The October 2015 IRLSSG Meeting Agenda

[figflower]

Here is the 2015 agenda for the International RLS Study Group (IRLSSG) and European RLS Study Group slated for October 22-26, 2015. I feel that I've been unfairly accused of negligently and intentionally emphasizing the role of iron, iron management and dopaminergic system in RLS, while down playing the role of histamine and glutamine by essentially each and every moderator on here. The international RLS community is on my side:
SESSION 1 Epidemiology
CO-CHAIRS Daniel Picchietti, Klaus Berger
SPEAKERS AND TITLE
Daniel Picchietti How has epidemiological research helped the field of WED/RLS?
(brief introduction)
Stephen van den Eeden Opportunities and limits of secondary data sources in WED/RLS research
Lorene M. Nelson What needs to be done in WED/RLS epidemiological
(Stanford) research?—an “outside” expert’s view
Klaus Berger Convergence of WED/RLS epidemiological research with genetic,
biologic, and other areas of WED/RLS research
Daniel Picchietti Summary
and Klaus Berger
SESSION 2 Animal models for RLS phenotype
CO-CHAIRS Bryon Jones, David Rye
SPEAKERS AND TITLE
Juliane Winkelmann The role of Meis1, a gene nominated by GWAS, in behaviors
mimicking RLS
Yunqing Li The role of Btbd9, a gene nominated by GWAS, in behaviors and
iron regulation related to RLS
Subhabrata Sanyal Ubiquitination in Drosophila as related to RLS
Richard Allen BXD 40, a mouse that when fed an iron-poor diet, exhibits
endo- and exo-phenotypes mimicking RLS
Byron Jones Discussion
and David Rye
SESSION 3 Genetics
CO-CHAIRS Guy Rouleau, Juliane Winkelmann
SPEAKERS AND TITLE
Juliane Winkelmann The search for common variants: GWAS studies – an update
Barbara Schormair The search for rare variants: WES and WGS studies of RLS
Guy Rouleau Genetic architecture of RLS”, including “common variants” and
“rare variants” and thoughts about “missing heritability.”
David Rye From genotype to phenotype in RLS and PLMS
Juliane Winkelmann Summary and discussion
SESSION 4 Spinal and cortical excitability/hyperarousal
CO-CHAIRS Liborio Parrinoco, Walter Paulus
SPEAKERS AND TITLE
Imad Ghorayeb Spinal physiology in non-human primate models of RLS
(Bordeaux)
Cornelius Bachmann Physiology of spinal sensory processing in RLS alternatively RLS
and its relation to pain at a spinal level
Walter Paulus Spinal excitability and methods of stimulation
Yuping Wang Cortical excitability
Giuseppe Lanza Discussion on spinal and cortical excitability hyperarousal
Walter Paulus Summary
and Liborio Parrino
SESSION 5 PLMS*
CO-CHAIRS Raffaele Ferri, Stephany Fulda
SPEAKERS AND TITLE
Jacques Montplaisir PLMS as a cardiovascular risk factor: evidence and mechanisms
*no overlap with cardiovascular
Stephany Fulda Evidence-based criteria are needed to score PLMS
Liborio Parrino Neurophysiological mechanisms of driving PLMS
Raffaele Ferri Discussion
and Stephany Fulda
SESSION 6 The role of iron
CO-CHAIRS James Connor, Richard Allen
SPEAKERS AND TITLE
James Connor Blood Brain Barrier iron - CSF from RLS patient
Stephanie Patton Iron – Hypoxia interaction: central and peripheral effects including
effects on genes and peripheral myelin
Richard Allen Pre-clinical and clinical data on effects of iron deficits and
iron treatments
Konrad Oexle Genetic factors of iron
Richard Allen Discussion
and James Connor
SESSION 7 The dopaminergic system and RLS: where are we and what next
CO-CHAIRS Chris Earley, Stephan Clemens
SPEAKERS AND TITLE
Sergi Ferre DA receptor heteromers as possible new targets for RLS
George Uhl DAergic systems and cell adhesion molecules. How might they
inform us about RLS, augmentation and novel therapeutic targets
Chris Earley The state of the DAergic system in RLS
Stefan Clemens The spinal DAergic system and relevance to RLS
Chris Earley Discussion
and Stephan Clemens
SESSION 8 Opioids and pain in RLS
CO-CHAIRS Claudia Trenkwalder, Walter Zieglgänsberger
SPEAKERS AND TITLE
Walter Zieglgänsberger The interaction of pain physiology and the opioid system:
from animals to humans
Birgit Hoegl The contribution of Sleep and Sleep deprivation for pain
Sam Ahmedzai Actions of commonly used opioid medications; mechanisms and
actions of opioids
Claudia Trenkwalder Possible mechanisms of action for opioid treatment in RLS -
lessons from clinical trials
Claudia Trenkwalder Discussion; What type of pain is occurring in RLS patients
SESSION 9 RLS and cardiovascular disease: current evidence and a roadmap
for future research*
CO-CHAIRS John Winkelman, Virend Somers
SPEAKERS AND TITLE
John Winkelman Epidemiologic evidence linking RLS and other sleep disorders to
cardiovascular disease
Virend Somers Neural mechanisms linking RLS and other sleep disorders to
cardiovascular disease
John Floras Vascular mechanisms linking RLS and other sleep disorders to
cardiovascular disease
Naresh Punjabi Inflammatory/metabolic mechanisms linking RLS and other sleep
disorders to cardiovascular disease
John Winkelman Open discussion on how relates to RLS.
and Virend Somers
SESSION 10 Brain imaging and connectivity
CO-CHAIRS Giovanni Rizzoco, Yong Won Cho
SPEAKERS AND TITLE
Giovanni Rizzo Brain MRI in RLS. Include both
1) Iron level to possible structural changes
2) Regional brain metabolic dysfunctions in RLS patients:
magnetic resonance spectroscopy findings
Maria I. Argyropoulou Task-evoked functional MRI for studying RLS
Enzo Tagliazucchi Investigating brain connectivity from resting state functional MRI
recordings: methodological aspects
Yong Won Cho Resting state functional MRI assessments in RLS
Giovanni Rizzo Discussion
and Young Won Cho
SESSION 11 New treatment implications of current science*
CO-CHAIRS Diego Garcia-Borreguero, Sergi Ferre
SPEAKERS AND TITLE
Chris Earley A possible role of adenosine, histamine, and glutamate in RLS
Diego Garcia- Role of drugs acting on the calcium channels
Borreguero
Mauro Manconi The future of animal models for drug development of RLS;
Animal models for rapid screening of RLS
Sergi Ferre Getting mechanistic with new in vivo models of cortico-striatal
neurotransmission
Diego Garcia- Summary discussion of future treatments with interactive
Borreguero questions and answers 30
SESSION 12 Clinical updates
CO-CHAIRS Luigi Ferini-Strambi, S Chokroverty
SPEAKERS AND TITLE
Marco Zucconi Summary review of the PLMS task force
Ferini-Strambi Discussion of PLMS task force
and Chokroverty
Mike Silber Summary review of the treatment algorithm from the augmentation
task force
Ferini-Strambi Discussion of treatment algorithm
and Chokroverty
Bill Ondo Deep brain stimulation and RLS: Pathophysiology considerations
Ferini-Strambi Discussion of DBS and overall summary of clinical updates
and Chokroverty

[figflower]

I don't see histamine or glutamine mentioned, at least not directly in the agenda. Bottom line - we have lousy dopamine receptors because of low levels of brain iron. Figure out a way to get some iron to your brain and you have a darn good treatment. Wait, there is a way...iron bis-glycinate, empty stomach, with water only, during an attack. Then go about up-regulating your receptors with something other than iron - under-eat, fast, get your gut and gut microbiome in order, anaerobic exercise, magnesium that also crosses the BBB (in the morning), or uridine 5 monophosphate and CDP choline (in the morning). Then once you're feeling good stop for a while and start up again when things go south.

But NEVER take my advise or anyone's without doing your own research first and talking about it with a professional you trust. And when you're talking about substances that cross the BBB, IN MY OPINION, a little goes a long way. Less is more. Go VERY slow. This is powerful stuff. I've taken the iron bis-glycinate and awakened on the living room floor at 4am because that's where I dropped an hour after taking the iron. The same is true with the Uridine. Only it had the opposite affect of the iron. It gave me all night restless body, three times and I was expecting the best night's sleep of my life. The amount I took was 1/3 the size of a tic tac.

[badnights]

Yes, they discuss iron investigations. Iron is incredibly ipmortant. Who says it isn't? I object to the leaps made from that fact, and the fact that dopamine is involved, to saying that the The cure is to build more dopamine receptors by ingestintg anything that acts like a dopamine agonist under some conditions.

They're devoting an entire section to opioids in RLS/WED - I wonder if they'll mention one of my favorite studies there. (It showed that opioids protect mouse brain cells in vitro from death by iron deprivation) (no mention of dopamine.)

They'll have a number of talks on genetic variants, common and rare, which belies your earlier statement that RLS is a single clear-cut entity as well understood as the common cold.

They will even discuss spinal and cortical hyperexcitability - possibly the glutamate connection, and/or other non-dopamine non-iron controls.

One of their topics is Iron – Hypoxia interaction - goodness, could that be the hypoxia I mentioned as yet another factor besides iron and dopamine that is involved in the disease state?

They get into the histamine connection.

They will discuss the effect of drugs that act on calcium-ion channels (wasn't I just mentioning these).

With so many discussions on the agenda that illustrate our point, that the RLS/WED disease system is complex and probably is not going to be treated or cured by a simplified view of needing more dopamine receptors, I have to wonder why you placed mocking laughter everywhere iron or dopamine was mentioned. It seems you didn't actually read it, or if you did, you didn't understand it; or worse, maybe you haven't understood the points that Steve and I have been trying to make to you.

You have a good mind for science, but you need to open it up, embrace some checks and balances, never get married to a favorite idea so you never have to suffer a messy divorce from it (or an embarrassing clinging to it after the love has died), and read more deeply in each subject. It's best to assume you don't know, rather than that you do know, at this stage of your learning. Hope you take this advice to heart.

[figflower]

Here's an article on cortical excitability from one or two of the guest speakers. No mention of histamine or glutamine. I never disagreed with you about hypoxia. Hypoxia might be one way to up-regulate our receptors. How's your gut microbiome doing these days. I think you and I know that is probably the ultimate cause of RLS and potential cure. But that's for another day and possibly another universe.

http://www.sleep-journal.com/article/S1389-9457(14)00444-4/fulltext?mobileUi=0

[figflower]

Ok, I missed that one line on the agenda about the possible role adenosine, histamine and glutamine. Except for several glutamine blogs from this blogger (who like me), who thinks that he's found the one sole cause of RLS, inflammation, I could find only one article on glutamine and RLS. I also found one article by the guest speakers on adenosine but in that article, low levels of iron is the root of the tree that gives rise to dysfunction in the adenosine, gaba, dopamine, and glutamine systems. But here's the ONE that I believe Rustsmith has referred to:

http://www.sciencedaily.com/releases/20 ... 134600.htm

[badnights]

every paragraph in my post is one or more talks on the agenda - not one line you missed, but many lines

it's glutamate not glutamine (EDIT: searching for the right term is helpful in returning results)

The number of pages turning up in a google search has nothing to do with the validity of a subject. (Nothing. Seriously: nothing.)

Re gut microbes: I think they are important in a lot of cases of WED/RLS. I suspect they are not important in every case.

[Rustsmith]

A copy of the abstracts for the presentations given at the IRLSSG meeting this past week can be found at

http://irlssg.org/wp-content/uploads/2015/05/RLS-Science-Summit-abstracts-ver100915.pdf