European Journal of Neuroscience

Cover image for Vol. 35 Issue 12


June 2012

Volume 35, Issue 12

Pages 1810–1950


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      Early brain repair and protection (page 1810)

      Jean-Marc Fritschy and Martin Sarter

      Version of Record online: 19 JUN 2012 | DOI: 10.1111/j.1460-9568.2012.08173.x

    2. What does the developing brain tell us about neural diseases? (pages 1811–1817)

      Esther T. Stoeckli

      Version of Record online: 19 JUN 2012 | DOI: 10.1111/j.1460-9568.2012.08171.x

      Neural diseases are a major burden for society with respect to both health care cost and suffering of the affected individuals. Despite major efforts from the pharmaceutical industry there are almost no drugs to cure neural diseases. In my article I try to make the point that progress in drug development will require more investment in basic research. Better understanding of brain development and function will be the prerequisite to find cures and therapies for neural diseases in the future.

    3. RNA-binding proteins involved in RNA localization and their implications in neuronal diseases (pages 1818–1836)

      Marco Tolino, Martin Köhrmann and Michael A. Kiebler

      Version of Record online: 19 JUN 2012 | DOI: 10.1111/j.1460-9568.2012.08160.x

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      RNA-binding proteins (RBPs) exert crucial functions in mRNA localisation and in the control of local protein synthesis at the activated synapse. In this review, we outline the process of mRNA localisation and the role RBPs play in it. We further discuss how mis-regulation of many of these RBPs are linked to various neuronal diseases and how the latest advances in our understanding encourage early intervention strategies for treatment.

    4. Engrailed signaling in axon guidance and neuron survival (pages 1837–1845)

      Julia Fuchs, Olivier Stettler, Daniel Alvarez-Fischer, Alain Prochiantz, Kenneth L. Moya and Rajiv L. Joshi

      Version of Record online: 19 JUN 2012 | DOI: 10.1111/j.1460-9568.2012.08139.x

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      The study of Engrailed signaling in retinal axon guidance and in the survival of adult dopaminergic neurons has revealed an unsuspected link between a homeoprotein and mitochondrial activity. Engrailed-mediated effects involve translation regulation as well as cooperation with classical signaling pathways. These findings highlight the crucial role of cellular energy metabolism in neuron development, survival and neurodegeneration, and may help to identify novel therapeutic targets.

    5. Timing of developmental sequences in different brain structures: physiological and pathological implications (pages 1846–1856)

      N. Dehorter, L. Vinay, C. Hammond and Y. Ben-Ari

      Version of Record online: 19 JUN 2012 | DOI: 10.1111/j.1460-9568.2012.08152.x

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      Brain development is associated with developmental sequences of voltage and transmitter gated currents and network patterns. We compare these sequences in different brain structures and show how they timely shift to behaviourally relevant ones for instance in the basal ganglia to enable targeted locomotion. In keeping with the ‘neuroarcheology’ concept, interruption or alteration of these sequences is a major signature of neurological disorders since neurons keep their immature features.

    6. Neonatal seizures: controversies and challenges in translating new therapies from the lab to the isolette (pages 1857–1865)

      Kevin E. Chapman, Yogendra H. Raol and Amy Brooks-Kayal

      Version of Record online: 19 JUN 2012 | DOI: 10.1111/j.1460-9568.2012.08140.x

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      Translating basic science research into clinical practice involves overcoming multiple hurdles. Neonatal seizures have unique properties that have proved challenging for both clinicians and basic science researchers with new effective therapies developing slowly. This article will discuss barriers that exist for the development of new therapies for neonatal seizures and the challenges inherent in bringing new therapies from the bench to the bedside.

    7. Cortical interneurons, immune factors and oxidative stress as early targets for schizophrenia (pages 1866–1870)

      Patricio O’Donnell

      Version of Record online: 19 JUN 2012 | DOI: 10.1111/j.1460-9568.2012.08130.x

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      Cortical interneurons are affected in schizophrenia, and animal models reveal their protracted developmental trajectory is affected by diverse manipulations, yielding behavioral anomalies with a peri-adolescent onset. Immune activation and oxidative stress are likely factors that contribute to GABA interneuron alterations during development in these models and perhaps in schizophrenia as well. These observations suggest novel preventive approaches may be identified with translational efforts.

    8. Cortical circuit dysfunction and cognitive deficits in schizophrenia – implications for preemptive interventions (pages 1871–1878)

      David A. Lewis

      Version of Record online: 19 JUN 2012 | DOI: 10.1111/j.1460-9568.2012.08156.x

      Schizophrenia is a common, usually chronic, and very costly illness with no proven means of prevention. Impairments in certain cognitive processes are the core feature of schizophrenia, reflect abnormalities in specific cortical circuits, and arise during childhood-adolescence. The implications of these findings for the development of preemptive, disease-modifying interventions in individuals at high risk for a clinical diagnosis of schizophrenia are discussed.

    9. An integrated approach to design novel therapeutic interventions for demyelinating disorders (pages 1879–1886)

      Oscar G. Vidaurre, Jia Liu, Jeffery Haines, Juan Sandoval, Richard Nowakowski and Patrizia Casaccia

      Version of Record online: 19 JUN 2012 | DOI: 10.1111/j.1460-9568.2012.08118.x

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      In this review we will discuss the current studies available in the literature regarding the genetics, pharmacogenomics and epigenetics of multiple sclerosis and propose an integrated view of disease pathogenesis, with the aim of opening a debate regarding the feasibility of future potential integrated approaches to therapy.

    10. Mitochondrial sirtuins – a new therapeutic target for repair and protection in multiple sclerosis (pages 1887–1893)

      C. M. Rice, M. Sun, K. Kemp, E. Gray, A. Wilkins and N. J. Scolding

      Version of Record online: 19 JUN 2012 | DOI: 10.1111/j.1460-9568.2012.08150.x

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      Mitochondrial sirtuins are NAD-dependent protein deacetylases associated with control of metabolism, aging and stem cell proliferation and differentiation. Their role in inflammatory demyelinating disease has not been fully characterised and is the subject of on-going research. Here, we expound the rationale behind selecting mitochondrial sirtuins as a therapeutic target in demyelinating disease.

    11. Cognitive dysfunction and depression in Parkinson’s disease: what can be learned from rodent models? (pages 1894–1907)

      Hanna S. Lindgren and Stephen B. Dunnett

      Version of Record online: 19 JUN 2012 | DOI: 10.1111/j.1460-9568.2012.08162.x

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      Although Parkinson’s disease has been considered a pure motor disorder, cognitive impairment and depression are increasingly recognized non-motor symptoms with significant clinical impact. This review will focus on these neuropsychological symptoms and consider whether, and how, these deficits can best be modelled in rodent models of the disorder. Since only a few of these symptoms respond to dopamine-replacement therapies, the quest for other approaches remains a major research effort, and success in this area will be dependent on appropriate rodent models.

    12. AMPA receptors as drug targets in neurological disease – advantages, caveats, and future outlook (pages 1908–1916)

      Philip K.-Y. Chang, David Verbich and R. Anne McKinney

      Version of Record online: 19 JUN 2012 | DOI: 10.1111/j.1460-9568.2012.08165.x

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      Many neurological diseases are manifested by changes in synaptic transmission and plasticity. As AMPA receptors are the workhorses in excitatory neurotransmission, we review the potential, as well as pitfalls, for targeting these receptors in four different neuropathologies.

    13. The early contribution of cerebrovascular factors to the pathogenesis of Alzheimer’s disease (pages 1917–1937)

      Pedro M. Pimentel-Coelho and Serge Rivest

      Version of Record online: 19 JUN 2012 | DOI: 10.1111/j.1460-9568.2012.08126.x

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      In this review, we summarize recent findings about the role of cerebrovascular disease and vascular dysfunction as early events contributing to the progression of cognitive deficits and neurodegeneration in Alzheimer’s disease. We also discuss potential preventive therapies targeting these early vascular alterations.

    14. Extrusion of misfolded and aggregated proteins – a protective strategy of aging neurons? (pages 1938–1950)

      Jana Doehner, Christel Genoud, Claudine Imhof, Dimitrije Krstic and Irene Knuesel

      Version of Record online: 19 JUN 2012 | DOI: 10.1111/j.1460-9568.2012.08154.x

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      Three-dimensional immunoelectron microscopy in the aging hippocampus reveals that neurons might utilise an extrusion mechanism to remove misfolded/damaged proteins which are then cleared by glia. This protective strategy appears to be impaired under chronic neuroinflammatory conditions, resulting in increased accumulation of aggregation-prone peptides and potentially facilitating the formation of amyloid plaques.