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Journal of Neurochemistry

Cover image for Vol. 123 Issue 2

October 2012

Volume 123, Issue 2

Pages 203–336

  1. REVIEW

    1. Top of page
    2. REVIEW
    3. SYSTEMATIC REVIEW
    4. ORIGINAL ARTICLES
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      Matrix metalloproteinase-3 in the central nervous system: a look on the bright side (pages 203–216)

      Inge Van Hove, Kim Lemmens, Sarah Van de Velde, Mieke Verslegers and Lieve Moons

      Article first published online: 3 SEP 2012 | DOI: 10.1111/j.1471-4159.2012.07900.x

  2. SYSTEMATIC REVIEW

    1. Top of page
    2. REVIEW
    3. SYSTEMATIC REVIEW
    4. ORIGINAL ARTICLES
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      Citicoline in pre-clinical animal models of stroke: a meta-analysis shows the optimal neuroprotective profile and the missing steps for jumping into a stroke clinical trial (pages 217–225)

      Alejandro Bustamante, Dolors Giralt, Lidia Garcia-Bonilla, Mireia Campos, Anna Rosell and Joan Montaner

      Article first published online: 23 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07891.x

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      Citicoline meta-analysis in experimental stroke Translation of neuroprotective drugs into clinical practice has repeatedly failed. The meta-analysis here conducted aimed to verify the described neuroprotective benefits of citicoline therapy on animal stroke models. Although these effects were verified, we found that STAIR criteria have not been fulfilled and we identified several factors that may be important for a better translation into clinical trials.

  3. ORIGINAL ARTICLES

    1. Top of page
    2. REVIEW
    3. SYSTEMATIC REVIEW
    4. ORIGINAL ARTICLES
    1. Gene regulation & Genetics

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      Positive feedback regulation of Akt-FMRP pathway protects neurons from cell death (pages 226–238)

      Se Jin Jeon, Seol-Heui Han, Sung-Il Yang, Ji woong Choi, Kyoung Ja Kwon, Seung Hwa Park, Hahn Young Kim, Jae Hoon Cheong, Jong Hoon Ryu, Kwang Ho Ko, David G Wells and Chan Young Shin

      Article first published online: 22 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07886.x

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      Neurological insults such as excessive glutamate or stroke induce FMRP expression and activation of PI3K-Akt pathway in primary cortical neurons, which may form positive feedback activation loop resulting in up-regulation of anti-apoptotic Bcl-xL expression and increased cell survival. This study provides experimental evidences that stimuli-induced FMRP expression underlies well-regulated neuronal cell survival system under excitotoxic insult conditions by modulating PI3K-Akt pathway.

    2. Signal Transduction & Synaptic Transmission

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      Expression of A1 adenosine receptors in the developing avian retina: in vivo modulation by A2A receptors and endogenous adenosine (pages 239–249)

      Rafael Brito, Mariana Rodrigues Pereira, Roberto Paes-de-Carvalho and Karin da Costa Calaza

      Article first published online: 3 SEP 2012 | DOI: 10.1111/j.1471-4159.2012.07909.x

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      Retinas exposed to A1 agonist (CHA) or antagonist (DPCPX) reduced or increased, respectively, A1 receptor expression. A2A agonist (CGS21680) increased while A2A antagonists (SCH58261/ZM241385) decreased A1 receptor Levels. [3H]DPCPX binding kinetics showed that treatment with CHA reduced and CGS21680 increased the Bmax but did not affect Kd values.These data demonstrated an in vivo regulation of A1 receptor expression.

    3. Neuroinflammation & Neuroimmunology

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      Endothelial Japanese encephalitis virus infection enhances migration and adhesion of leukocytes to brain microvascular endothelia via MEK-dependent expression of ICAM1 and the CINC and RANTES chemokines (pages 250–261)

      Ching-Yi Lai, Yen-Chuan Ou, Cheng-Yi Chang, Hung-Chuan Pan, Chen-Jung Chang, Su-Lan Liao, Hong-Lin Su and Chun-Jung Chen

      Article first published online: 23 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07889.x

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      Brain microvascular endothelial cells act as crucial target for Japanese encephalitis-associated recruitment of peripheral immune cells. The characteristics and specific cell types associated with Japanese encephalitis-associated leukocyte trafficking are not understood. JEV infection activates brain microvascular endothelial cells and promotes their interaction with leukocytes. JEV infection could make brain microvascular endothelial cells favorable for the recruitment and adhesion of circulating leukocytes, thereby together with other unidentified barrier-disrupting mechanisms contributing to Japanese encephalitis and associated neuroinflammation.

    4. Neuronal Plasticity & Behavior

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      Neuron-specific non-classical release of prothymosin alpha: a novel neuroprotective damage-associated molecular patterns (pages 262–275)

      Sebok Kumar Halder, Hayato Matsunaga and Hiroshi Ueda

      Article first published online: 23 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07897.x

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      Neuron-specific non-classical release of prothymosin alpha, a novel neuroprotective DAMPsWe have firstly investigated the cell type-specific non-classical release of ProTα from brain after cerebral ischemia. The novel finding is that only neurons have the machineries to release ProTα upon cerebral ischemic stress in vivo. The discovery cell type-specific mechanisms of ProTα signaling in the brain may provide a novel solution to protect chronic cellular damages in stroke.

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      Comparative peptidomics analysis of neural adaptations in rats repeatedly exposed to amphetamine (pages 276–287)

      Elena V. Romanova, Ji Eun Lee, Neil L. Kelleher, Jonathan V. Sweedler and Joshua M. Gulley

      Article first published online: 3 SEP 2012 | DOI: 10.1111/j.1471-4159.2012.07912.x

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      Complex chemical adaptations in the brain reward circuit that occur during AMPH-stimulated behavioral sensitization are measured via mass spectrometry-based peptidomics. Quantified changes in pathways that regulate energy/metabolism, neurotransmission, apoptosis, neuroprotection, neuritogenesis, cytoskeleton integrity, and neuronal morphology imply that diverse pathways other than the mesolimbic dopamine system contribute to the effect of chronic AMPH exposure on behavior.

    6. Molecular Basis of Disease

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      Amphetamine and methamphetamine reduce striatal dopamine transporter function without concurrent dopamine transporter relocalization (pages 288–297)

      Christopher L. German, Glen R. Hanson and Annette E. Fleckenstein

      Article first published online: 23 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07875.x

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      Previous work has found that in vitro application of amphetamine to heterologous cell lines and striatal synaptosomes causes drug-induced internalization of the dopamine (DA) transporter (DAT), implicating transporter endocytosis in reduced DAT function following drug exposure. In contrast, this study found no evidence that single or repeated in vivo administrations of amphetamine or methamphetamine caused acute (within 1 h) striatal DAT relocalization, despite reduced DAT function. Consequently, factors other than internalization are likely responsible for acute and persistent DAT dysfunction following exposure to amphetamines in vivo.

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      Glucocerebrosidase Mutations alter the endoplasmic reticulum and lysosomes in Lewy body disease (pages 298–309)

      Marzena Kurzawa-Akanbi, Peter S Hanson, Peter G Blain, Debra J Lett, Ian G McKeith, Patrick F Chinnery and Christopher M Morris

      Article first published online: 22 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07879.x

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      Glucocerebrosidase Mutations in Lewy Body Disease Mutations in glucocerebrosidase (GBA) increase the risk of Lewy body disease (LBD). Based on the analysis of post-mortem frontal cortex from LBD and controls with GBA mutations, we report on decreased glucocerebrosidase activities, lysosomal abnormalities and impaired unfolded protein response, a potential cause of α-synuclein accumulation. Defects in glucocerebrosidase lead to abnormalities underlying the vulnerability of neurons to α-synuclein dismetabolism.

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      Cholesterol metabolism is associated with soluble amyloid precursor protein production in Alzheimer's disease (pages 310–316)

      Julius Popp, Piotr Lewczuk, Heike Kölsch, Sabrina Meichsner, Wolfgang Maier, Johannes Kornhuber, Frank Jessen and Dieter Lütjohann

      Article first published online: 23 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07893.x

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      Alzheimer's Disease: Cholesterol metabolism is associated with soluble amyloid precursor protein production Alterations of the cholesterol metabolism may contribute to cerebral pathology in Alzheimer's disease (AD). In this study, cerebrospinal fluid cholesterol, 24S-hydroxycholesterol and 27-hydroxycholesterol as well as plasma 27-hydroxycholesterol concentrations predicted the cerebrospinal fluid soluble amyloid precursor protein (sAPP) levels in patients with AD. The results suggest that both peripheral and cerebral cholesterol metabolisms are linked to sAPP production in AD.

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      Swim training attenuates oxidative damage and promotes neuroprotection in cerebral cortical slices submitted to oxygen glucose deprivation (pages 317–324)

      Hércules R. Leite, Flávio A. G. Mourão, Luciana E. Drumond, Talita H. Ferreira-Vieira, Danielle Bernardes, Josiane F. Silva, Virgínia S. Lemos, Márcio F. D. Moraes, Grace S. Pereira, Juliana Carvalho-Tavares and André R. Massensini

      Article first published online: 23 AUG 2012 | DOI: 10.1111/j.1471-4159.2012.07898.x

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      Swim training and cortical neuroprotection.The mechanisms underlying neuroprotective effects of regular exercise are still not fully understood. Here, we showed that swim training promotes neuroprotection decreasing the effects of oxidative stress on lipid membrane damage, as well as, on glutamate and nitric oxide release from brain cortical slices. Our data reinforce the idea that exercise affords a neuroprotective effect.

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      Unregulated brain iron deposition in transgenic mice over-expressing HMOX1 in the astrocytic compartment (pages 325–336)

      Wei Song, Hillel Zukor, Shih-Hsiung Lin, Adrienne Liberman, Ayda Tavitian, Jeannie Mui, Hojatollah Vali, Carine Fillebeen, Kostas Pantopoulos, Ting-Di Wu, Jean-Luc Guerquin-Kern and Hyman M. Schipper

      Article first published online: 3 SEP 2012 | DOI: 10.1111/j.1471-4159.2012.07914.x

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      This study was performed to determine the effects of astroglial HMOX1 expression on brain iron deposition in vivo. The main finding was that over-expression of human HO-1 in astrocytes promotes unregulated brain iron deposition and mitophagy in novel GFAP.HMOX1 transgenic mice. Suppression of glial HO-1 activity may mitigate pathological iron deposition and neuronal damage in Parkinson disease, Alzheimer disease and other aging-related human neurodegenerative disorders.

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