Research

IBM unveils fingernail sensor that can monitor PD

July 1, 2019 Life, Research

Recently IBM unveiled its latest innovation that could change the way how we monitor health. It’s prototype AI-powered fingernail sensor will let its users place the sensor over their fingernail to detect symptoms and track disease progression.

According to IBM, the innovation can help track cognitive functions in schizophrenics, check the effectiveness of medication in a person with Parkinson’s disease and even individuals’ cardiovascular health.

Although there are skin sensors that can monitor body activities, it is hard to place them on people with Parkinson’s disease as a majority of them are older patients with brittle skin and might lead to infection.

But by shifting the sensors to the nail, not only did they avoid the problem of skin rash that could arise from skin sensors, they were able to track the activities of hand for throughout the day which is a key factor in diagnosing degenerative neurological diseases such as in the case of Parkinson’s disease.

“Our fingernails deform — bend and move — in stereotypic ways when we use them for gripping, grasping, and even flexing and extending our fingers. This deformation is usually on the order of single digit microns and not visible to the naked eye,” said Katsuyuki Sakuma, from IBM’s Thomas J. Watson Research Center in New York.

The system consists of strain gauges attached to the fingernail and a small computer that collects data and communicates with a smart watch, which is equipped with machine learning models to rate bradykinesia, tremor, and dyskinesia which are all symptoms of Parkinson’s disease.

The AI-powered sensor monitors the bending and movement of a patient’s nail to calculate their grip strength. It then transmits the information which includes matters like nail wrap, motions, gestures, finger-writing, grip strength, and activation time from the wearable sensors to an off-finger device for interpretation and draws meaningful insight.

With this invention, IBM says that it is one step closer to materialising their longtime challenge of using AI to help clinicians monitor individuals in their natural environments. “By pushing computation to the end of our fingers, we’ve found a new use for our nails by detecting and characterising their subtle movements,” Sakuma said in closing.

Article from Analytics India Magazine.

Using EEG data to diagnose Parkinson’s disease

July 1, 2019 Research

Currently, diagnosis of Parkinson’s disease relies on a neurologist’s professional opinion. Researchers behind a new study believe that an EEG may be a more effective alternative.

Parkinson’s disease affects more than 10 million people worldwide, but no scan has been proved to definitively diagnose it.

Instead, a neurologist will assess a person by asking them to carry out certain tasks. These may include writing or drawing, walking, and speaking.

They will also examine the face and limbs to check for signs of tremors and facial expression difficulties.

As diagnosis is currently rather subjective, researchers have been trying to find an easier and more scientific method. A team from the University of Oregon, in Eugene, and the University of California, San Diego, has studied the possibilities of an EEG.

An EEG records electrical activity produced by the brain via small sensors attached to the scalp. Attempts to use EEG readings for Parkinson’s disease diagnosis have not always produced the results that researchers have been looking for.

Nicole Swann, Ph.D., the principal investigator of the new study and an assistant professor at the University of Oregon’s Department of Human Physiology, says that this is because, in the past, sine waves were the focal point. These are beta waves filtered to appear rounder.

A search for sharpness

But it is the angles and sharpness of brain waves that could hold the key to detecting Parkinson’s, according to the new study’s findings, which appear in the journal eNeuro.

While working on his doctorate at the University of California, San Diego, fellow study author Scott Cole, Ph.D., realized a potential link between the disease and sharp brain waves.

Using EEG readings taken from 15 Parkinson’s patients and 16 healthy individuals, the team honed in on the unfiltered waves.

“The raw signals go up and down like sine waves but with more asymmetry,” explains Swann, adding, “The steepness — the slant — turns out to be important in Parkinson’s patients.”

Indeed, the team noticed that Parkinson’s patients who were not taking medication had a sharper peak at the top of their brain wave, compared with the bottom.

Finding that a noninvasive method such as an EEG could be a promising diagnostic tool may have important consequences for the future of the disease. The team is hoping that doctors and researchers can use the test to track changes related to Parkinson’s in the brain over the years.

“We don’t know yet whether this approach will be better, but it could provide easily obtained brain measurements that would be helpful and possibly used in tandem with clinical observations and other EEG measurements,” notes Swann.

Changing the course of treatment

The EEG method could also have an effect on treatment. Currently, doctors can prescribe medication or implant an electric stimulator into the brain.

“If there were real-time measures of how effective treatments are at reducing the negative symptoms of Parkinson’s disease, treatments could be adjusted in real time,” says co-author and University of California neuroscientist Bradley Voytek, Ph.D.

“In the case of an invasive brain stimulator, this might mean only applying electric stimulation when it’s needed.”

“In the case of pharmacology, it would mean adjusting a drug’s dose, much like continuous glucose monitoring done by an implant can signal a pump to adjust insulin levels as needed.”

For the researchers, a bigger study examining EEG data, medical histories, and self-reports from patients is on the cards.

If the results prove to be consistent, people with Parkinson’s could eventually carry out their own EEGs at home, sending the data straight to a neurologist for immediate analysis.

The only issue with this, notes Voytek, is that obtaining the right brain waves is not easy to do in a home environment. Further research will prove whether this, too, can be changed.

Article from Medical News Today.

Developing a Biomarker for Parkinson Disease

June 1, 2019 Education, Research

Identifying, studying, and verifying a potential biomarker can be a lengthy affair. However, success often means clinicians have a new tool to better diagnose a condition like Parkinson disease and to diagnose the condition earlier in the disease progression.

A biomarker for Parkinson disease might mean that patients can begin receiving treatment before irreversible neurological damage occurs.

Sarah Hamm-Alvarez, PhD, Professor of Ophthalmology at the USC Roski Eye Institute at the Keck School of Medicine of USC, spoke with MD Magazine® about this biomarker research, which she presented at the 2019 Annual Meeting of the Association for Research in Vision and Ophthalmology (ARVO) in Vancouver, BC.

Hamm-Alvarez highlighted the collaborative nature of the project that has included colleagues from the neurology, pharmacy, and preventive medicine departments.

“Part of the passion for the project is driven by the clinical need that I sense from my neurology colleagues and their frustration that they don’t have better ways to diagnose patients at early disease states,” said Hamm-Alvarez.

In part 1 of the interview, Hamm-Alvarez introduced the study and the team’s reasons for investigating tears for a Parkinson biomarker. In part 2, she described the study methods and the differences they found in basal and reflex tears.

What’s the process for developing a biomarker?

First you start by establishing a correlation, which we have done. And right now what we’re doing is that we are actually recruiting patients with Parkinson’s disease that are at different times from disease diagnosis and this, we think, will reflect disease severity. So, what we’re trying to do is to see if the levels of oligomeric α-synuclein are correlated with time from disease diagnosis. So, we’re going to try to get a sense of the disease severity. We also are eventually planning to try to test this in patients without a diagnosis, as well as patients who exhibit symptoms that overlap with Parkinson’s disease, such as patients with atypical parkinsonian syndromes and patients with other neurological disorders, of course, to determine how specific this may be, and also whether this has predictive ability going forward if a patient is at an early stage of Parkinson’s disease.

How have various departments collaborated in this project?

This project is very much a team effort we have a whole team at the University of Southern California including colleagues in neurology and pharmacy and preventive medicine. We work very closely with Mark Liu in neurology, who is a neurologist, and who is very excited about the potential for applying this in his clinic. So, I think that part of the passion for the project is driven by the clinical need that I sense from my neurology colleagues and their frustration that they don’t have better ways to diagnose patients at early disease states.

Article from MD Magazine.

Virtual reality reduced PD symptoms for 10 people

June 1, 2019 Life, Research

A new virtual reality game has helped Parkinson’s sufferers keep walking without losing their balance, falling or struggling to turn.

Over time, the incurable neurodegenerative disease restricts muscles more and more, limiting a person’s mobility, ability to turn and balance. But a new technique developed by researchers at the University of Utah restored dynamic movement in 10 patients who trained on the system three times a week for six weeks.

Experts believe the repetitive activity – walking, running and turning on a treadmill as they hop over virtual objects on a cave-like screen in front of them – helped to keep their muscle memory active and ward off deterioration.

‘The primary advantage is that they can encounter multiple obstacles and terrains while a safe environment is maintained using equipment such as a fall restraint tether,’ said K. Bo Foreman, PhD, associate professor and director of the Motion Capture Core Facility at the University of Utah.

‘Participants enjoyed the experience and thought it was fun, not just exercise. They liked training and challenging themselves without the fear of falling.’

The virtual reality experience is projected onto semi-circle-shaped wall facing the patient, who is on a very wide treadmill. The patient wears a headset, shoes and clothing with sensors on them, and they are tethered to a pole behind them for control.

Some of the tasks seem more straight forward than others – walking straight through a field, for example, rather than jumping up onto the curb of a road. But the fusion of everything together forces patients to exercise various skills which can quickly become challenging, if not impossible, for people with Parkinson’s.

Once we’ve learned to walk, we become adept at nimbly switching from walking to running, from walking straight forward, to walking diagonally to the right. We can speed up or slow down, and step to the left or right, or up or down.

Researchers are still working to fully understand how Parkinson’s restricts movement and gait. There is evidence that the drop in dopamine levels plays a role. However, there is growing evidence that physical activity can stave off the decline. For example, revered actor Alan Alda, who revealed his Parkinson’s diagnosis last summer, has taken up boxing to stay mobile.

Dr Foreman’s team at Utah believe VR, much-hyped for its potential use in clinics, is worth the fan-fare. ‘We are hopeful that this improved performance relates to decreased falls in their everyday life,’ Dr Foreman said. ‘Parkinson’s disease is a progressive disease, and anything we can do to impact the progression is a step in the right direction.’

Article from Daily Mail.

Turn, stop, then sit: A research-based guide for Parkinson’s patients

May 1, 2019 Awareness, Education, Exercise, Research

Tel Aviv University team studies why patients with Parkinson’s disease have difficulty transitioning from walking to sitting, leading to greater instability and falls

People with Parkinson’s disease — a debilitating degenerative disorder that affects the motor system, causing tremors, shaking and rigidity — are known to have difficulty in turning around and then sitting down.

A new Tel Aviv University study provides an understanding as to why these patients may have difficulty transitioning from walking though turning around to sitting. The results suggest new ways to help improve the rehabilitation of these kind of patients.

“Parkinson’s patients can be challenged when they try to turn as they walk,” said Prof. Jeffrey Hausdorff of Tel Aviv University’s Sackler Faculty of Medicine and the Center for the Study of Movement, Cognition, and Mobility at Tel Aviv Sourasky Medical Center.

While most healthy older adults turn and then sit in a precise sequence that clearly distinguishes the two components of the task, in contrast “we found that most Parkinson’s patients start to sit while they are still turning,” he said.

“We originally speculated that, when transitioning from a walking or standing position to a sitting position, people with Parkinson’s would first turn and then start the process of sitting,” Hausdorff said. “But we found that this wasn’t true.”

The research was led by Hausdorff in collaboration with Prof. Anat Mirelman and Prof. Nir Giladi, also of the university and the Tel Aviv Medical Center, and colleagues at Rush University in Chicago. It was published in January in the journal Gait & Posture.

According to the study, when healthy older adults turn to sit, about 80 percent of them complete the turn before starting to sit, in what the researchers called a “distinct strategy.” But in about 20% of the subjects, part of the turning and sitting take place at the same time, in what the researchers called an “overlapping strategy.”

The researchers evaluated the strategies employed by people with Parkinson’s as they transitioned from standing through turning to sitting. In one experiment, 96 participants with Parkinson’s, assessed both on medication and after its effects wore off, were asked to turn to sit while wearing a body-fixed sensor. The researchers then quantified the turning-to-sitting transition and determined whether the distinct or the overlapping strategy had been employed. The use of the sensor revealed subtle but important distinctions that were previously overlooked based on visual observation alone.

The scientists then stratified the cases, using models adjusted for age, gender, height and weight, to identify the associations with their sitting strategies and with the Parkinsonian characteristics and cognition.

“Interestingly, we found that the individuals who employed the overlapping strategy experienced more severe postural instability compared to those who used the distinct strategy,” Hausdorff said.

They also found that anti-Parkinsonian medications did not affect the strategy choice, “suggesting that the decision may be regulated by networks and brain areas that are less directly affected” by the drugs.

Hausdorff said that it is important for people who suffer from Parkinson’s disease and their physical therapists and others to be aware of this issue.

Based on the study, he said in an emailed comment to The Times of Israel, “one can speculate that some of the rehabilitation and continuous care process should be devoted to teaching people with Parkinson’s that when they are turning to sit down, they should break the process into two separate pieces: first turn, briefly stop, and then sit down.”

“This is the way that healthy young and healthy older adults generally carry out this common task,” and they are much less prone to falls than people with Parkinson’s disease, he said.

Stopping along the turn “may, therefore, be safer and less prone to problems than doing this movement all at once,” he said.

Even so, he added, “it remains to be seen” if interventions designed to make this change in the turning process are indeed effective.

Article from Times of Israel.

Digital Management of Parkinson Disease: Is Technology the Future?

May 1, 2019 Education, Life, Research

With the ever-increasing integration of technology into nearly every aspect of modern life, its applications in medicine continue to expand, including in the area of Parkinson disease (PD).

A recent randomized controlled trial of 195 patients with PD, for example, found that physician care delivered via telemedicine into patients’ homes was as effective as in-person care.1 Additional emerging research supports the benefits of other digital tools in this patient population.

In a review published online in the Journal of Parkinson’s Disease, Clint Hansen, PhD, of the Department of Neurology at Christian-Albrechts-Universität Kiel and the University Hospital Schleswig-Holstein, Campus Kiel in Kiel, Germany, and colleagues explored current and future directions regarding the use of technologies such as the electronic health record (EHR) and wearable sensors in PD management.2

Although many institutions and private practices have replaced paper-based medical records with EHRs, there are often limitations on how these are used in clinical decision making. This is likely to change significantly within the next decade, as most “countries with established health structures will then have nationwide provision of innovative EHRs with cloud storage solutions, and most of these EHRs will be patient-controlled,” Dr Hansen and colleagues noted.

In addition, they wrote, EHRs will “communicate with clinical data warehouses that consolidate hospital- and practice-derived data, with population health analytics databases that will provide information about disease risk and prevention, and with digital technology that is used by… the patient.”2 They also expect that moving forward, data protection laws will become more stringent, thus reducing the risk for privacy violations and increasing patient acceptance of EHRs.

With the growing use of digital devices to provide personalized feedback on measures of health, including those worn on the wrist or contained in shoes, it is conceivable that similar tools could be designed to facilitate the continuous monitoring of disease manifestations in patients with PD. These systems “will most probably be easily and widely used and not [require] an active interaction with the user, will be approved by regulatory authorities and the costs will be covered by health insurances,” noted Dr Hansen and colleauges.2

As a template for such devices intended for application in PD, the authors pointed to continuous subcutaneous glucose monitors that are used in patients with diabetes. Other possibilities include integrated detection systems in hearing aids, glasses, and earphones to allow patient interaction with the environment; analysis of mobility data such as reaction times and multitasking ability; insertable cardiac monitors; use of a smartphone as an accelerometer platform to gauge the treatment efficacy of deep brain stimulation; and remote assessment of autonomic features and gut motility. Many of these systems should be easily individualized to each patient.

In another review published in the same journal issue, the authors propose the use of a sensor-based system to analyze gait and detect falls in patients with PD, which would include decision support based on big data sources.3 One benefit of this type of approach is the “standardization of real-life medical data derived from individual patients into longitudinal multimodal disease trajectories…[which] will allow matching and clustering of different patient trajectories for individualized prediction about the expected treatment efﬁcacy of particular interventions,” wrote Jochen Klucken, MD, of the Department of Molecular Neurology at Friedrich-Alexander University, and colleagues, in the Journal of Parkinson’s Disease. “Ultimately, the growing amount of medical data derived from individualized real-life treatment contexts will enable academic and industrial research to further improve objective outcomes and better tailor individual care.”

To glean further insights pertaining to the use of digital health technology in the realm of PD, Neurology Advisor spoke briefly with Alberto J. Espay, MD, MSc, professor of neurology and director and endowed chair of the James J. and Joan A. Gardner Center for Parkinson’s Disease and Movement Disorders at the University of Cincinnati Academic Health Center. Dr Espay is also chair of the Movement Disorders Society Task Force on Technology, which promotes the development of digital health systems that will achieve the goals mentioned above.4

Neurology Advisor: What is a key example of how digital health technologies could be used to improve PD care?

Dr Espay: Digital health technologies have the capacity of capturing intraday fluctuations with the kind of granularity that no scales, diaries, or questionnaires can.

Neurology Advisor: How can clinicians support these developments?

Dr Espay: Clinicians can stimulate their patients’ participation in a variety of technology-integration projects through many organizations. This is a great time to participate and contribute.

There will be a variety of ongoing studies aimed at developing a new version of the diary in electronic format for the digital age, integrated with mobile health technologies (“e-diary/tracker”). This is being coordinated through the Task Force on Technology of the International Parkinson’s and Movement Disorders Society. Efforts such as these are ongoing or will soon occur in many countries in the world.

Neurology Advisor: What should be next steps in terms of research or development in this area?

Dr Espay: The future development of a unifying platform for integrating and synchronizing the data from multiple technologies, one of the goals of the Movement Disorders Society Technology Task Force, could provide the most comprehensive picture of patients’ function than anything we currently have.

Neurology Advisor: Would you like to note any additional takeaways on the topic?

Dr Espay: Technology offers us the means to improving the ends of health care delivery. In the future it will weave seamlessly into patients’ lives to enhance the capture of data, help anticipate periods in which changes are needed, and empower patients to apply strategies to enhance their quality of life.

References

1. Beck CA, Beran DB, Biglan KM, et al. National randomized controlled trial of virtual house calls for Parkinson disease. Neurology. 2017;89(11):1152-1161.

2. Hansen C, Sanchez-Ferro A, Maetzler W. How mobile health technology and electronic health records will change care of patients with Parkinson’s disease. J Parkinsons Dis. 2018;8(Suppl 1):S41-S45.

3. Klucken J, Krüger R, Schmidt P, Bloem BR. Management of Parkinson’s disease 20 years from now: towards digital health pathways. J Parkinsons Dis. 2018;8(Suppl 1):S85-S94.

4. Espay AJ, Bonato P, Nahab FB, et al. Technology in Parkinson’s disease: challenges and opportunities.Mov Disord. 2016;31(9):1272-1282.

Article from NeurologyAdvisor.

Can Imaging Genetics Analysis Effectively Identify Depression In Parkinson Disease?

May 1, 2019 Research

A model using imaging genetics analysis was able to predict and explain the degree of depression in Parkinson disease (PD) with a lower error and higher correlation than other models over a 5-fold cross-validation, according to the results of a study published in PLoS One.

Ji Hye Won, a PhD student from the Department of Electrical and Computer Engineering, Sungkyunkwan University and the Center for Neuroscience Imaging Research, Institute for Basic Science, Suwon, Korea, and colleagues conducted a retrospective analysis of de-identified data. They used diffusion MRI, T1-weighted MRI, and DNA genotyping data obtained from the Parkinson’s Progression Markers Initiative database for 81 patients with PD. Researchers obtained DNA samples genotyped by NeuroX genotyping arrays from the Parkinson’s Progression Markers Initiative and used the least absolute shrinkage and selection operator (LASSO) algorithm to identify regional imaging features that could characterize depression in Parkinson disease. They assessed depression clinically, using the geriatric depression scale.

The investigators identified imaging features that related significantly to the degree of depression, using the LASSO. The selected imaging features correlated strongly with the geriatric depression scale score. Using the LASSO framework, the researchers selected 3 single nucleotide polymorphisms associated with the geriatric depression scale: exm2267347, exm1187499, and exm-rs9303521. The investigators then created a linear regression model with the genetic features from the imaging genetics approach to describe clinical scores suggesting the degree of depression. They constructed other models using imaging and genetic features based on references to validate their models. These models were tested in a 5-fold cross-validation.

The investigators asserted that imaging genetics represents a powerful bottom-up approach to illuminating the mechanisms involved in psychiatric disease. They suggested that imaging genetics could be used to pinpoint neural circuits that translate genetic influences into behavior.

“Our model combining imaging and genetics information could be applied whenever a patient undergoes new imaging and thus could be used for the early prediction of depression. If detected, patients could be directed to many non-drug therapy options that are only available in the early stages of depression,” the researchers concluded.

Article from PsychiatryAdvisor.

Manganese and Parkinson’s: Mechanism may explain link

April 1, 2019 Research

New research, published in the journal Science Signaling, details the mechanism through which exposure to manganese can trigger protein misfolding in the brain — which may, in turn, lead to Parkinson’s-like symptoms. The findings may enable an earlier diagnosis of the neurological condition.

Manganese is an essential nutrient present in “legumes, pineapples, beans, nuts, tea, and grains.”

In the human body, manganese aids blood sugar regulation, bone formation, and immunity.

However, exposure to excessive levels of manganese may trigger Parkinson’s-like neurological symptoms. Manganese builds up in the basal ganglia area of the brain.

Researchers have known about these links between manganese and Parkinson’s for decades, but new research helps elucidate the mechanisms behind these associations.

Anumantha Kanthasamy, the Linda Lloyd Endowed Chair of Neurotoxicology at Iowa State University in Ames, led the new research.

Manganese helps transfer a faulty protein

Parkinson’s disease is characterized by clumps formed by misfolded alpha-synuclein protein. These protein aggregates are toxic to neurons.

Kanthasamy and colleagues set out to investigate how these misfolding proteins might interact with manganese to trigger the progression of Parkinson’s.

To do so, they examined data from mice and blood serum samples collected from eight welders. As a group, welders have a higher risk of prolonged manganese exposure. The research also examined a control group of 10 people.

The analyses revealed that welders with exposure to manganese had higher levels of misfolded alpha-synuclein, which puts them at a higher risk of Parkinson’s.

Additional cell culture tests showed that misfolded alpha-synuclein was secreted through small vesicles called exosomes into the extracellular space. In other words, the vesicles enabled the proteins to travel from cell to cell and further spread the misfolded protein.

The scientists also isolated alpha-synuclein-containing exosomes from alpha-synuclein-expressing cells that had exposure to manganese and delivered them to a brain area in the mice called the corpus striatum. This induced Parkinson’s-like symptoms in the mice.

Manganese seemed to accelerate the “cell-to-cell transmission” of alpha-synuclein, which, in turn, led to neurotoxicity. Kanthasamy and colleagues explain:

“Together, these results indicate that [manganese] exposure promotes [alpha-synuclein] secretion in exosomal vesicles, which subsequently evokes proinflammatory and neurodegenerative responses in both cell culture and animal models.”

“[W]e identified a possible mechanism involving the exosome-mediated, cell-to-cell transmission of [alpha-synuclein] during exposure to the environmental neurotoxicant,” write the authors.

Findings may lead to earlier detection

According to the National Institutes of Health (NIH), around 50,000 individuals in the United States receive a diagnosis of Parkinson’s each year, and 500,000 people currently live with the condition.

Though the condition does not yet have a cure, diagnosing it earlier may prevent irreversible brain damage and help accelerate human clinical trials of new drugs.

The results that Kanthasamy and colleagues have just published may help scientists devise a new diagnostic test for Parkinson’s that could detect the disease much earlier on. The results may also help scientists test how effective new Parkinson’s drugs are.

“As the disease advances, it’s harder to slow it down with treatments,” Kanthasamy says. He adds: “Earlier detection, perhaps by testing for misfolded alpha-synuclein, can lead to better outcomes for patients. Such a test might also indicate whether someone is at risk before the onset of the disease.”

However, the study authors also caution that their findings are still experimental, and that such a diagnostic test may not be available for years.

Article from Medical News Today.

Can We Repair the Brain?

March 1, 2019 Research

Cell replacement may play an increasing role in alleviating the motor symptoms of Parkinson’s disease (PD) in future. Writing in an open access special supplement to the Journal of Parkinson’s Disease, experts describe how newly developed stem cell technologies could be used to treat the disease and discuss the great promise, as well as the significant challenges, of stem cell treatment.

The most common PD treatment today is based on enhancing the activity of the nigro-striatal pathway in the brain with dopamine-modulating therapies, thereby increasing striatal dopamine levels and improving motor impairment associated with the disease. However, this treatment has significant long-term limitations and side effects. Stem cell technologies show promise for treating PD and may play an increasing role in alleviating at least the motor symptoms, if not others, in the decades to come.

“We are in desperate need of a better way of helping people with PD. It is on the increase worldwide. There is still no cure, and medications only go part way to fully treat incoordination and movement problems,” explained co-authors Claire Henchcliffe, MD, DPhil, from the Department of Neurology, Weill Cornell Medical College, and Department of Neurosurgery, Memorial Sloan Kettering Cancer Center, New York, NY, USA; and Malin Parmar, PhD, from the Wallenberg Neuroscience Center and Lund Stem Cell Center, Lund University, Lund, Sweden. “If successful, using stem cells as a source of transplantable dopamine-producing nerve cells could revolutionize care of the PD patient in the future. A single surgery could potentially provide a transplant that would last throughout a patient’s lifespan, reducing or altogether avoiding the need for dopamine-based medications.”

The authors have analyzed how newly developed stem cell technologies could be used to treat PD, and how clinical researchers are moving very quickly to translate this technology to early clinical trials. In the past, most transplantation studies in PD used human cells from aborted embryos. While these transplants could survive and function for many years, there were scientific and ethical issues: fetal cells are in limited supply, and they are highly variable and hard to quality control. Only some patients benefited, and some developed side effects from the grafts, such as uncontrollable movements called dyskinesias.

Recent strides in stem cell technology mean that quality, consistency, activity, and safety can be assured, and that it is possible to grow essentially unlimited amounts of dopamine-producing nerve cells in the laboratory for transplantation. This approach is now rapidly moving into initial testing in clinical trials. The choice of starting material has also expanded with the availability of multiple human embryonic stem cell lines, as well as the possibilities for producing induced pluripotent cells, or neuronal cells from a patient’s own blood or skin cells. The first systematic clinical transplantation trials using pluripotent stem cells as donor tissue were initiated in Japan in 2018.

“We are moving into a very exciting era for stem cell therapy,” commented Dr. Parmar. “The first-generation cells are now being trialed and new advances in stem cell biology and genetic engineering promise even better cells and therapies in the future. There is a long road ahead in demonstrating how well stem cell-based reparative therapies will work, and much to understand about what, where, and how to deliver the cells, and to whom. But the massive strides in technology over recent years make it tempting to speculate that cell replacement may play an increasing role in alleviating at least the motor symptoms, if not others, in the decades to come.”

“With several research groups, including our own centers, quickly moving towards testing of stem cell therapies for PD, there is not only a drive to improve what is possible for our patients, but also a realization that our best chance is harmonizing efforts across groups,” added Dr. Henchcliffe. “Right now, we are just talking about the first logical step in using cell therapies in PD. Importantly, it could open the way to being able to engineer the cells to provide superior treatment, possibly using different types of cells to treat different symptoms of PD like movement problems and memory loss.”

“This approach to brain repair in PD definitely has major potential, and the coming two decades might also see even greater advances in stem cell engineering with stem cells that are tailor-made for specific patients or patient groups,” commented Patrik Brundin, MD, PhD, Van Andel Research Institute, Grand Rapids, MI, USA, and J. William Langston, MD, Stanford Udall Center, Department of Pathology, Stanford University, Palo Alto, CA, USA, Editors-in-Chief of the Journal of Parkinson’s Disease. “At the same time, there are several biological, practical, and commercial hurdles that need circumventing for this to become a routine therapy.”

Article from IOS Press.

Coffee and Parkinson’s: Protection in the Making?

March 1, 2019 Research

For years, drinking coffee has been associated with having a reduced risk of developing Parkinson’s disease (PD). In fact, a 1968 study suggested that coffee drinkers were less like to get PD (Nefzger, Quadfasel, & Karl, 1968). Since then, multiple epidemiologic studies have confirmed the PD/coffee connection (Ascherio et al., 2003; Ascherio et al., 2004; Fujimaki et al., 2018). Researchers have mostly attributed the protective effect to the caffeine component (Lee et al., 2013).

However, coffee is more than a caffeine delivery system. Coffee has more than 1,000 different compounds, including organic acids, sugars, amino acids and fatty acids. One such fatty acid called Eicosanoyl-5-hydroxytryptamide (EHT) has been getting quite a bit of buzz in the PD research community; and, for good reason. A recently published study titled, “Synergistic neuroprotection by coffee components eicosanoyl-5-hydroxytryptamide and caffeine in models of Parkinson’s disease and DLB” (Yan et al., 2018), provides some compelling insights into the possible biochemical protective mechanisms of our cup of joe. A recently published study in the journal, Neuropsychopharmacology, sought to determine if having ADHD and/or its treatment, increases the risk of having basal ganglia and cerebellar diseases. In this 20-year follow-up retrospective cohort study, a total of 190,586 patient records (31,796 with ADHD and 158,790 without ADHD) from Utah were examined. People with no prior PD diagnosis or symptoms, no basal ganglia/cerebellar disease and those with a history of substance abuse were excluded from participating in the study.

Here’s what the researchers did: over a six-month period, they treated groups of two different PD model mice with various combinations of caffeine and EHT (caffeine alone, EHT alone, or caffeine and EHT together) to study their effects on both brain and behavior. There was also a group of mice that received no treatment. Then they performed several behavioral tests to study their movement, as well as study their brains for signs of alpha-synuclein clumps (which result in Lewy bodies, the pathological hallmark of PD), neurodegeneration and inflammation. The study found that the untreated mice had significant amounts of clumped α-synuclein in their brains, increased inflammation and loss of neurons, as well as significant deficits on three different behavioral tests. In general, the mice treated with EHT or caffeine alone showed either no or minimal improvement in any of these measures. However, the mice treated with the combination of EHT and caffeine together showed significant improvements in all of these measures.

Results

More specifically, mice treated with both EHT and caffeine together:
Had less alpha-synuclein clumping in the brain
Maintained better neuron integrity and function
Had less brain inflammation
Displayed less movement symptoms

What Does This Mean?

In this study, a synergistic combination of EHT and caffeine was shown to slow down the progression of the neurodegeneration associated with PD in mice — which has potentially readily available therapeutic implications. In addition, previous research has demonstrated that caffeine enhances dopamine signaling in the brain (Volkow et al., 2015); and, it’s the death of dopamine-producing cells that results in movement symptoms of PD (and why dopamine replacement medication is the gold standard treating PD symptoms).

For years, coffee consumption has been suggested to play a protective role in developing PD. However, it was never clear what exactly in coffee had this effect. This study suggests that two compounds, caffeine and the fatty acid EHT, work together to protect against alpha- synuclein clumps and dopamine neuron loss in two different PD models of mice. Interestingly, these effects were seen even using very low doses of the compounds. If the results of this study can be replicated by other researchers, then identifying that delicate balance of safety and effectiveness for humans is likely an essential step that researchers will be investigating in the future.

References

Ascherio, A., Chen, H., Schwarzschild, M. A., Zhang, S. M., Colditz, G. A., & Speizer, F. E. (2003). Caffeine, postmenopausal estrogen, and risk of Parkinson’s disease. Neurology, 60(5), 790-795.

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Coffee and Parkinson’s: Protection in the Making?

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Coffee and Parkinson’s: Protection in the Making?