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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Russian Researchers Create Software that Predicts Parkinson’s Symptoms

software program predictive

A new software can predict with an accuracy of 96 percent the form of Parkinson’s disease and future symptoms that a patient may experience.

The software was the result of a collaboration between researchers at Peter the Great St. Petersburg Polytechnic University (SPbPU), the Institute of Experimental Medicine, and ITMO University, in Russia.

This technology may improve early diagnosis, promote preventive care, and ultimately enhance patients’ overall health.

The program was developed based on a discriminant analysis method that allows researchers to dissect a great amount of data more easily and create groups that share similar features. The technology combines clinical information, test results, and disease progression data, which may provide common patterns used to identify patients or particular features according to those specific characteristics.

This strategy allows clinicians to evaluate which treatments would be more likely to work for a patient or group of patients. Also, the software could predict if patients were likely — or not — to develop certain disorders or symptoms.

For instance, in a previous study researchers found that Parkinson’s patients who have very low blood levels of copper have increased chances of developing abnormal posture.  “If a doctor knows about a potential threat in advance, he or she can start preparing for the treatment beforehand,” Marina Karpenko, PhD, associate professor at the biophysics department of SPbPU, said in a press release.

Built on the basis of artificial intelligence, the software has the capacity to constantly improve its predictive abilities, as Karpenko explained: “The program can be ‘trained’: the more information is uploaded in it, the more precise conclusions and recommendations it will provide,” she said.

Overall, the software may empower clinicians to diagnose Parkinson’s disease earlier, which will support prompt and targeted treatments to provide the best patient care and outcomes.

Researchers expect to make the software available in the near future, in a format that can be installed in any computer or smartphone.

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Survey Shows Canadian Parkinson’s Community’s Key Concerns

Canadian Parkinson's survey

Long waits for diagnosis, limited access to specialized treatments and services, and out-of-pocket healthcare costs are among key concerns of Parkinson’s patients, caregivers, and medical-service providers, according to a Parkinson Canada survey.

The organization created the 30-minute online survey to better understand the challenges that patients, caregivers, and providers face. It was conducted between Sept. 29 and Oct. 24, 2017.

Fifty-seven percent of the patients who participated were men, and most were aged 65-74 years. About four in five were married or living with a partner. Seven in 10 were retired.

An important finding was that patients face long waits for a diagnosis, with two out of 10 saying they waited over one year. Almost one in four patients classified their ability to gain access to medical specialists as poor or very poor. Sentiment was similar on accessing movement disorder clinics, a Parkinson’s nurse specialist, and long-term care facilities.

Three in five patients said they needed additional information from Parkinson Canada or one of its support groups. Four in 10 reported depression, anxiety, stress, sadness, and loss of confidence. Access and waiting times for mental health services were a problem for many patients.

In contrast, nine of 10 patients and caregivers rated access to oral treatments and to a family doctor as good, very good or excellent.

Providers were more critical. Over half reported poor or very poor access to movement disorder clinics, and three out of 10 rated access to speech and swallowing therapy as poor or very poor.

Providers were even more negative on waiting times for specialized services and treatments, with four in 10 rating them as poor or very poor.

The patient barriers that providers mentioned included too few medical specialists, limited information and understanding of Parkinson’s, scarce availability of educational resources, insufficient counseling resources, and too few support groups.

The findings also showed the toll that Parkinson’s takes on caregivers. More than one in four reported that they care for a patient while having a full-time job. Seventy-seven percent of caregivers were women and most were aged 75 years or older.

Nearly half of caregivers said access to long-term care facilities was poor or very poor. They were also concerned about access to movement disorder clinics, Parkinson’s nurse specialists, and mental health services.

Among the health problems that caregivers experienced were stress, exhaustion and feeling guilty that they were not doing enough. They also mentioned frustration towards the patient, helplessness and anxiety.

“People with Parkinson’s often suffer from complex physical and non-motor [non-movement] health disorders, which can affect the whole family,” Joyce Gordon, the CEO of Parkinson Canada, said in a press release. “We know that caregivers are heavily burdened, financially and emotionally. Our mission is to help close the gap for them and build awareness of Parkinson’s.”

The disease also represents a significant financial burden. Four in 10 respondents reported difficulty paying health care bills, including medication, exercise, physiotherapy, and speech and swallowing therapy.

About three-fourths of patients and care partners reported paying for exercise programs. Forty-four percent said they paid for physiotherapy and a third said they paid for at least one type of medication. Four out of 10 said paying for medication imposes a major financial burden on them if it’s not reimbursed by insurers.

Three out of four care providers perceived medication and other therapies as a major burden without financial assistance

“It’s important that individuals receive a correct diagnosis as early as possible and have adequate access to ongoing specialized care. Even this care is limited and follow-up visits are too far apart,” said David Grimes, lead author of the “Canadian Guidelines on Parkinson’s Disease.

“If the survey shows that Canadians are experiencing considerable gaps and delays to care, this hinders [providers] from effectively recommending treatments and lifestyle changes that would help patients better manage the disease,” he said.

Parkinson Canada plans to share the survey results with governments and others during Parkinson Awareness Month in April. The goal is to raise awareness as a way of improving access and decreasing wait times. It will also share the information with the public and donors.

It called for more effort on research and services for Parkinson’s at a time when healthcare demand is increasing as the population ages. It also called for more investment to provide medical professionals with educational opportunities and healthcare resources.

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An Introduction to ‘Slow Is the New Fast’: How Did I Get Here?

column, perspective, shared advice

I am not a writer.

A little history

In 2010, I retired from a 37-year career in the information technology industry. For many years, I relied on the analytical side of my brain. While in retirement, I decided the time was right to exercise the more visual and perceptual side of my brain. Graphic design was a natural next step for me, so I began to do the creative work for the event business of my life partner, Steve.

Graphic design seemed to make sense, but I never envisioned myself as a creative writer after I retired from my computer career. My writing experience primarily consisted of developing contractual documents related to phone-system deployments.

A turning point

When Steve took his own life on March 15, 2015, my world changed dramatically. We were together for over 33 years. I took solace in writing about Steve and found purpose in trying to bring more awareness to suicide by telling Steve’s story.

About six months before Steve took his own life, he was suffering from a panic attack in our living room. Seeing someone you love in such a state is devastating. I remember helplessly dropping to the floor while my body was wracked with sobs. Steve was in so much mental pain and our relationship and “fairy tale” life was falling apart. I clearly remember feeling something “snap” in the back of my head. It was not pain, but I recalled thinking to myself that this was an ominous occurrence that would impact my long-term health. I did not think about that moment again until I received my PD diagnosis seven months after Steve died. More than one neurologist has told me emotional trauma I suffered before and after Steve passed might have triggered the onset of my PD.

Why do I write?

While blogging about suicide and grieving, I have been encouraged by many to continue writing. Comments left on my blogs indicated that many no longer feel alone in what they felt after they have read my stories.

Now that I have PD, I hope to be a voice for people afflicted with this disease. One of my other goals will be to help others better understand what one who has the illness struggles with on a daily basis. While I will continue to write about Steve and suicide-related topics, I will now also share my PD journey in this column.


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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New Smartphone App Seen to Quickly and Ably Assess Parkinson’s Symptoms

machine learning and apps

A new smartphone application can be used to remotely assess Parkinson’s disease symptoms in a rapid and objective way, with the potential to transform how a range of neurological diseases are evaluated, the research team that created it report.

The study, “Using Smartphones and Machine Learning to Quantify Parkinson Disease Severity, The Mobile Parkinson Disease Score,” was published in JAMA Neurology.

Although studies regarding smartphone use to assess Parkinson’s disease have previously been published, only specific features, such as gait, were considered — neglecting overall symptoms of the disease.

Johns Hopkins and University of Rochester researchers developed a smartphone application that can assess Parkinson’s and its severity based on several disease features. 

The Android smartphone application, called HopkinsPD, was designed to evaluate five activities: voice, finger tapping, gait, balance, and reaction time. It also allows users to report the use of medication.

The team used a new machine-learning–based approach to generate a mobile Parkinson disease score (scaled from 0 to 100, where higher scores indicate greater severity) that could objectively weight features derived from each smartphone activity, such as stride length from the gait activity.

A total of 250 people with Parkinson’s downloaded HopkinsPD, with 129 fulfilling requirements for the study’s development arm. Another 23 Parkinson’s plus 17 healthy controls constituted the clinic group.

Participants ranged in age from a mean of 58.7 years in the development group, to 64.6 years and 54.2 years in the clinic group (Parkinson’s patients and controls, respectively).

All completed standard in-person assessments of their disease using the smartphone app for six months.

Results showed a good-to-excellent correlation between the mobile Parkinson disease score and current standard assessments, such as the Movement Disorder Society Unified Parkinson Disease’s Rating Scale (MDS-UPDRS), proving this method could provide an objective measure of symptoms. Importantly, this method can be performed frequently, remotely, and rapidly compared to other tests.

Despite limitations, such as the demographic of the participants (who were mostly white and college-educated) and the fact that they generally owned Android smartphones and are not representative of the broader Parkinson’s population, the study is the largest of its kind. It is also consider a proof of concept for the use of mobile phone applications in assessing the severity of neurological conditions.

“Using a novel machine-learning approach, we created and demonstrated construct validity of an objective PD [Parkinson’s] severity score derived from smartphone assessments. This score complements standard PD measures by providing frequent, objective, real-world assessments that could enhance clinical care and evaluation of novel therapeutics,” the team concluded.

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New PET Tracer with Potential to Diagnose Parkinson’s to Be Tested in First-in-Human Study

PET tracer

An innovative Positron Emission Tomography (PET) tracer that has the potential to diagnose Parkinson’s disease will soon be tested in humans for the first time.

Led by Switzerland-based AC Immune, which developed the technology, the study is expected to begin in the second half of 2018. The company recently presented the data on its new product at the AAT-AD/PDTM Focus Meeting 2018 in Turin, Italy.

“We are excited about this significant step in our development of potentially the first ever PET tracer for earlier and more accurate diagnosis of Parkinson’s,” Andrea Pfeifer, CEO of AC Immune, said in a press release. “This important milestone underlines our vision to become a global leader in precision medicine of neurodegenerative diseases, leveraging our proprietary technology platform.”

The company used its Morphomer platform, designed to interact with misfolded and aggregated proteins, to develop the PET tracer, which is highly selective for alpha-synuclein, enabling an earlier and more accurate Parkinson’s diagnosis.

AC Immune’s technology is aimed at not only detecting alpha-synuclein in patients, but also monitoring the effects of treatments targeting protein clumps. The research program has been spotting small molecules selective for alpha-synuclein and suitable for development as PET tracers.

Upon entering the brain, the new imaging agent, called a PET tracer, binds to abnormal or misfolded alpha-synuclein. Its radioactive label enables the imaging device to detect bound alpha-synuclein, informing clinicians on the amount and distribution of pathological brain alpha-synuclein.

If successful, the new PET tracer would be the first alpha-synuclein tracer to receive regulatory approval for commercial distribution. Its specificity would be important not only for Parkinson’s patients, but also for other disorders characterized by aggregated alpha-synuclein, collectively called synucleinopathies.

AC Immune has been collaborating with Biogen on this program since April 2016. The companies will proceed with the development and seek clinical validation for the use of the PET tracer as an imaging biomarker for Parkinson’s.

The Michael J. Fox Foundation for Parkinson’s Research (MJFF) is supporting this project. “We are very pleased about this next important step in the development of an alpha-synuclein imaging agent,” Jamie Eberling, PhD, director of research programs at MJFF, said.

“Having a PET tracer to detect and track Parkinson’s disease would be transformative for Parkinson’s research and patient care,” she said.

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Noticing the Signs of Parkinson’s Disease in a Loved One

Sherri Journeying Through

This is written for loved ones who might have a sense that something isn’t quite right with the one they care about. It is a list of early signs you may notice before your spouse, friend, child, or parent does and how you might help them.

Most people notice the tremors as the first symptom of Parkinson’s disease (PD) in someone they know. However, did you know that there are other signs that are a clue that someone may have PD? Clues that are often overlooked, even by medical doctors?

On one of my earlier visits to my neurologist, I learned one of the first signs of PD can be depression. Looking back, it was true for me. There was no reason for me to feel down or anxious, but I did. I talked to my general practitioner about it, and she was the one who first put me on an antidepressant. There are many other reasons a person can feel depressed, so don’t jump to conclusions that the one you’re concerned about has PD. For a diagnosis to be confirmed, several symptoms must be present. A diagnosis of PD isn’t made solely because a person is depressed.

So, what if they have tremors and seem down? Again, there is a list of symptoms your neurologist will look for in making a correct diagnosis of PD. Adding tremors to the mix with depression will not necessarily mean Parkinson’s disease.

Is your mate having a hard time sleeping? Restless? Tired during the day from lack of a good night’s rest? Having vivid dreams? Nightmares? Acting out while dreaming? All on a regular basis? If you are married and find yourself wanting to go to the guest room frequently because your spouse is, how shall I put this, too active in bed? It may be a cause for concern. Sleep disorders can be evidence that something may be going on.

Parkinson’s can snitch your sniffer, so your loved one may not smell things as well or at all. The ability to smell may return for the short-term at random times, though.

PD can also cause a person to drag their foot or have a slight shuffle when they walk.

No one likes people to enter the room and ask, “What’s wrong with you?” But that can happen when early signs of PD show — such as the masked face. What is “masked” face? When the muscles in the face have tightened. Because of this, people with PD have a harder time smiling or showing facial emotion. It’s also been called a stone face — showing no expression. You’ve heard the saying, “Don’t judge a book by its cover.” Well, in PD we say, “Don’t judge the mood by the face.” OK, maybe only I have said that. But it’s true.

Another symptom I struggle(d) with is a soft voice. I have a soft voice to begin with, and getting softer only served to aggravate those around me. It also makes for lousy conversation on the part of the person with PD, as no one hears you participating in the conversation, so you end up being constantly interrupted, never able to finish your sentences. Plus, well, you just don’t feel like talking at all.

It takes several signs/symptoms to make a diagnosis of Parkinson’s disease, and it should be done by a neurologist or a movement disorder specialist. It’s important to remember that everyone lives with PD differently. Some are affected more by tremors, some by stiffness, some by pain, and some deal with it all. And some may have some of the signs, but don’t actually have PD. Don’t make your diagnosis. Ask questions until you are satisfied with the answers, and don’t give up. We’re in this together.


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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Biomarkers Identified That Could Help Predict Individuals at Risk for Parkinson’s, Study Says

DOPA, DOPAC levels

Low levels of two dopamine-related molecules in cerebrospinal fluid can help identify patients in the early stages of preclinical Parkinson’s disease, a study suggests.

The study, “Cerebrospinal fluid biomarkers of central dopamine deficiency predict Parkinson’s disease,” was published in Parkinsonism & Related Disorders.

Parkinson’s disease is mainly recognized by its motor symptoms, such as uncontrolled tremors, gait difficulties, and slow movement. However, by the time these symptoms appear, a significant loss of brain cells sensitive to dopamine has already occurred.

Because of this, there is a need for sensitive markers of early brain cell loss that can be used to track disease progression.

DOPAC and DOPA are two dopamine-related molecules whose levels are reduced in patients with untreated Parkinson’s. However, it was not clear if measuring levels of both proteins could help identify asymptomatic, healthy people who are at risk of developing Parkinson’s disease.

A team led by David Goldstein, MD, PhD, principal investigator at the National Institutes of Health, evaluated the levels of DOPAC and DOPA in cerebrospinal fluid samples collected from 26 at-risk people.

This analysis was integrated in the PDRisk prospective study of the National Institute of Neurological Disorders and Stroke (NINDS), which intends to identify early biomarkers of Parkinson’s disease.

Participants had to have at least three previously defined risk factors for Parkinson’s disease, including direct family history of the disease, loss of sense of smell, impaired sleep or abnormal sleep behavior, and low resting blood pressure.

Patients who were already showing signs of Parkinson’s-related motor symptoms during the enrollment phase were excluded from the study.

Of the 26 participants, four developed clinical Parkinson’s disease during the three-year follow-up period. These patients were found to have significantly lower levels of both DOPA and DOPAC in cerebrospinal fluid than the 22 participants who did not develop Parkinson’s for at least a mean follow-up of 4.2 years.

Researchers determined that the optimal cutoff value for defining low diagnostic DOPAC was 1.22 pmol/mL, which accurately predicted Parkinson’s risk in 84.1% of cases. For DOPA, the cutoff value was 2.63 pmol/mL, accurately predicting disease risk in 90.3% of cases.

These data suggest that early dopamine deficiency in at-risk individuals — defined by low DOPAC and DOPA levels — is linked to an increased likelihood of developing clinical Parkinson’s disease within three years.

Researchers believe the identified “predictive strength” reflects the important role of these neurochemical biomarkers in the underlying mechanisms of disease, suggesting that “neurochemical biomarkers of central dopamine deficiency identify the disease in a pre-clinical phase.”

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Better Biomarkers Needed to Diagnose, Predict Risk of Mild Cognitive Impairment

Parkinson's mild cognitive impairment

There still are no reliable biomarkers for early detection, or to characterize and predict risk of dementia, in Parkinson’s disease, according to a recent analysis.

Several studies on the cognitive deficits, progression to dementia, potential biomarkers and the mechanisms underlying Parkinson’s disease mild cognitive impairment (PD-MCI) were analyzed by University College London researchers in the review study “Mild Cognitive Impairment in Parkinson’s Disease—What Is It?,” which was published in the journal Current Neurology and Neuroscience Reports.

Large-scale studies have shown that PD-MCI is not only important, but also common, even at the earliest stages of Parkinson’s disease. In fact, MCI signs can be detected before the onset of Parkinson’s motor symptoms.

About half of Parkinson’s patients with cognitive impairment will progress to dementia in the first 10 years after diagnosis. But considerable variation exists among this patient population regarding the type of cognitive domains affected, the timing, severity and risk of progression to dementia.

Accordingly, PD-MCI is emerging as an intermediate stage between normal cognition and dementia, similarly to the stage of amnestic mild cognitive impairment in Alzheimer’s disease.

Epidemiological studies report that 25 to 50 percent of Parkinson’s patients have MCI, depending on the population and the clinical setting. Identifying individuals with early signs of PD-MCI or at risk of dementia is important to provide early interventions, estimate prognosis, and discover therapeutic targets.

In an effort to clarify the diagnosis of PD-MCI, a task force from the International Parkinson and Movement Disorder Society (MDS) provided a unified definition. According to the new criteria, PD-MCI is defined as an “insidious decline in cognitive abilities reported by patient or informant or observed by the clinician, not caused by other comorbidities.”

Unlike dementia, MCI deficits are detectable, but do not interfere with patients’ autonomy.

The nature and severity of PD-MCI is quite variable. The dominant manifestation does not involve memory. But there are other subtypes with deficits in attention, memory, executive function, psychomotor speed and visuospatial abilities. In some people the deficits can involve multiple cognitive domains.

The MDS has recommended a battery of tests to assess involvement of single or multiple domains and report exactly which domains are affected.

In general, patients with PD-MCI are at higher risk of progressing to dementia than Parkinson patients without MCI. Importantly, studies report that 11 to 28 percent of patients with PD-MCI revert to normal cognition during follow-up.

The variability of these results is likely to reflect differences in study populations, assessment methods and definitions.

Some factors can increase risk of cognitive deficits in Parkinson’s, including being older than 70, akinetic rigid phenotype (freezing and/or falls), poor verbal fluency and higher rates of comorbidities. Higher rates of progression to dementia are associated with older age, depression and a non-tremor clinical manifestations.

Exploring biomarkers

Biomarkers such as amyloid beta protein in the cerebrospinal fluid, and magnetic resonance imaging of the brain, may become important for providing insights into mechanisms of cognitive involvement and for accessing disease progression.

The mechanisms underlying PD-MCI likely involve a combination of factors. Brain aggregates of the proteins alpha synuclein, beta amyloid and tau — the latter two also characteristic of Alzheimer’s disease —  are likely to play a role.

Besides, some studies suggest that changes in specific neurotransmitters — chemical messengers used to communicate between neurons, including acetylcholine, noradrenaline and dopamine — also contribute to cognitive impairment.

Some questions regarding PD-MCI remain unresolved. One of them is the distinction between dementia with Lewy bodies (intracellular accumulations of alpha synuclein) and Parkinson’s dementia.

Dementia with Lewy bodies emerges early, before or within the first year of Parkinsonism, while Parkinson’s dementia is defined as a progressive decline appearing at least one year after motor symptoms are noticeable.

However, given the reports of people with cognitive deficits even before characteristic manifestations of Parkinson’s, perhaps cognitive impairments are the first signs of Parkinson’s disease and may start earlier than believed.

Some studies report that some PD-MCI sub-groups, particularly those with deficits in visuospatial performance, are at the highest risk of dementia.

This underscores the need for better assessment methods and biomarkers of PD-MCI to allow well-defined characterizations of the cognitive deficits and predict who is more prone to dementia.

Although the antipsychotics Nuplazid (pimavanserin) and Clozaril (clozapine) are the only therapies shown to improve Parkinson’s disease psychosis (PDP) symptoms without impairing motor function, there currently are no pharmacological treatments specifically for PD-MCI.

The effect of current experimental therapies on cognition is unknown. Some studies suggest that cognitive training can improve overall cognition in Parkinson’s patients, although the effect seems small.

Physical exercise shows more promising results. Several studies report that moderate intensity aerobic exercises performed two to three times a week lead to some improvement in executive and language functions.

However, Acadia Pharmaceuticals, Nuplazid’s manufacturer, is planning to conduct additional studies of the therapy in PD psychosis patients with a broader range of cognitive abilities and formal cognitive diagnoses, including mild cognitive impairment and dementia.

“Maintaining wide definitions, with poorly differentiated cognitive profiles, prevents accurate comparisons across studies,” researchers wrote. “There is clearly a need for better cognitive phenotyping to enable well-defined sub-groups that are more likely to show similar rates of disease progression.”

“Recognizing the earliest stages of cognitive involvement will allow disease stratification and personalized treatment, with the potential for early intervention. It will enable better-powered clinical trials, and potential outcome measures, ultimately to develop treatments to prevent the progression of dementia in PD,” the review concluded.

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