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

July 7, 2010 By vani 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

Filed Under: International News Tagged With: Asya, atrophy, award ceremony, Ceremony Took Place, fens, fetal development, immobility, Marlies, National Institute For Health, nature genetics, Nervous System Diseases, Neuron, neuroscience research, Neurosciences, novel therapies, Scientific Publications, Spinal Cord Motoneurons, Translation Of Mrna, weizmann institute of science, Young Scientists

Network problem harms brain in Alzheimer’s disease!

March 29, 2010 By vani Leave a Comment

Mon, Mar 29 12:02 PM

In what could pave the way for new strategies for early diagnosis and effective treatment of Alzheimer’s, scientists have found that the disease makes parts of the brain shrink “as messages fail to get through”.

The findings, published in the ‘Neurology’ journal, suggest a build-up of deposits of the protein amyloid-beta in a region of the brain known as temporal inferior cortex which is connected to the hippocampus involved in memory.

Alzheimer’s disease is characterised by two factors –a build-up of amyloid-beta plaques in the brain, and a loss of neurons.

Lead scientist Dr Cassandra Szoeke of CSIRO said the puzzle for them was that the parts of the brain that had shrunk (atrophied) due to neuron loss were not the same as those showing increased deposits of amyloid-beta.

Using MRI scans to study Alzheimer’s disease affected brain tissue, the scientists found that shrinking (atrophy) of the hippocampus was associated with plaque deposits in the temporal inferior cortex.

The results indicate that the increased accumulation of amyloid in temporal inferior cortex disrupts connections with the hippocampus, causing the neurons to die, say the scientists.

“By helping to better understand the mechanisms involved in the progression of the disease, the study may guide the development of new strategies for early diagnosis,” Dr Szoeke said.
Agencies

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Healthy older brains not smaller than younger ones

September 8, 2009 By admin Leave a Comment

Washington, Sept 8 (ANI): The belief that healthy older brains are substantially smaller than younger brains has been deemed incorrect by Dutch researchers.

The authors suggest that previous findings may have overestimated atrophy and underestimated normal size for the older brain.

The new study tested participants in Holland’s long-term Maastricht Aging Study who were free of neurological problems such as dementia, Parkinson’s disease or stroke.

Once participants were deemed otherwise healthy, they took neuropsychological tests, including a screening test for dementia, at baseline and every three years afterward for nine years.

MRI scans were used to measure seven different parts of the brain, including the memory-laden hippocampus, the areas around it, and the frontal and cingulate areas of the cognitively critical cortex.

The participants were later divided into two groups: one group with 35 cognitively healthy people who stayed free of dementia (average starting age 69.1 years), and the other group with 30 people who showed substantial cognitive decline but were still dementia-free (average starting age 69.2 years).

In contrast to the 35 people who stayed healthy, the 30 people who declined cognitively over study-period showed a significant effect for age in the hippocampus and parahippocampal areas, and in the frontal and cingulate cortices.

In short, among the people whose cognition got worse, older participants had smaller brain areas than younger participants.

Thus, the seeming age-related atrophy in gray matter more likely reflected pathological changes in the brain that underlie significant cognitive decline than aging itself, wrote the authors.

As long as people stay cognitively healthy, the researchers believe that the gray matter of areas supporting cognition might not shrink much at all.

If future longitudinal studies find similar results, our conception of ‘normal’ brain aging may become more optimistic,” said lead author Saartje Burgmans, who is due to receive her PhD later this year.

The study appears in journal Neuropsychology. (ANI)

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Smoking may lead to brain damage in multiple sclerosis patients

August 18, 2009 By admin Leave a Comment

Washington, Aug 18 (ANI): Cigarette smoking can cause brain damage in patients with multiple sclerosis (MS), according to a new study.

Scientists at the University at Buffalo have shown that MS patients who smoked for a little as six months during their lifetime had more destruction of brain tissue and more brain atrophy than the patients who never smoked.

“Cigarette smoking is one of the most compelling environmental risk factors linked to the development and worsening of MS,” said Dr Robert Zivadinov, UB professor of neurology, director of the Buffalo Neuroimaging Analysis Centre (BNAC) where the research was conducted and first author on the study.

“The biological basis of the potential link between smoking and MS has not yet been fully elucidated.

“In addition to nicotine, cigarette smoke contains hundreds of potentially toxic components, including tar, carbon monoxide and polycyclic aromatic hydrocarbons.

“In MS patients, smoking was associated with higher increased lesion burden and greater brain atrophy. Our results indicate that a wide range of quantitative brain MRI markers are affected by smoking in MS patients,” he added.

The study involved 368 patients from the Baird Multiple Sclerosis Center of the Jacobs Neurological Institute (JNI), where 128 had a history of smoking: 96 were active smokers who had smoked more than 10 cigarettes-per-day in the three months prior to the study start and 32 were former smokers who had smoked cumulatively for at least six months sometime in the past.

The remaining 240 participants were lifelong nonsmokers.

They found that that smokers with MS had a greater breakdown of the blood-brain barrier.

They had nearly 17 percent more brain lesions – patches of inflammation in the sheath surrounding the nerve fibres that impair their function – than nonsmokers with MS, and also had less brain volume.

Smoking also was associated with increased physical disability.

“The findings underscore the detrimental effect of smoking, providing a link between smoking and a more severe brain injury in MS patients,” said Dr Bianca Weinstock-Guttman, director of the Baird MS Center, UB associate professor of neurology and a principal co-author on the study.

The study appears in Neurology(r), the medical journal of the American Academy of Neurology. (ANI)

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Indian-origin boffin offers potential new spinal muscular atrophy treatment

July 29, 2009 By admin Leave a Comment

Washington, July 28 (ANI): A team of researchers led by Indian origin scientist has come up with a potential new treatment for spinal muscular atrophy, the second-leading cause of infant mortality in the world.

Ravindra Singh, associate professor in biomedical sciences at Iowa State University’s College of Veterinary Medicine said that more than 95 percent of the sufferers have a mutated or deleted gene called Survival Motor Neuron 1 (SMN1) that doesn’t correctly do its job of creating functional SMN proteins.

He suggested that replacing poor-performing gene with another gene could help treat the disease.

Humans need a certain level of SMN protein to ward off Spinal Muscular Atrophy.

When SMN1 fails to create functioning proteins, Spinal Muscular Atrophy is the result.

There is a gene already in humans that looks very much like SMN1, so much so that it’s called SMN2. The SMN2 gene doesn’t seem to serve any function that researchers can identify.

Singh has discovered a way of using SMN2 to produce the working SMN protein. When SMN2 makes enough SMN, it compensates for the mutated or malfunctioning SMN1 gene.

However, SMN2 doesn’t produce normal protein because of the presence of a specific intronic sequence in the gene or DNA.

To make SMN2 behave as SMN1, Singh has introduced a small antisense oligonucleotide that blocks this specific intronic sequence.

When the intronic sequence is blocked, SMN2 produces normal proteins and acts, in effect, like SMN1.

“The significance of our work is that we have this stuff called junk DNA in SMN2,” said Singh.

“We found that we could get SNM2 to behave as SMN1 by introducing a small oligonucleotide. It is a very simple experiment if you think about it,” he added.

The resulting proteins are normal just like a regular cell – free from Spinal Muscular Atrophy.

“Our cells are healthy and survive. From that point of view, this is a major achievement,” he added.

The study appears online in Landes Bioscience.(ANI)

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7 in 10 women ‘feel uncomfortable’ talking about vaginal dryness, pain

May 19, 2009 By admin Leave a Comment

Washington, May 19 (ANI): A new study has revealed that nearly 70 pct of postmenopausal women feel embarrassed to talk about vaginal dryness and pain, and hesitate to seek medical help.

The survey showed that nearly 39 pct of post-menopausal women experience these symptoms of vaginal atrophy and 40 percent agree that it interferes with their sex life.

Local symptoms such as painful intercourse, vaginal dryness, itching, burning, and soreness are caused, like other menopausal symptoms, by the gradual decline of oestrogen production in ovaries.

Seven out of ten said they were reluctant to talk about the problem with their physician.

As result a quarter would wait for over a year before finally contacting their physician.he survey showed only 30 percent of women considered talking to a gynaecologist, and only 29 percent considered talking to a GP.

“The results of this survey really highlight my experiences of treating menopausal women and in my practice in Italy it is even worse. I see many women who have vaginal dryness and pain post-menopause, and the most alarming aspect is that they wait for so long, with only 17 percent of surveyed women taking a treatment to counteract these symptoms.” said Dr. Rossella Nappi, Director of the Gynecological Endocrinology and Menopause Unit at the Maugeri Foundation, University of Pavia, Italy.

“In addition to the physical pain that affects the women, there is an emotional impact on them and their partner as well.

“There is definitely a taboo factor involved as the survey shows that, of those who have experienced vaginal dryness and pain, 47 percent would rather speak to a female physician than a male physician about the problem,” she added.

The survey also showed that 67 percent of those who have had or are currently taking treatment experience improvements, including an improved quality of life, a return to normal sexual activity, and an improvement in the relationship with their partner.

“Vaginal dryness and pain don’t need to be considered as a natural part of growing older and effective treatment options, such as vaginal oestrogen tablets, pessaries, creams or rings are available and can easily be prescribed by their healthcare professional.” said Professor Henry Burger, Consultant Endocrinologist, Jean Hailes Foundation for Women’s Health, Melbourne, Australia.

The study was presented at the European Congress on Menopause in London. (ANI)

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Shrinkage of hippocampus could predict Alzheimer’s development

March 17, 2009 By admin Leave a Comment

Washington. Mar 16 (ANI): A new study has revealed that people who have lost cells in the hippocampus area of the brain are more likely to develop dementia.

For the study, researchers involved 64 people with Alzheimer’s disease, 44 people with mild cognitive impairment, which is the stage of memory problems that precedes Alzheimer’s disease, and 34 people with no memory or thinking problems.

They performed MRI scans on all of the participants at the beginning of the study and again an average of a year and a half later.

During that time, 23 of the people with mild cognitive impairment had developed Alzheimer’s disease, along with three of the healthy participants.

The researchers measured the volume of the whole brain and the hippocampus area, which is affected by Alzheimer’s disease, at the beginning and end of the study, and calculated the rate of shrinkage in the brain over that time.

For people who did not have dementia at the beginning of the study, those with smaller hippocampal volumes and higher rates of shrinkage were two to four times as likely to develop dementia as those with larger volumes and a slower rate of atrophy.

“This finding seems to reflect that at the stage of mild cognitive impairment, considerable atrophy has already occurred in the hippocampus,” said study author Wouter Henneman, MD, of VU University Medical Center in Amsterdam, The Netherlands.

“In people who already have Alzheimer’s disease, the loss of nerve cells is more widespread throughout the brain,” Henneman added.

The study has been published in the March 17, 2009, print issue of Neurology, the medical journal of the American Academy of Neurology. (ANI)

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Two glasses of milk a day can help prevent Alzheimer’s

March 2, 2009 By admin Leave a Comment

London, Mar 1 (ANI): Just two glasses of milk a day can help prevent Alzheimer’s disease in old age, suggests a new study.

University of Oxford researchers have identified a vitamin that is believed to cut neurological damage to the brain that can lead to dementia.

They have found that older adults with low levels of the vitamin B12 suffer twice as much shrinkage of the brain as those with higher levels of the vitamin in their bodies.

The researchers suggest that increasing vitamin B12 intake in elderly could help slow cognitive decline.

Professor David Smith, from the Oxford Project to Investigate Memory and Ageing, said drinking just two glasses of milk a day would be enough to increase levels of vitamin B12 to an adequate level.

“Our study shows that consuming around half a litre of milk or more per day, and it can be skimmed milk, could take someone who has marginal levels of B12 into the safe range. But even drinking just two glasses a day can protect against having low levels,” the Telegraph quoted him as saying.

While meat contain some of the highest levels of the vitamin B12, it was poorly absorbed by the body when eaten.

Professor Smith, along with scientists from Oslo University and Bergen University, in Norway, found the highest levels of vitamin B12 absorbed by the body came from milk, despite having lower B12 concentrations than meat.

The study showed that around 55 per cent of the vitamin in milk entered the blood stream.

“In meat, B12 can be tightly bound to protein and this bond has to be broken down by acid in the stomach before the body can use it,” said Smith.

“Older people have lower levels of acid and so it is much harder for them to get B12 from certain foods. In milk, the binding is readily reversible,” he added.

During the study, brain scans of patients who have a vitamin B12 deficiency have revealed that they suffer more brain loss, or atrophy, than those with higher intake of the vitamin.

“We are currently preparing to unmask a two-year trial of 180 people over the age of 70 with memory problems, who were either given Vitamin B12 or a placebo,” he said.

“We have been taking volumetric MRI scans to look at whether the vitamin treatment has slowed down the atrophy in the brain,” he added.

The research is published in the American Journal of Clinical Nutrition. (ANI)

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