Brain Research 2009 Young Investigator Award Winners
Elsevier is delighted to announce four Brain Research Young Investigator Award winners in 2009.
Access the winning articles below.
Giovanni Grasso Universityof Palermo, Palermo, Italy
Description of the paper: In the study Grasso and co-workers demonstrated that recombinant human erythropoietin confers neuroprotection in an in vivo model of traumatic brain injury and emphasizes its beneficial effect on neurological dysfunction, brain edema formation, blood-brain barrier dysfunction, and cerebral tissue injury extent following a cryogenic model of brain damage. These results strongly indicate that further studies should be made in order to assess additional information about a possible clinical use of erythropoietin after the onset of traumatic brain injury.
Giovanni Grasso, MD, PhD, is Aggregate Professor at the University of Palermo, in the Department of Clinical Neurosciences, Neurosurgical Unit. He has led research programs, some of them still ongoing, into neurological and neurosurgical diseases, with the goal of translating scientific discovery into clinically important treatments. Prominent amongst these various lines of research is the study of tissue-protective cytokines in the safe treatment of devastating diseases and injuries of the nervous system. The results from these studies have contributed strongly to the initiation of clinical trials.
Charlotte D'Hulst HunterCollege, City University of New York, New York, NY, USA (formerly at: Dept of Medical Genetics, University of Antwerp, Antwerp, Belgium)
Description of the paper: D’Hulst and co-workers investigated the expression of the different GABAA receptor subunits in fragile X syndrome, the main cause of inherited mental retardation and the leading known genetic form of autism affecting 1/2500 individuals.
Using a well validated mouse model and real-time PCR they found decreased expression of 7 out of 19 subunits which make up this receptor. Interestingly, downregulation of the GABAergic system seemed to be an evolutionary conserved hallmark of fragile X syndrome as we could also demonstrate under expression of the much simpler GABA receptor system in the fragile X fruitfly.
Because GABAA receptors are the major inhibitory receptors in brain, involved in anxiety, depression, insomnia and learning and memory, processes also disturbed in fragile X patients, the GABAA receptor might be a novel target for rational therapy of fragile X syndrome.
Charlotte D’Hulst, PhD, graduated in 2003 in Bio-engineering Sciences at the Catholic University of Leuven, Belgium. In 2009 she got her PhD degree in Professor Frank Kooy’s lab in the Department of Medical Genetics of the University of Antwerp, Belgium. During het PhD period she was mainly interested in identifying new targets for rational therapy of the underlying molecular defects of fragile X syndrome. Recently she joined Professor Jason Dictenberg’s lab in the Department of Biology, Laboratory for Molecular Neurobiology and Research in Cognitive Developmental Disorders at Hunter College, CUNY, New York as a post-doc research fellow. The main goal of this lab is the visualization of gene expression dynamics in living neurons and the regulation of synaptic plasticity, using fragile X syndrome as a working model.
Sowmini K. Oomman TexasTech University, Lubbock, TX, USA
Description of the paper: Caspases belong to a family of cysteine proteases that has been well implicated in executing cell death. Some of the caspases such as caspase-8,-3 and -14 have been considered as proapoptotic caspases. In this study Oomman and co-workers were able to demonstrate that caspase-3, an executor caspase has a non–apoptotic role. Using a Bergmann glial (BG) preparation, it was shown that differentiating BG cells express nuclear active caspase-3, and that transformation into a proliferating state was attained by blocking the function of active caspase-3. This novel understanding of the function of caspase-3 will provide avenues to treat/target glial based tumors through caspase-mediated signaling.
Because tumor cells represent a dedifferentiated state, increasing capsase-3 activity in them potentially could induce differentiation or apoptosis depending on the degree to which it is activated and thus prevent tumor progression.
Sowmini Oomman, MD, PhD, finished her medical school training in India in 1999, after which she began her PhD dissertation work in Physiology in Dr. Jean Strahlendorf’s lab in the Department of Physiology of Texas Tech University Health Sciences Center School of Medicine. Her PhD focused on the idea of non-apoptotic functions of caspase-3. She received her PhD in 2004. She then worked as Postdoctoral researcher for 1½ years in the laboratory of Dr. Jean Strahlendorf before joining the Neurology residency program at the University of Arkansas which she will complete in 2010.
Micha M.M. Wilhelmus Free University of Amsterdam, Amsterdam, The Netherlands (Formerly at: Radboud University Medical Centre, Nijmegen, The Netherlands)
Description of the paper: Wilhelmus and co-workers investigated the role of small heat shock proteins in the amyloid-beta (Ab) aggregation process, which leads to neuronal loss in Alzheimer’s disease. Using an array of biochemical techniques, i.e. surface plasmon resonance, circular dichroism spectroscopy and electron microscopy, they found that small heat shock proteins did not only bind to Ab, but also affects Ab aggregation. Interestingly, it was observed that members of the small heat shock protein family reduced or completely inhibited aggregation of Ab and that Ab-mediated toxicity towards human cerebrovascular cells was strongly reduced by co-incubation of small heat shock proteins with Ab. It was therefore concluded that small heat shock proteins may regulate Ab aggregation and serve as a potential antagonists of the neurotoxic action of Ab in Alzheimer’s disease.
Micha Wilhelmus, PhD: During his PhD period at the Department of Pathology and Neurology of the Radboud University Nijmegen Medical Centre, The Netherlands, Micha Wilhelmus focused on various aspects of amyloid-beta (Aβ) aggregation and toxicity in Alzheimer’s disease (AD). He worked on the role of Apolipoprotein E in neurotoxicity, and in a parallel study on the role of small heat shock proteins in Aβ aggregation, neurotoxicity and complement activation. In the final year of his PhD project, he added a new line of research investigating the role of cell surface receptors in Aβ-mediated toxicity.
After receiving his PhD degree, Micha Wilhelmus decided to focus more on identification of drugable targets in the Aβ cascade. In order to do this, he joined Dr. Benjamin Drukarch’s group at the Department of Anatomy and Neurosciences at the Free University Medical Center in Amsterdam, The Netherlands, which is interested in the development of neuroprotective strategies for neurodegenerative diseases. Currently, he is investigating mechanisms of protein-protein interactions and enzyme-driven posttranslational modifications of the Aβ protein in the Aβ cascade.
Giovanni Grasso, MD, PhD, is Aggregate Professor at the University of Palermo, in the Department of Clinical Neurosciences, Neurosurgical Unit. He has led research programs, some of them still ongoing, into neurological and neurosurgical diseases, with the goal of translating scientific discovery into clinically important treatments. Prominent amongst these various lines of research is the study of tissue-protective cytokines in the safe treatment of devastating diseases and injuries of the nervous system. The results from these studies have contributed strongly to the initiation of clinical trials.
Charlotte D’Hulst, PhD, graduated in 2003 in Bio-engineering Sciences at the Catholic University of Leuven, Belgium. In 2009 she got her PhD degree in Professor Frank Kooy’s lab in the Department of Medical Genetics of the University of Antwerp, Belgium. During het PhD period she was mainly interested in identifying new targets for rational therapy of the underlying molecular defects of fragile X syndrome. Recently she joined Professor Jason Dictenberg’s lab in the Department of Biology, Laboratory for Molecular Neurobiology and Research in Cognitive Developmental Disorders at Hunter College, CUNY, New York as a post-doc research fellow. The main goal of this lab is the visualization of gene expression dynamics in living neurons and the regulation of synaptic plasticity, using fragile X syndrome as a working model.
Sowmini Oomman, MD, PhD, finished her medical school training in India in 1999, after which she began her PhD dissertation work in Physiology in Dr. Jean Strahlendorf’s lab in the Department of Physiology of Texas Tech University Health Sciences Center School of Medicine. Her PhD focused on the idea of non-apoptotic functions of caspase-3. She received her PhD in 2004. She then worked as Postdoctoral researcher for 1½ years in the laboratory of Dr. Jean Strahlendorf before joining the Neurology residency program at the University of Arkansas which she will complete in 2010.
Micha Wilhelmus, PhD: During his PhD period at the Department of Pathology and Neurology of the Radboud University Nijmegen Medical Centre, The Netherlands, Micha Wilhelmus focused on various aspects of amyloid-beta (Aβ) aggregation and toxicity in Alzheimer’s disease (AD). He worked on the role of Apolipoprotein E in neurotoxicity, and in a parallel study on the role of small heat shock proteins in Aβ aggregation, neurotoxicity and complement activation. In the final year of his PhD project, he added a new line of research investigating the role of cell surface receptors in Aβ-mediated toxicity.
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