ERA-Net NEURON Announces Winners of the First Excellent Paper in Neuroscience Award

July 7, 2010 By Leave a Comment

AMSTERDAM–(Business Wire)–
ERA-Net NEURON, an initiative of the European Commission aimed at advancing
transnational European research in the field of disease-related neuroscience,
announced today the winners of the Excellent Paper in Neuroscience award for
young scientists for the year 2009. The two winners, awarded each a prize of
€3,000, are Dr. Heidi O. Nousiainen from the National Institute for Health and
Welfare, Biomedicum, Finland and Dr. Asya Rolls from the Weizmann Institute of
Science, Israel. The award ceremony took place during the 7th Forum of European
Neuroscience Societies (FENS) yesterday in Amsterdam. Dr. Heidi Nousiainen was
invited to the Conference as the special ERA-Net NEURON Young Investigator
lecturer.

“The first Excellent Paper in Neuroscience Award is awarded to outstanding
scientific publications by young researchers in the field of disease related
neurosciences,” said Dr. Marlies Dorlöchter, coordinator of ERA-Net NEURON. “The
two winners, chosen out of seven candidates, have made significant contributions
towards our understanding of disease and injury of the nervous system as well as
the development of novel therapies. Their achievements emphasize the high
quality neuroscience research undertaken in Europe.”

About the Chosen Papers

Dr. Heidi O. Nousiainen received the award on her publication in Nature Genetics
(2008)1 describing and identifying the gene underlying two fatal nervous system
diseases (LCCS1 and LAAHD) that are characterized by marked atrophy of spinal
cord motoneurons and fetal immobility, and who are lethal already during fetal
development or shortly after birth. Dr. Nousiainen discovered that the disease
causing gene is GLE1 which encodes for a protein that has been shown to
participate in mRNA export from the nucleus as well translation of mRNA into
protein. This discovery adds a new and important member to the increasing number
of RNA processing molecules linked to neurodegenerative diseases. This study
provides significant new information about the molecular background of fetal
motoneuron disease, but at the same time also gives insight into the mechanisms
that are essential for the normal development as well as maturation and
functioning of motoneurons.

Dr. Asya Rolls received the award on her publication in PLoS Medicine (2008)2
for elucidating the role of scar tissue formation in spinal cord repair after
injury. It has been accepted for quite some time that lack of nerve regeneration
in the central nervous system is due to formation of a deleterious scar tissue.
Dr. Rolls addressed the question of why should the body invest so much energy in
scar formation after traumatic spinal cord injury (SCI) only to inhibit spinal
cord repair. She showed that initial formation of the scar, and in particular a
protein called CSPG, is part of an `SOS` response crucial for recovery. In fact,
inhibiting the formation of CSPG at the early stages of spinal cord injury
actually harms the recovery process. On the other hand, CSPG inhibition during
the later subacute phase, improves functional recovery and can benefit
regeneration. This study thus identified an endogenous repair mechanism of the
body and may have considerable implications for the treatment of SCI.

About ERA-Net NEURON

ERA-Net NEURON, an initiative funded by the European Commission, has been set up
to establish sustained co-operation between national funding bodies and to
coordinate their research programs on disease-related neuroscience. Coordinated
by Dr. Marlies Dorlöchter from Germany, the participating ERA-Net NEURON partner
countries and funding institutions include: Austria, The Austrian Science Fund
(FWF); Canada, The funding agency for health research in Québec (FRSQ); Finland,
Academy of Finland (AKA); France, The National Agency for Research (ANR), the
French National Centre for Scientific Research (CNRS) and the National Institute
for Health and Medical Research (INSERM); Germany, Project Management Agency in
the German Aerospace Centre (PT-DLR) for the Federal Ministry of Education and
Research (BMBF); Israel, The Chief Scientist Office, Ministry of Health
(CSO-MOH); Italy, Ministry of Health (MOH); Luxemburg, National Research Fund
(FNR); Poland – National Centre for Research and Development (NCBiR); Romania,
Ministry of Education and Research (ANCS-MEdR) and National Centre for
Programmes Management (CNMP); Spain – Ministry of Education and Science (MICINN)
and Fund for Health Research (ISCIII-FIS); Sweden, Swedish Research Council
(SRC); and United Kingdom, Medical Research Council. For further information,
please visit www.neuron-eranet.org.

1 Heidi O Nousiainen H.O., Marjo Kestilä M., Pakkasjärvi N., Honkala H., Kuure
S., Tallila J., Vuopala K., Ignatius J., Herva R. and Peltonen L. (2008).
Mutations in mRNA export mediator GLE1 result in a fetal motoneuron disease.
Nature Genetics, 2:155-7

2 Rolls A., Shechter R., London A., Segev Y., Jacob-Hirsch J., N., Rechavi G.,
Schwartz M. (2008). Two Faces of Chondroitin Sulfate Proteoglycan in Spinal Cord
Repair: A Role in Microglia/Macrophage Activation. PLoS Medicine, 5:1262-1277

ERA-Net NEURON
Tsipi Haitovsky, Media Liaison
+972-52-598-9892
tsipih@netvision.co.il

Copyright Business Wire 2010

Filed Under: International News Tagged With: , , , , , , , , , , , , , , , , , , ,

How genetic mutations lead to diabetes

April 20, 2010 By Leave a Comment

Washington, April 20 (ANI): Scientists at The Scripps Research Institute have finally cracked the 40-year-old mystery of how certain genetic mutations lead to Type 1 diabetes.

According to researchers, their findings could lead to novel therapies for Type 1 diabetes and other autoimmune diseases.

“People have been looking for the mechanism linking HLA and autoimmunity for 40 years. This study provides a big leap forward in understanding and suggests a critical new target to intervene in type 1 diabetes,” said Scripps Research Professor Luc Teyton, who led the study with Scripps Research Professor Ian Wilson.

While genes predispose people to many different types of diseases in many different ways, specific genetic variations are especially strong predictor of the development of type 1 diabetes.

Three genetic variations in particular (HLA-DQ2, HLA-DQ8, and HLA-DR0405)-all located in the region of the genome called HLA for “human leukocyte antigen”-are known to dramatically increase risk of coming down with the condition.

These three genes encode molecules that present peptides (protein fragments) to the body”s T cells. T cells then determine whether the peptide being presented is dangerous and needs to be eliminated from the body-as in the case of foreign invaders such as bacteria or viruses-or whether the peptide is “self,” part of the host and something the immune system needs to leave alone. However, in the context of type 1 diabetes, T cells aggressively attack the body”s own cells.

The scientists wanted to know on a molecular level how mutations in the immune surveillance machinery could lead to type 1 diabetes.

Research Associate Adam Corper of the Wilson lab, who was first author of the paper with Kenji Yoshida of the Teyton lab, said: “We were interested in trying to understand why certain MHC molecules (which are molecules in mice analogous to HLA molecules in humans) are linked to autoimmune disease, particularly type 1 diabetes. In particular, we wanted to know why a single residue at position 57 on the ß chain of HLA molecules seems to be linked to the disease.”

In the new research, the team used a series of structural and biophysical studies to answer that question.

The study was published in an advanced, online issue of the Journal of Clinical Investigation on April 19, 2010, and will appear in the May print edition of the journal. (ANI)

Filed Under: International News Tagged With: , , , , , , , , , , , , , , , , , , ,

How genetic mutations lead to diabetes

April 20, 2010 By Leave a Comment

Washington, April 20 (ANI): Scientists at The Scripps Research Institute have finally cracked the 40-year-old mystery of how certain genetic mutations lead to Type 1 diabetes.

According to researchers, their findings could lead to novel therapies for Type 1 diabetes and other autoimmune diseases.

“People have been looking for the mechanism linking HLA and autoimmunity for 40 years. This study provides a big leap forward in understanding and suggests a critical new target to intervene in type 1 diabetes,” said Scripps Research Professor Luc Teyton, who led the study with Scripps Research Professor Ian Wilson.

While genes predispose people to many different types of diseases in many different ways, specific genetic variations are especially strong predictor of the development of type 1 diabetes.

Three genetic variations in particular (HLA-DQ2, HLA-DQ8, and HLA-DR0405)-all located in the region of the genome called HLA for “human leukocyte antigen”-are known to dramatically increase risk of coming down with the condition.

These three genes encode molecules that present peptides (protein fragments) to the body”s T cells. T cells then determine whether the peptide being presented is dangerous and needs to be eliminated from the body-as in the case of foreign invaders such as bacteria or viruses-or whether the peptide is “self,” part of the host and something the immune system needs to leave alone. However, in the context of type 1 diabetes, T cells aggressively attack the body”s own cells.

The scientists wanted to know on a molecular level how mutations in the immune surveillance machinery could lead to type 1 diabetes.

Research Associate Adam Corper of the Wilson lab, who was first author of the paper with Kenji Yoshida of the Teyton lab, said: “We were interested in trying to understand why certain MHC molecules (which are molecules in mice analogous to HLA molecules in humans) are linked to autoimmune disease, particularly type 1 diabetes. In particular, we wanted to know why a single residue at position 57 on the ß chain of HLA molecules seems to be linked to the disease.”

In the new research, the team used a series of structural and biophysical studies to answer that question.

The study was published in an advanced, online issue of the Journal of Clinical Investigation on April 19, 2010, and will appear in the May print edition of the journal. (ANI)

Filed Under: International News Tagged With: , , , , , , , , , , , , , , , , , , ,

Autism may be reversible

April 2, 2009 By Leave a Comment

Washington, Apr 2 (ANI): Proposing a new theory of autism, scientists have revealed that the brains of autistic people are structurally normal but dysregulated, which implies that the disorder might be reversible.

The theory put forward by scientists at Albert Einstein College of Medicine of Yeshiva University is centred on the principle that autism is a developmental disorder caused by impaired regulation of the locus coeruleus-a bundle of neurons in the brain stem that processes sensory signals from all areas of the body.

The new theory is the result of decades of anecdotal observations that some autistic children seem to improve when they have a fever, only to regress when the fever recedes.

A previous study has already shown that autistic children experience behaviour changes during fever.

“On a positive note, we are talking about a brain region that is not irrevocably altered. It gives us hope that, with novel therapies, we will eventually be able to help people with autism,” said theory co-author Dr. Mark F. Mehler, chairman of neurology and director of the Institute for Brain Disorders and Neural Regeneration at Einstein.

The researchers reckon that scientific evidence clearly indicates that the locus coeruleus-noradrenergic (LC-NA) has a major role to play in autism.

“The LC-NA system is the only brain system involved both in producing fever and controlling behavior,” said co-author Dominick P. Purpura.

“What is unique about the locus coeruleus is that it activates almost all higher-order brain centers that are involved in complex cognitive tasks,” said Mehler.

The researchers hypothesized that in autism, the LC-NA system is dysregulated by the interplay of environment, genetic, and epigenetic factors (chemical substances both within as well as outside the genome that regulate the expression of genes).

In their opinion, stress plays a central role in dysregulation of the LC-NA system, especially in the latter stages of prenatal development when the foetal brain is particularly vulnerable.

And for evidence they pointed to a 2008 study, which found that maternal exposure to severe storms at mid-gestation resulted in the highest prevalence of autism.

According to the researchers, in autistic children, fever stimulates the LC-NA system, temporarily restoring its normal regulatory function.

“This could not happen if autism was caused by a lesion or some structural abnormality of the brain. This gives us hope that we will eventually be able to do something for people with autism,” said Purpura.

Instead of advocating fever therapy (fever induced by artificial means), the scientists claimed that the future of autism treatment lies in drugs that selectively target certain types of noradrenergic brain receptors or, more likely, in epigenetic therapies targeting genes of the LC-NA system.

“If the locus coeruleus is impaired in autism, it is probably because tens or hundreds, maybe even thousands, of genes are dysregulated in subtle and complex ways,” said Mehler.

He added: “The only way you can reverse this process is with epigenetic therapies, which, we are beginning to learn, have the ability to coordinate very large integrated gene networks.”

The study has been published in Brain Research Reviews.(ANI)

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , , ,