sense of hopelessness was left in its place.

Isn’t the future uncertain for everyone, whether we have been diagnosed with a disease or not? No one knows how the end will turn out or when we will tuck our babies into bed at night for the last time.

I am reminded of one of my favorite quotes: “Dance as if no one is watching, sing as if no one is listening, and live every day as if it were your last.”

That is how I want to live each day — whether I am fighting PD or making peace with it. I want to dance without caution, even if I stumble. I want to sing at the top of my lungs, even if others think I’m whispering. And I want live each day as if it is my last, even if I get a tomorrow.

It is a difficult thing to live like that. There are so many distractions and reminders that we are not “whole.” Distractions push their way into our daily paths and our bodies struggle to be free from this disease. We can, however, choose to have the attitude of living life to its fullest and enjoying the journey. It may not be the journey we would have chosen for ourselves, but there is good in it. It’s always better to wear a face of hope than one of despair.

***

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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Protein Content in Tears May Help to Identify People with Parkinson’s Disease, Study Says

tears as possible biomarkers

An analysis of the protein content in tears may offer a non-invasive and inexpensive way of identifying people with probable Parkinson’s disease.

A study led researchers at the Keck School of Medicine of the University of Southern California reports that Parkinson’s patients have different levels of alpha-synuclein protein in tear fluid than do people who do not have the disease.

This finding suggests that tears may represent a reliable biomarker of Parkinson’s, one that might enhance early diagnosis of this progressive disorder.

The study, “Tear proteins as possible biomarkers for Parkinson’s disease,” was recently presented at the 2018 World Congress on Parkinson’s Disease and Related Disorders (IAPRD) in Lyon, France.

Parkinson’s disease is mostly recognized by selective loss of nerve cells in the brain that produce an important regulatory protein called dopamine. This is believed to be in part mediated by the accumulation of abnormal toxic protein clumps, mainly composed alpha-synuclein protein.

But disease effects are not restricted to the brain, and patients also experience progressive peripheral nerve cell damage.

As the secretory cells of the tear gland are stimulated by nerves, researchers hypothesized that nerve alterations observed in Parkinson’s disease could result in altered protein content in tears.

A research team led by Mark Lew, MD, collected and evaluated tear samples from 94 Parkinson’s patients and 60 healthy volunteers matched for age and sex.

The researchers found that total levels of normal, non-clumped, alpha-synuclein were about 35% lower in patients’ tear fluid compared to healthy controls.  In contrast, patients had an amount of alpha-synuclein toxic aggregates that was four times higher than controls  (3.43 nanograms per milligram of tear proteins compared to 0.84 nanograms). The team had reported similar results previously in a smaller group of patients.

Now, the researchers also evaluated the levels of other potentially relevant proteins, including chemokine ligand 2 (CCL-2 ) and DJ-1 (Park 7), but failed to find any changes between the two groups.

Supported by these results, the researchers believe that evaluation of “total alpha-synuclein and oligomeric [aggregated] synuclein may have potential to discriminate between tears of Parkinson’s disease patients and healthy controls.”

“To our knowledge this is the first report of tear collection and protein analysis as a possible non-invasive, inexpensive, and reliable biomarker for Parkinson’s,” they added.

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Valuable Advice for Parkinson’s Disease ‘Newbies’

self-care, lessons

Sherri Journeying Through

You have been asked to speak to a group of newbies in the Parkinson’s world. You have been asked to share with them wisdom you have gleaned from walking this journey of having Parkinson’s disease. What will you tell them? This is what I might say:

  • You must exercise! Exercise! Exercise! This is probably the most important piece of advice anyone can give or receive regarding dealing with Parkinson’s disease.
  • Leave your pride in the doctor’s office. Accept help.
  • Find a movement disorder specialist as soon as possible. There really is a big difference in the type of care you will receive.
  • It’s quite easy to be anxious about your diagnosis. It is not a death sentence, and many, many people with Parkinson’s disease have gone on to live very productive lives after being diagnosed.
  • You will find you are stronger than you ever imagined you could be.
  • Make your health a priority.
  • Take someone with you to your doctor’s appointments to help you remember what you wanted to ask and to help you remember what the answer was!
  • Fight for your life. There will be hard days, bad days, and oh, so great days. Relish the great ones and fight through the harder ones. You will get through!
  • Don’t spend quality time focused on what you can’t see or can’t know: the future. Don’t regret things from the past. Focus on living in the now.
  • You are not alone in this journey. There may not be a cure yet, but there is definitely a community.
  • Everyone wears the coat of PD differently.
  • PD is sooooooo unpredictable.
  • Try not to begin more than one medication at a time so you are able to tell how you are reacting to it.
  • Some friends will leave your circle of friendship because they can’t relate or understand what you’re now going through. That will leave room for new friends who do or want to understand.
  • Find out as much as you can about Parkinson’s but don’t believe everything you read.
  • Time is precious. Make the most of it, starting now.

What advice or encouragement would you offer someone who is newly diagnosed with Parkinson’s disease?

***

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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Some Thoughts About Treating Parkinson’s Disease

treated, neuroprotective medications

Sherri Journeying Through

Someone told you that you or someone you love has Parkinson’s disease (PD). You’ve also heard that it is incurable. Nevertheless, can it be treated? If so, what medicines are used?

First, let me say that I was diagnosed with PD over 10 years ago and misdiagnosed with lupus over 20 years ago. As stated earlier, Parkinson’s disease is not curable, but it is treatable, to a degree. Just maybe, the day you’ve reached your “last degree” will be the day they announce a cure.

No one I have ever met likes taking pills, and yet to treat Parkinson’s effectively, there is no way around it for the common patient. Patients must also understand that Parkinson’s disease affects each person differently, so each patient is treated differently and different medications will be used accordingly.

My drug therapy has been conservative, according to my neurologist. For example, one medication at a time is added at the time of my checkup, if needed. This is done so that the physician is able to correctly identify which medication a patient reacts to should side effects occur. This can be a much safer procedure than starting with eight pills, three times a day, and working backward.

Pharmaceutical companies would go out of business if they were not constantly coming up with improvements to the treatments already available on the market. That, in and of itself, says the medical field is making progress in creating treatments for PD and other diseases.

While I said earlier that PD is incurable, it is treatable. Treatable, however, will look different for you than it does for me or another patient. Some will be behind you in their progression of the disease, some ahead. It also depends on how each individual doctor believes or thinks the disease should be best treated. As you can see, many different factors come into play when a physician must come up with a custom treatment that best suits a patient.

Of the medications available that physicians choose for their patients, some of the more tolerated and beneficial seem to be Mirapex (although it is noted to have serious side effects for some), Sinemet, Artane, Requip, and Comtan. Doctors might add other various medications be added to the mix depending on a patient’s symptoms and needs. These could include Azilect, Lexapro or another antidepressant (as one of the first notable symptoms of PD is depression), and Symmetrel, etc.

Each patient is unique and different and, therefore, patients’ needs and reactions to their treatment will be different. What works for one may not be tolerated or work well for another. Hopefully, the drug treatment is scaled to your individual needs and will treat your symptoms, but only your doctor can decide with you what is best and what is needed. New steps are taken every day, and progress is made at nearly the same rate worked toward a cure. Until then, it is best for patients to follow their regimented treatments until something better comes along. It will if we all keep fighting and do not give up.

***

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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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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Nerve Damage in Hearts of Parkinson’s Patients Can Be Monitored with Imaging Tools, Animal Study Reports

cardiovascular damage

Cardiovascular damage in Parkinson’s patients, due to nerve cell loss in the heart, can be captured by imaging stress and inflammation molecules — a process that may help to determine the mechanisms behind such damage and ways of treating neurodegeneration in the heart, researchers report.

The study by researchers at the University of Wisconsin-Madison, “In vivo imaging of inflammation and oxidative stress in a nonhuman primate model of cardiac sympathetic neurodegeneration,” was published in the journal npj Parkinson’s Disease.

Virtually all Parkinson’s patients experience, to some extent, a loss of the nerve cells controlling the heart, specifically those involved in the sympathetic nervous system that regulates the heartbeat in response to changes in physical activity and blood pressure. This degeneration is independent of motor symptoms and can lead to fatigue, exercise difficulties (poor cardiac response), and dizziness and fainting, putting patients at a greater risk of falls and injury.

“This neural degeneration in the heart means patients’ bodies are less prepared to respond to stress and to simple changes like standing up,” Marina Emborg, the study’s senior author, a UW-Madison professor, and a researcher at the Wisconsin National Primate Research Center, said in a university news article by Chris Barncard.

Because nearly 60 percent of Parkinson’s patients have evidence of cardiac nerve loss at diagnosis, it has been suggested that tests of such damage might be a Parkinson’s marker  in patients considered at disease risk but asymptomatic in terms of tremors or motor control.

The researchers created radio-labeled compounds that could monitor nerve loss through positron emission tomography (PET) scans.

The compounds target molecules involved in inflammation and oxidative stress, which are believed to play a key role in Parkinson’s neurodegeneration.

Investigators tested three radioligands – PBR28, ATSM, and MHED – in monkeys with induced cardiac nerve cell loss, mimicking the features of Parkinson’s in humans. These compounds had been deemed safe in mice and humans.

The monkeys underwent PET scans, a imaging approach that detects radio-labeled compounds, once before and twice after receiving the molecules.

Researchers focused particularly on changes in the left ventricle, the strongest blood-pumping chamber of the heart, and found that they could trace damage, inflammation, and oxidative stress over time.

“We know there is damage in the heart in Parkinson’s, but we haven’t been able to look at exactly what’s causing it,” said Jeanette Metzger, the study’s first author. “Now we can visualize in detail where inflammation and oxidative stress are happening in the heart, and how that relates to how Parkinson’s patients lose those neuronal connections in the heart.”

Researchers also hypothesized that the tracers could be used to monitor the efficacy of treatments aiming to protect these neurons. They tested a drug called pioglitazone – approved to treat diabetes by lowering blood sugar levels – because it has anti-inflammatory and anti-oxidative effects.

Compared to placebo monkeys, those given pioglitazone were found to be significantly better at preventing signs inflammation and oxidative stress in the heart, which ultimately was associated with reduced nerve cell damage.

“The recovery of nerve function is much greater in the pioglitazone-treated animals,” Emborg said. “And what’s interesting is this method allows us to identify very specifically the differences the treatment made — separately for inflammation and for oxidative stress — across the heart.”

The researchers suggested this new technique may  be useful in better understanding the mechanisms of early nerve damage occurring in the hearts of Parkinson’s patients, as well as those with other cardiac disorders.

“The present study in rhesus macaques demonstrated that PET with the radioligands MHED, PBR28, and ATSM successfully detected changes over time and across the cardiac left ventricle in sympathetic innervation, inflammatory response, and oxidative stress during neurotoxin-induced neurodegeneration and PPARγ [pioglitazone]-associated neuroprotection,” they wrote.

“Our findings strongly support future preclinical and clinical studies using these radioligands to evaluate the role of inflammation and oxidative stress in peripheral sympathetic neurodegeneration,” the study concluded.

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Source: Parkinson's News Today