Our presentation at Society for Neuroscience meeting in SanDiego

reposted from 

https://community.sfn.org/t/poster-highlight-dance-for-parkinsons-disease/9593

Dance for Parkinson’s Disease

During a Gairdner award lecture by Dr. Eric Kandel at the Toronto Reference Library, Kandel prescribed 2 miles of walking a day for protecting against age-related memory declines. Kandel, Nobel prize laureate and expert on the neurobiological basis of memory, described how his research demonstrates that osteocalcin mediates long-term memory formation. Osteocalcin is a hormone released from bones particularly during weight-bearing exercises such as walking.

Fast-forward one year to SFN 2018 in San Diego: Instead of walking, “Dr. Kandel, you should try dancing!” joked Dr. Joseph DeSouza, York University researcher who examines the effects of dance on Parkinson’s Disease.

“I do love some salsa!”, laughed Dr. Eric Kandel, now 88 years old.

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(Left to right: Dr. Joseph DeSouza, Dr. Torsten Wiesel, Dr. Eric Kandel, and unknown)

Parkinson’s disease is a neurodegenerative disorder in which there is degeneration of dopaminergic cells in the substantia nigra which causes a host of motor symptoms such as tremors and slow, stiff movements. Dr. DeSouza’s poster presentation displays research conducted by PhD student Karolina Bearss. Their research examined the effect of dance lessons on the progression of Parkinson’s disease. They used both behavioural and neuroimaging methods which included Unified Parkinson’s Disease Rating Scale to measure the behavioural symptoms of the disease and functional neuroimaging to assess neural changes caused by training. They showed that weekly exercise classes protected against disease progression in the behavioural measure. The neuroimaging analysis is still ongoing however, the preliminary results suggest that the behavioural protection afforded by the dance lessons may be attributable to increased activation in the supplementary motor area.

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Dance is a highly complex social activity which involves coordination of movements to an instructor and music. This workout for the body is certainly also a workout for the brain. While enjoying San Diego, hopefully you get to experience some of the local culture, put on your own dancing shoes, and experience some of the same benefits as the patients with Parkinson’s disease.

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Dana Swarbrick
See more on Twitter: @DanaSwarbrick

reposted from https://www.frontiersin.org/articles/10.3389/fneur.2018.00068/full  and it suggests how important circadian rhythms are for life.....

EDITORIAL ARTICLE

Front. Neurol., 16 February 2018 | https://doi.org/10.3389/fneur.2018.00068

Editorial: Intrinsic Clocks

Timo Partonen1* and Daniela D. Pollak2

• 1Department of Public Health Solutions, National Institute for Health and Welfare (THL), Helsinki, Finland
• 2Department of Neurophysiology and Neuropharmacology, Medical University of Vienna, Vienna, Austria

Editorial on the Research Topic

Intrinsic Clocks

The existence of living organisms on our planet has been dependent on and co-evolved with the foreseeable variations in environmental conditions oscillating over recurring periods. All species have responded to these exogenous rhythms by developing endogenous clocks that allow for an approximate, but reliable estimation of the periodic changes and elicit corresponding adaptive processes.

The importance of these mechanisms for health and disease has been highlighted by the 2017 award of the Nobel Prize in Physiology or Medicine to Jeffrey C. Hall, Michael Rosbash, and Michael W. Young for their discoveries of the genetic control of the daily biological rhythm. They explained in molecular terms how the gene named as period contributed to the emergence (eclosion from the pupal case) rhythm of a population and to the locomotor activity of individual flies (Drosophila melanogaster). The key to the explanation was the discovery of transcription-translation feedback loops of the so-called “clock genes.”

This research topic on Intrinsic Clocks which appeared earlier comprises a well-balanced collection of original research and review articles on endogenous rhythms from seasonal and monthly to daily and hourly oscillations in different experimental model systems with analytical approaches from systemic to cellular and molecular levels.

Serchov and Heumann in their review focus on the role of Ras, an enzyme which hydrolyzes guanosine triphosphate and dependent intracellular signaling cascades in the regulation of the circadian rhythm in mice. They elegantly summarize how Ras activity forms a molecular bridge between entrainment of the suprachiasmatic nucleus that is the master clock in the brain and synaptic plasticity in dependent brain regions, such as the hippocampus, and corresponding functions. The extensive study by Chiang et al. specifically investigated rhythmic alterations in the murine hippocampus. They characterized the protein phosphorylation using a mass spectrometry approach with which they provided large-scale quantitative analysis of the daily oscillation of hippocampal phosphorylation events over a range of biological pathways. The hippocampus is a key focus also in the review by Urs Albrecht. It features the role of circadian proteins in the control of adult hippocampal neurogenesis, reciprocally implicated in depression and antidepressant responses. He discusses neurobiological mechanisms implicated in the pathogenesis of mood disorders, such as monoaminergic neurotransmission and stress response by the hypothalamic–pituitary–adrenal axis. The hypothalamus and the pituitary are further involved in seasonal cycles as highlighted in the review by Lewis and Ebling who elaborate in detail on the role of tanycytes, pituitary radial glial cells, in the regulation of circannual clocks in hamsters. They provide evidence supporting their hypothesis that tanycytes serve as central organizers of seasonal rhythms in the adult hypothalamus. Raible et al. present in their review on marine animals the current insight in the cellular mechanisms in molecular detail the monthly or semi-monthly rhythms. They express their worry about light pollution and further review the relevance of circalunar rhythms to mammalian physiology and reproduction in specific. They speculate that these rhythms may be the remnant of evolutionary ancient clocks, which were uncoupled from a natural entrainment mechanism.

Bourguignon and Storch summarize recent findings of the cellular substrate and mechanism, which generate locomotor activity with periods of 2–6 h. Such rhythms are normally integrated with circadian rhythms, but often lack the period stability and expression robustness. They further review the concept of the dopaminergic ultradian oscillator and show that ultradian locomotor rhythms rely on cells in the brain using dopamine for transmission. Intriguingly, Monje et al. report in their study on interleukin-6 knockout mice that the ultradian locomotor rhythm was impaired under both light-entrained and free-running conditions, whereas the circadian period and the level of locomotor activity as well as the phase shift response to light exposure at night remained normal. During the day, Cry1 and Bhlhe41 expression levels were increased whereas those of Nr1d2 were decreased in the hippocampus. Liu and Zhang first created mutants of cryptochrome circadian clock 1 (Cry1) protein at potential phosphorylation sites and conducted thereafter a screen in Cry1/Cry2 double deficient cells. They targeted at identifying mutations that disrupted circadian rhythms. They found that these single amino acid substitutions changed not only the circadian period, but also repression activity, protein stability, or cellular localization of the protein. Concerning the circadian period, Narasimamurthy and Virshup elucidate in their review the molecular mechanisms that regulate an enigma of the clock. Unlike other chemical reactions, the output of the clock as measured with the period remains nearly constant with fluctuations in ambient temperature. This is called as temperature compensation. The key lies especially in the mechanism that controls the stability of period circadian clock 2 protein. Clock-enhancing small molecules have become of particular interest as candidate chronotherapeutics, since there is a close association of circadian amplitude dampening with progression of chronic diseases, especially that of mood disorders. Gloston et al. present in their review an update of the regulatory mechanisms of circadian amplitude and the current status of these small molecules of therapeutic interest. Millius and Ueda introduce the readers to study of biology which takes advantage of engineering and mathematical tools to model and test the behaviors of the intrinsic clocks. It has evolved through the development of both wet lab and in silico work. The goal here is to understand the clocks that are made up of a range of complex properties of cells, tissues, and organisms.

The cross-section of studies comprised in this research topic on Intrinsic Clocks highlights the vibrant scientific activity in the field of the investigation of endogenous biological rhythms and their relevance for physiology and pathology.

Author Contributions

TP and DP planned and wrote the manuscript together.

Conflict of Interest Statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Keywords: circadian rhythm, depression, marine biology, mouse model, plasticity, seasonality, small-molecule, systems biology

Citation: Partonen T and Pollak DD (2018) Editorial: Intrinsic Clocks. Front. Neurol. 9:68. doi: 10.3389/fneur.2018.00068

Received: 04 December 2017; Accepted: 29 January 2018;
Published: 16 February 2018

Edited and Reviewed by: Yves A. Dauvilliers, Hôpital Gui De Chauliac, France

Copyright: © 2018 Partonen and Pollak. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Timo Partonen, timo.partonen@thl.fi

reposted from

Giants of Circadian Biology Win Nobel Prize

The award in Physiology or Medicine goes to chronobiologists Jeffrey Hall, Michael Rosbash, and Michael Young.

By Catherine Offord | October 2, 2017

Jeffrey Hall, Michael Rosbash, Michael YoungNOBEL MEDIA. III. N. ELMEHEDThe 2017 Nobel Prize in Physiology or Medicine has been jointly awarded to Jeffrey Hall, Michael Rosbash, and Michael Young for their work on circadian rhythms. The trio is recognized for research on the period gene in Drosophila—a central regulator of the circadian clock whose discovery led to the identification of such genes in humans and other animals—plus the protein machinery governing the timing of biological rhythms.

In the course of their research, collaborators Rosbash and Hall at Brandeis University and Young independently at Rockefeller University, “solved the mystery of how an inner clock in most of our cells in our bodies can anticipate daily fluctuations between night and day to optimize our behavior and physiology,” Thomas Perlmann, secretary general for the Nobel Assembly and Nobel Committee, says in a statement.

Russell Foster, head of the Sleep and Circadian Neuroscience Institute at the University of Oxford, tells The Scientist that he’s “thrilled and delighted” by the news. “These are the people who gave us our first working model of how the molecular clock might tick. The three of them . . . have formed the platform of our understanding of the molecular basis of circadian rhythms, not only in flies, but it’s informed the work in mice and humans.”

Retired since 2008, Jeffrey Hall was at Brandeis University from 1974, where he took an early interest in the biology of circadian rhythms in Drosophila. His initial work with period showed that the gene played an important role in regulating the rhythm of courtship song cycles produced by male fruit flies (PNAS, 77:6729-33, 1980).

Hall later began collaborating with Brandeis colleague Michael Rosbash—a neuroscientist he got to know primarily through sport, colleagues say. The pair went on to isolate the period gene—which had been described in the 1970s by Seymour Benzer and Ronald Konopka—and showed that it produced a protein, PER, that cycles on a daily rhythm (Cell, 39:369-76, 1984). Rockefeller’s Michael Young and colleagues simultaneously isolated period, publishing the findings in Nature the same year (312:752-54).

These are the people who gave us our first working model of how the molecular clock might tick.—Russell Foster,
University of Oxford

The research laid the groundwork for other researchers to map similarly essential circadian genes in mice and other animals. “What’s extraordinary is that the basic building blocks of the clock discovered in flies are very similar in mice and humans,” says Foster. “It’s broadly the same genes and broadly the same proteins.”

The trio went on to pin down the details of the protein machinery governing circadian rhythms. Working with postdoctoral researcher Paul Hardin, Hall and Rosbash showed that mRNA transcripts from the period gene also cycle, allowing the PER protein to regulate its own production via a feedback loop (Nature, 343:536-40, 1990). “It was a great experience working as a postdoc,” Hardin tells The Scientist, adding that he is pleased and not overly surprised about today’s news. “Their work for a number of years has merited an award of this magnitude. I was so happy to hear the news this morning.”

Young, meanwhile, discovered a number of other genes influencing period protein dynamics. In 1994, his group identified timeless, a clock gene that produces a protein, TIM, that binds to PER, and is required for the latter’s entry into the nucleus to regulate period gene expression (Science, 263:1603-6). A few years later, the team described another gene, double-time, which regulates the accumulation of the period protein (Cell, 94:83-95, 1998). “He’s just a terrific scientist,” says collaborator Brian Crane, a biochemist at Cornell University. “His impact is huge. I figured that sooner or later this would happen, but it’s nice to see it materialize.”

It’s not the first time the laureate trio has been recognized for contributions to biology and the research into human circadian rhythms that has followed. In 2009, the Gruber Foundation awarded the Neuroscience Prize to Hall, Rosbash, and Young for the establishment of “a direct link between genes and behavior” that could later be extended beyond fruit flies into humans and, indeed, “all living organisms.”

In 2012, the three were recognized again with the Canada Gairdner International Award for pioneering science’s understanding of the circadian rhythm. “The medical relevance of these findings has become apparent as it was found that changes in these clock genes are associated with a series of sleep disorders in humans,” Young said in an interview at the time. “There are strong indications that some forms of depression are linked to the control of circadian rhythms.”

All three have made an impression inside and outside the lab. “Being in the room with them, you realize you have to keep concentration to keep up with the discussion,” notes Michael Hastings, a molecular neurobiologist working on circadian rhythms at the University of Cambridge, who sees both Rosbash and Young frequently at research gatherings. “[They have] an enormous intellectual appetite and curiosity.”

On announcing the prize, Rosbash’s first response to the news of the award this morning was “you are kidding me,” Perlmann told the audience. “That’s a classic Michael response,” Hardin says. “He’s quite the jokester.”

Update (October 2): The article has been updated to include reaction from Brian Crane.

Tags

sleep/wake cycle, sleep, physiology, Nobel Prize, neuroscience, disease/medicine, circadian rhythms,circadian clocks and chronobiology