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But meta-analysis includes only two Taiwanese claims studies
VANCOUVER -- A common insomnia drug may raise the risk of developing Parkinson's disease, according to a meta-analysis presented here.
Although only two studies were of high enough quality to be included in the review, pooled data showed a 2.5-fold increased risk of Parkinson's disease among patients taking zolpidem (Ambien), Salman Hussain, PhD, of Hamdard University in New Delhi in India, reported at the Movement Disorders Society meeting here:
The hitch was that both of these retrospective, observational studies relied on a health claims database from Taiwan, and thus can't be generalized to other populations, Hussain cautioned.
"We found that there's an increased risk of getting Parkinson's disease among zolpidem users, but to confirm the association and make it robust, more study is needed, Hussain told MedPage Today.
It's not clear as to why zolpidem may raise the risk of developing Parkinson's, he said. It's highly selective for GABAA receptors, and two decades ago it was actually being investigated as a treatment for Parkinson's disease. But the two studies in the meta-analysis -- one by Yang et alpublished in 2014, and the other byHuang et al in 2015 -- found the sleep aid was associated with a higher risk of Parkinson's.
For their review, Hussain and colleagues searched the PubMed, Cochrane, and Embase databases for studies assessing any potential links between zolpidem and Parkinson's, using the Newcastle-Ottawa Scale to rate study quality.
Ultimately, they came up with only two retrospective, observational studies, both of which relied on the National Health Insurance Research Database from Taiwan.
The Yang study included 101,719 patients treated for 5 years, and the Huang study included 14,805 patients treated for 10 years. There were 42,171 zolpidem users and 809 Parkinson's cases in the Yang study and 2,961 zolpidem users and 157 Parkinson's cases in the Huang study.
Overall, both the Yang study (RR 2.57, 95% CI 2.22 to 2.96) and the Huang study (RR 2.62, 95% CI 2.15 to 3.19) revealed a higher risk of developing Parkinson's among zolpidem users. The Huang study subjects had taken zolpidem for at least 3 months, and the relationship with Parkinson's was more prevalent among those who had depression. In the Yang study, there was a U-shaped relationship between number of doses of zolpidem and Parkinson's risk.
When pooling the data, Hussain and colleagues found a significantly increased risk of developing Parkinson's disease among those taking zolpidem (RR 2.58, 95% CI 2.30 to 2.90).
Although the findings indicate a possible link between zolpidem and development of Parkinson's disease, Hussain urged that more robust evidence is needed, particularly from well-designed randomized controlled trials.
Summary: Researchers have identified a neural system involved in making decisions based on preference.
Source: University of Glasgow.
Previously it was unclear where the brain implements preference-based choices and whether it uses a mechanism similar to when we make decisions purely based on the perceptual properties of the alternatives (like choosing the bigger of two items). NeuroscienceNews.com image is credited to University of Glasgow.
Researchers have found a direct window into the brain systems involved in making every day decisions based on preference.
The study, led by a team of neuroscientists at the University of Glasgow’s Institute of Neuroscience and Psychology, and published today in Nature Communications, offers crucial insight into the neural mechanisms underlying our decision-making process, opening up new avenues for the investigation of preference-based choices in humans.
Whether we decide to opt for a piece of apple or a piece of cake is, for example, a preference-based decision. How our brains arrive at such decisions – as well as choices that rely on our subjective valuation of different alternatives – is currently a popular research topic.
Previously it was unclear where the brain implements preference-based choices and whether it uses a mechanism similar to when we make decisions purely based on the perceptual properties of the alternatives (like choosing the bigger of two items).
Study lead Dr Philiastides said: “Our research suggests that preference-based and perceptual decisions might share a common underlying mechanism in the brain. Our findings also suggest that preference-based decisions might be represented in the same brain areas that plan the action to execute the decision, i.e. the hand reaching to grab the preferred item.”
He added: “Our findings have important implications for a broad range of socioeconomic problems ranging from public policy analysis, like informing health behaviours, to brain-informed advertisement strategies and product design.
“In addition, the work can improve our understanding of mental and neurodegenerative disorders known to compromise one’s decision-making faculties, like depression, schizophrenia and Parkinson’s disease by offering a direct window into the brain systems involved in goal-directed choices.”
The study presented participants with pairs of snacks, like a chocolate bar and a pack of crisps, and asked them to choose their preferred item. To identify the brain areas involved in these decisions, the team used a state-of-the-art multimodal brain imaging procedure. Volunteers wore an EEG cap (to measure their brain electrical activity) whilst being simultaneously scanned in an MRI machine.
An EEG cap records neural activity (tiny electrical signals on the surface of the scalp), providing information about “when” a certain event takes place in the brain and how it unfolds in time, while functional MRI provides information on “where” this activity happens in the brain.
The EEG revealed that decision activity unfolds gradually over time and persists until one commits to a choice. This EEG activity was then localised with fMRI in the posterior medial frontal cortex of those who participated in the study, a brain region that has not been previously linked directly with preference-based decisions.
Andrea Pisauro, the first author of the paper, said: “This is similar to when we make perceptual decisions, like choosing the larger of two slices of cake. The brain accumulates information supporting one of the decision alternatives until an internal criterion is reached and a decision is made.”
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Funding: The work was funded by the BBSRC and ESRC.
Image Source:NeuroscienceNews.com image is credited to University of Glasgow.
Original Research: Full open access research for “Neural correlates of evidence accumulation during value-based decisions revealed via simultaneous EEG-fMRI” by M. Andrea Pisauro, Elsa Fouragnan, Chris Retzler & Marios G. Philiastides in Nature Communications. Published online June 9 2017 doi:10.1038/ncomms15808
Abstract
Neural correlates of evidence accumulation during value-based decisions revealed via simultaneous EEG-fMRI
Current computational accounts posit that, in simple binary choices, humans accumulate evidence in favour of the different alternatives before committing to a decision. Neural correlates of this accumulating activity have been found during perceptual decisions in parietal and prefrontal cortex; however the source of such activity in value-based choices remains unknown. Here we use simultaneous EEG–fMRI and computational modelling to identify EEG signals reflecting an accumulation process and demonstrate that the within- and across-trial variability in these signals explains fMRI responses in posterior-medial frontal cortex. Consistent with its role in integrating the evidence prior to reaching a decision, this region also exhibits task-dependent coupling with the ventromedial prefrontal cortex and the striatum, brain areas known to encode the subjective value of the decision alternatives. These results further endorse the proposition of an evidence accumulation process during value-based decisions in humans and implicate the posterior-medial frontal cortex in this process.
“Neural correlates of evidence accumulation during value-based decisions revealed via simultaneous EEG-fMRI” by M. Andrea Pisauro, Elsa Fouragnan, Chris Retzler & Marios G. Philiastides in Nature Communications. Published online June 9 2017 doi:10.1038/ncomms15808
Summary: According to researchers, people who consumed at least three servings of low fat dairy a day were had a 34% higher risk of developing Parkinson’s disease.
Source: AAN.
Those who consumed at least three servings of low-fat dairy a day had a 34 percent greater chance of developing Parkinson’s than people who consumed less than one serving per day. NeuroscienceNews.com image is for illustrative purposes only.
Consuming at least three servings of low-fat dairy a day is associated with a greater risk of developing Parkinson’s disease compared to consuming less than one serving a day, according to a large study published in the June 7, 2017, online issue of Neurology. In addition, drinking more than one serving of low-fat or skim milk per day is associated with a greater risk of developing Parkinson’s disease compared to drinking less than one serving per week. The study results do not show that dairy products cause Parkinson’s disease–they just show an association.
“Our study is the largest analysis of dairy and Parkinson’s to date,” said Katherine C. Hughes, ScD, of the Harvard T.H. Chan School of Public Health in Boston. “The results provide evidence of a modest increased risk of Parkinson’s with greater consumption of low-fat dairy products. Such dairy products, which are widely consumed, could potentially be a modifiable risk factor for the disease.”
For the study, researchers analyzed approximately 25 years of data on 80,736 women enrolled in the Nurses’ Health Study and 48,610 men enrolled in the Health Professionals’ Follow-up Study. Participants in these studies completed health questionnaires every two years and diet questionnaires every four years. During that time, 1,036 people developed Parkinson’s.
Researchers examined what kinds of dairy each person consumed, including milk, cream, cheese, yogurt, ice cream, butter, margarine and sherbet. They then looked at whether full-fat dairy, as whole milk, was associated with a risk of Parkinson’s disease; there was no association. However, those who consumed at least three servings of low-fat dairy a day had a 34 percent greater chance of developing Parkinson’s than people who consumed less than one serving per day. The researchers also found that when looking specifically at skim and low-fat milk consumption, there was a 39 percent greater chance of developing Parkinson’s for people who consumed more than one serving per day compared to those who consumed less than one serving per week. Eating sherbet or frozen yogurt also was linked to a modest increased risk.
In a meta-analysis, looking at a group of studies, the researchers found that total dairy intake was associated with an increased risk of Parkinson’s disease.The overall conclusions from these studies was that frequent consumption of dairy products was associated with a modest increased risk of Parkinson’s disease.
It is important to note that the risk of developing Parkinson’s was still very low. Of the 5,830 people who consumed at least three servings per day of low-fat dairy at the start of the study, only 60 people, or 1 percent, developed the disease over the study period. In comparison, of the 77,864 people who consumed less than one serving per day of low-fat dairy, 483 people, or 0.6 percent, developed Parkinson’s.
“Frequently consuming low-fat dairy products was associated with a modest increased risk of Parkinson’s disease,” said Hughes.One limitation of the study was that early Parkinson’s symptoms may have affected the dietary behaviors and questionnaire responses of study participants.
More research is needed before recommendations can be made about dairy consumption.
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Funding: The study was supported by the National Institutes of Health and the U.S. Department of Defense.
Summary: Researchers solve a long standing mystery of the neural mechanism behind the Lombard effect.
Source: Johns Hopkins University.
This is a bat trained to stand on a platform and await delivery of its prey. NeuroscienceNews.com image is adapted from the Johns Hopkins University news release.
Astonishingly speedy brain mechanism helps bats get louder when necessary.
When trying to be heard over noise, humans and animals raise their voices. It’s a split-second feat, from ear to brain to vocalization, and Johns Hopkins University researchers are the first to measure just how fast it happens in bats: 30 milliseconds. That’s just a tenth of the time it takes to blink an eye, and a record for audio-vocal response.
Because this action, known as the Lombard effect, happens so very fast, the researchers were also able to solve a longtime mystery regarding the neural mechanism behind it. In a paper published online this week by the journal Proceedings of the National Academy of Sciences, they conclude it must be a fundamental temporal reflex rather than, as previously thought, a deeper cognitive behavior that would take more processing time. The findings, which shed light on the underpinnings of human speech control, also reveal how species as diverse as fish, frogs, animals and people share the ability to be heard over the fray.
“Scientists have been wondering for a century: Could there be a common auditory process to explain how this phenomenon happens in fish to frogs to birds to humans, species with wildly different hearing systems?” said co-author Ninad Kothari, a Johns Hopkins graduate student in psychological and brain sciences. “We resolved this question.”
The new information could lead to better treatment for diseases where the Lombard effect can be amplified, such as Parkinson’s disease, and could also help to build assistive medical devices.
The researchers studied bats, which rely on sonar-like echolocation — emitting sounds and listening for echoes — to detect, track, and catch prey. Unlike humans, whose vocalizations are comparatively long and slow, bats are ideal for such a sensorimotor study. Their high-frequency chirps, undetectable to the human ear, are quick and precise, allowing researchers to test the limits of a mammalian brain.
The team trained big brown bats to remain perched on a platform while tracking insects moving towards them on a tether. While the bat hunted the insect, the researchers recorded the bat’s vocalizations with an array of 14 microphones. Sometimes the researchers allowed the bat to hunt in silence, other times they played bursts of interfering white noise, at varying intensities, from a speaker positioned in front of the bat.
The white noise interfered with the bat’s echolocation and caused the bat to emit louder and louder chirps, not unlike someone trying to be heard, first over a loud radio, then over the clamor of a lawn mower and then over the blare of a passing fire engine. When the noise stopped, the bat would stop shouting, so to speak, and vocalize at a more typical level.
The researchers, who were able to create a computational model for the Lombard effect that applies to all vertebrates, concluded that the brain of a bat, or a person, or a fish, constantly monitors background noise and adjusts the vocal level as necessary.
First the auditory system detects background noise. The auditory system then measures the sound pressure level and adjusts the vocalization amplitude to compensate. When the background noise ends, the sound pressure level dissipates, and so does the level of vocalization.
This entire elaborate process happens in just 30 milliseconds, the authors found. Even in terms of near-instantaneous brain reactions, they call this reflex “remarkably short.”
“Typically, we breathe every three to five seconds, our heart beats once per second, and eye blinking takes one third of a second. If we believe that eye blinking is fast, the speed at which an echolocating bat responds to ambient noise is truly shocking: 10 times faster than we blink our eyes,” said lead author Jinhong Luo, a Johns Hopkins postdoctoral fellow.
Scientists had believed the Lombard effect was much slower: about 150 milliseconds for birds and bats and approximately150 to 175 milliseconds for humans.
“Our study features echolocating bats as valuable animal models for understanding connections between hearing and vocalizations, including speech control in humans,” said Cynthia Moss, a Johns Hopkins professor of psychological and brain sciences and of neuroscience and a co-author.
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Funding:Support for this research came from the National Science Foundation (IOS-1010193 and IOS-1460149), the Human Frontiers Science Program (RGP0040 and LT000279/2016-L9, the Office of Naval Research (N00014-12-1-0339), and the Air Force Office of Scientific Research (FA9550-14-1-0398).
Image Source:NeuroscienceNews.com image is adapted from the Johns Hopkins University news release.
Video Source:Video credited to JHU.
Original Research:Abstract for “Sensorimotor integration on a rapid time scale” by Jinhong Luo, Ninad B. Kothari, and Cynthia F. Moss in PNAS. Published online June 5 2017 doi:10.1073/pnas.1702671114
Abstract
Sensorimotor integration on a rapid time scale
Sensing is fundamental to the control of movement: From grasping objects to speech production, sensing guides action. So far, most of our knowledge about sensorimotor integration comes from visually guided reaching and oculomotor integration, in which the time course and trajectories of movements can be measured at a high temporal resolution. By contrast, production of vocalizations by humans and animals involves complex and variable actions, and each syllable often lasts a few hundreds of milliseconds, making it difficult to infer underlying neural processes. Here, we measured and modeled the transfer of sensory information into motor commands for vocal amplitude control in response to background noise, also known as the Lombard effect. We exploited the brief vocalizations of echolocating bats to trace the time course of the Lombard effect on a millisecond time scale. Empirical studies revealed that the Lombard effect features a response latency of a mere 30 ms and provided the foundation for the quantitative audiomotor model of the Lombard effect. We show that the Lombard effect operates by continuously integrating the sound pressure level of background noise through temporal summation to guide the extremely rapid vocal-motor adjustments. These findings can now be extended to models and measures of audiomotor integration in other animals, including humans.
“Sensorimotor integration on a rapid time scale” by Jinhong Luo, Ninad B. Kothari, and Cynthia F. Moss in PNAS. Published online June 5 2017 doi:10.1073/pnas.1702671114
Summary: CRISPR technology allows researchers to illuminate and monitor alpha synuclein in the brain.
Source: University of Central Florida.
Using the CRISPR technique, the Burnett team edited the alpha-synuclein gene and inserted a luminescent tag made from proteins that causes fireflies to light up. Every time the cell creates the alpha-synuclein protein, the tag gives off a light. NeuroscienceNews.com image is for illustrative purposes only.
A team of researchers at the University of Central Florida is using breakthrough gene-editing technology to develop a new screening tool for Parkinson’s disease, a debilitating degenerative disorder of the nervous system. The technology allows scientists in the lab to “light up” and then monitor a brain protein called alpha-synuclein that has been associated with Parkinson’s.
“Alpha-synuclein is a protein that is normally found in the brain. We all have it,” said Burnett School of Biomedical Sciences doctoral student Levi Adams, one of the lead researchers on the project. “But for some reason, when you have Parkinson’s the levels become abnormal. So if we can monitor this protein in the cell, we can start to measure what causes it to go up and also what treatments can cause it to go down.”
The team published its findings in the Scientific Reports journal. The National Institutes of Health (5R21NS088923-02 ) funded the work. The researchers believe their work is a crucial step toward identifying new drug therapies for Parkinson’s disease.
Adams is partnering with doctoral student Sambuddha Basu, associate professor and neurosciences researcher, Associate Professor Yoon-Seong Kim, and scientist Subhrangshu Guhathakurta to study Parkinson’s, which affects motor functions caused by a gradual loss of brain cells. There are about 60,000 new cases of Parkinson’s each year in the United States.
They are using CRISPR Cas9 (Clustered Regularly Interspaced Short Palindromic Repeats) gene-editing technology. The system is one of research’s fastest growing biomedical techniques that allows scientists to make specific changes in the DNA of plants and animals while not killing cells. The system is becoming instrumental in studying genetically based treatments for diseases including cancer and Parkinson’s.
“It’s the most powerful and widely used gene-editing technique in use because it allows us to change the DNA in living cells,” said Kim, who is also a medical doctor. “The innovation of this method is that it enables us to monitor this gene in real-time without killing the cell. Without the CRISPR Cas-9 method, you would have to extract all the proteins from the cell to measure them, which kills the cell.”
Using the CRISPR technique, the Burnett team edited the alpha-synuclein gene and inserted a luminescent tag made from proteins that causes fireflies to light up. Every time the cell creates the alpha-synuclein protein, the tag gives off a light. That reaction “makes it much easier to measure,” Adams said. “More light means an increased level of alpha-synuclein, which would be considered a diseased state.”
The team found that measuring light was a reliable method to measure alpha-synuclein production.
“If we take one of these modified cells and treat it with a particular drug, if it doesn’t produce light anymore, then this means the drug is a potential treatment for this disease,” Basu said.
With the engineered cells, researchers can screen new and existing drugs to see how they regulate alpha-synuclein level in patients.
“With an easy-to-measure reporter like light production, this will allow us to do high throughput screening, where you can test a large panel of drugs at once,” Guhathakurta said.
With the new technology, the scientists hope to identifying ways to reduce alpha-synuclein production that can possibly prevent Parkinson’s or its progression in patients diagnosed with the disease.
The team said research will focus on what aspects of the alpha- synuclein protein kill neurons during Parkinson’s disease.
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Funding: The study was funded by National Institutes of Health.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research:Full open access research for “A novel tool for monitoring endogenous alpha-synuclein transcription by NanoLuciferase tag insertion at the 3′end using CRISPR-Cas9 genome editing technique” by Sambuddha Basu, Levi Adams, Subhrangshu Guhathakurta & Yoon-Seong Kim in Scientific Reports. Published online April 4 2017 doi:10.1038/srep45883
Abstract
A novel tool for monitoring endogenous alpha-synuclein transcription by NanoLuciferase tag insertion at the 3′end using CRISPR-Cas9 genome editing technique
α-synuclein (α-SYN) is a major pathologic contributor to Parkinson’s disease (PD). Multiplication of α-SYN encoding gene (SNCA) is correlated with early onset of the disease underlining the significance of its transcriptional regulation. Thus, monitoring endogenous transcription of SNCA is of utmost importance to understand PD pathology. We developed a stable cell line expressing α-SYN endogenously tagged with NanoLuc luciferase reporter using CRISPR/Cas9-mediated genome editing. This allows efficient measurement of transcriptional activity of α-SYN in its native epigenetic landscape which is not achievable using exogenous transfection-based luciferase reporter assays. The NanoLuc activity faithfully monitored the transcriptional regulation of SNCA following treatment with different drugs known to regulate α-SYN expression; while exogenous promoter-reporter assays failed to reproduce the similar outcomes. To our knowledge, this is the first report showing endogenous monitoring of α-SYN transcription, thus making it an efficient drug screening tool that can be used for therapeutic intervention in PD.
“A novel tool for monitoring endogenous alpha-synuclein transcription by NanoLuciferase tag insertion at the 3′end using CRISPR-Cas9 genome editing technique” by Sambuddha Basu, Levi Adams, Subhrangshu Guhathakurta & Yoon-Seong Kim in Scientific Reports. Published online April 4 2017 doi:10.1038/srep45883
