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Journal of Neurochemistry

Cover image for Vol. 120 Issue 1

January 2012

Volume 120, Issue 1

Pages 1–198

  1. EDITORIAL HIGHLIGHTS

    1. Top of page
    2. EDITORIAL HIGHLIGHTS
    3. REVIEW ARTICLES
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    1. You have free access to this content
    2. You have free access to this content
  2. REVIEW ARTICLES

    1. Top of page
    2. EDITORIAL HIGHLIGHTS
    3. REVIEW ARTICLES
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    1. You have free access to this content
      Pathogenic implications of iron accumulation in multiple sclerosis (pages 7–25)

      Rachel Williams, Cassandra L. Buchheit, Nancy E. J. Berman and Steven M. LeVine

      Article first published online: 11 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07536.x

      Corrected by:

      Erratum

      Vol. 121, Issue 2, 326, Article first published online: 17 FEB 2012

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  3. SHORT COMMUNICATION

    1. Top of page
    2. EDITORIAL HIGHLIGHTS
    3. REVIEW ARTICLES
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
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      Phosphorylation of LRRK2 serines 955 and 973 is disrupted by Parkinson’s disease mutations and LRRK2 pharmacological inhibition (pages 37–45)

      Elizabeth A. Doggett, Jing Zhao, Christina N. Mork, Dongmei Hu and R. Jeremy Nichols

      Article first published online: 11 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07537.x

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      Phosphorylated residues as potential biomarkers for Parkinson’s Disease. The study reveals that phosphorylation of serines 955 and 973 is disrupted by acute inhibition of LRRK2 kinase activity and Parkinson’s disease mutations, concluding that these sites, along with Ser910 and Ser935, can be used as biomarkers for LRRK2 activity. Mutations in LRRK2 are a predominant cause of familial Parkinson’s disease.

  4. ORIGINAL ARTICLES

    1. Top of page
    2. EDITORIAL HIGHLIGHTS
    3. REVIEW ARTICLES
    4. SHORT COMMUNICATION
    5. ORIGINAL ARTICLES
    1. Signal Transduction & Synaptic Transmission

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      Angiotensin-(1–7) through Mas receptor up-regulates neuronal norepinephrine transporter via Akt and Erk1/2-dependent pathways (pages 46–55)

      María A. Lopez Verrilli, Martín Rodriguez Fermepín, Nadia Longo Carbajosa, Silvina Landa, Bruno D. Cerrato, Silvia García, Belisario E. Fernandez and Mariela M. Gironacci

      Article first published online: 24 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07552.x

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      Central NET upregulation by angiotensin-(1-7) in hypertension As angiotensin (Ang) (1–7) decreases norepinephrine (NE) content in the synaptic cleft, we investigated the effect of Ang-(1–7) on centrally NE neuronal uptake, the main mechanism for NE removal from the synaptic cleft, in hypothalamic neurons from hypertensive rats. We showed that Ang-(1–7) causes a long-term stimulatory effect on NE neuronal uptake by increasing NE transporter expression. This effect is coupled to Mas receptor activation acting through both MEK1/2-ERK1/2 and PI3-kinase/Akt-dependent pathways. In this way, Ang-(1–7) may regulate a pre-synaptic mechanism in maintaining appropriate synaptic NE levels during hypertensive conditions, thus contributing to the modulation of NE homeostasis and blood pressure regulation.

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      D2-Dopamine receptors target regulator of G protein signaling 9-2 to detergent-resistant membrane fractions (pages 56–69)

      Jeremy Celver, Meenakshi Sharma and Abraham Kovoor

      Article first published online: 24 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07559.x

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      The cellular compartmentalization of a D2-dopamine receptor signaling complex. The study investigated the molecular basis for the functionally important interactions between D2-dopamine receptors (D2R) and the striatally enriched RGS protein, RGS9-2. It was found that D2R is targeted to detergent-resistant membrane (DRM), and D2R in turn targets RGS9-2 to DRM. The results suggest that the D2R signaling complex is compartmentalized in cells via sequestration in detergent-resistant membrane rafts.

    3. Bioenergetics & Metabolism

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      RIP1 mediates the protection of geldanamycin on neuronal injury induced by oxygen-glucose deprivation combined with zVAD in primary cortical neurons (pages 70–77)

      Wei-Wei Chen, Hailong Yu, Hong-Bin Fan, Cui-Cui Zhang, Min Zhang, Caiyi Zhang, Yanbo Cheng, Jiming Kong, Chun-Feng Liu, Deqin Geng and Xingshun Xu

      Article first published online: 18 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07526.x

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      Although previous evidences demonstrated that geldanamycin protects against oxygen-glucose deprivation (OGD)-induced neuronal injury and cerebral ischemic injury, our findings first indicate that the protection of geldanamycin against OGD/zVAD-induced neuronal cell death was associated with decreased RIP1 protein level in primary cortical neurons. This study provides a therapeutic strategy of targeting RIP1 protein degradation by geldanamycin analogues or other reagents.

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      The antiretroviral protease inhibitors indinavir and nelfinavir stimulate Mrp1-mediated GSH export from cultured brain astrocytes (pages 78–92)

      Maria Brandmann, Ketki Tulpule, Maike M. Schmidt and Ralf Dringen

      Article first published online: 11 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07544.x

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      Antiretroviral drugs lower the GSH content of cultured astrocytes.Antiretroviral protease inhibitors are used as drugs for the combinatorial therapy of HIV infection. To test whether such compounds affect the glutathione metabolism of brain cells, cultured astrocytes were exposed to indinavir or nelfinavir. Both protease inhibitors stimulate the multidrug resistance protein 1-mediated export of glutathione, suggesting that continuous treatment of patients with such compounds may affect brain glutathione homeostasis.

    5. Neuroinflammation & Neuroimmunology

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      Neuropeptide Y inhibits interleukin-1 beta-induced microglia motility (pages 93–105)

      Raquel Ferreira, Tiago Santos, Luísa Cortes, Stéphanie Cochaud, Fabienne Agasse, Ana Paula Silva, Sara Xapelli and João O. Malva

      Article first published online: 17 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07541.x

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      Neuropeptide Y (NPY) has been increasingly assigned as a modulator of peripheral inflammatory processes. Herein, we investigated the effect of NPY on microglia motility as part of the inflammatory response to brain injury. We found that NPY limits cell motility upon LPS or interleukin-1β challenge. NPY, by reducing cell recruitment, may restrain the exacerbation of the inflammatory response while maintaining the neuroprotective properties of microglia.

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      Modulatory effects of the CCR5 antagonist maraviroc on microglial pro-inflammatory activation elicited by gp120 (pages 106–114)

      Lucia Lisi, Antonella Tramutola, Andrea De Luca, Pierluigi Navarra and Cinzia Dello Russo

      Article first published online: 17 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07549.x

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      Maroviroc affects microglial activation during HIV-1 infection Despite important clinical benefits of the highly active antiretroviral therapy, neurological disorders affect approximately 50% of AIDS patients. In the present study we tested the hypothesis that maraviroc, by blocking a chemokine receptor, affect microglial activation during HIV-1 infection. Maraviroc downregulated pro-inflammatory gene expression increased by gp120 (early infection), but increased pro-inflammatory activation elicited by gp120 and IFN? (chronic infection).

    7. Neuronal Plasticity & Behavior

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      Erythropoietin improves memory function with reducing endothelial dysfunction and amyloid-beta burden in Alzheimer’s disease models (pages 115–124)

      Soon-Tae Lee, Kon Chu, Jung-Eun Park, Keun-Hwa Jung, Daejong Jeon, Ji-Youn Lim, Sang Kun Lee, Manho Kim and Jae-Kyu Roh

      Article first published online: 11 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07534.x

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      Erythropoietin improves memory in an Alzheimer’s disease model. Neurovascular degeneration contributes to the pathogenesis of Alzheimer’s disease (AD), and erythropoietin (EPO) promotes endothelial regeneration. The study demonstrates that EPO improves memory and ameliorates endothelial degeneration induced by Aβ in AD models. This pre-clinical evidence suggests that EPO may be useful for the treatment of AD.

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      Ceruloplasmin deficiency results in an anxiety phenotype involving deficits in hippocampal iron, serotonin, and BDNF (pages 125–134)

      Sarah J. Texel, Simonetta Camandola, Bruce Ladenheim, Sarah M. Rothman, Mohamed R. Mughal, Erica L. Unger, Jean Lud Cadet and Mark P. Mattson

      Article first published online: 24 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07554.x

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      Low Iron and High Anxiety: A role for Ceruloplasmin in the HippocampusThe function of the iron-regulating protein ceruloplasmin (Cp) in the brain is unknown. We show that Cp-deficient mice exhibit reduced iron levels in the hippocampus, associated with reduced levels of serotonin, norepinephrine, and BDNF, and an anxiety phenotype. These findings suggest key roles for cellular iron handling in the regulation of neurotransmitter and neurotrophic factor signaling, and behaviors they control.

    9. Molecular Basis of Disease

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      Biliverdin reductase-A: a novel drug target for atorvastatin in a dog pre-clinical model of Alzheimer disease (pages 135–146)

      Eugenio Barone, Cesare Mancuso, Fabio Di Domenico, Rukhsana Sultana, M. Paul Murphy, Elizabeth Head and D. Allan Butterfield

      Article first published online: 9 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07538.x

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      Atorvastatin and Reduced risk of Alzheimer Disease: Could Biliverdin Reductase-A Play A Role? As statins reduce risk of Alzheimer disease (AD) and biliverdin reductase-A (BVR-A) is modified in AD, we evaluated the effect of atorvastatin treatment on BVR-A in a pre-clinical AD model (aged beagle). Atorvastatin significantly increased BVR-A levels, phosphorylation, and activity in a brain area affected in AD, improved cognitive function, and decreased AD-relevant BACE1 levels. We propose BVR-A as a novel atorvastatin target in AD.

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      Caveolin-1 regulates nitric oxide-mediated matrix metalloproteinases activity and blood–brain barrier permeability in focal cerebral ischemia and reperfusion injury (pages 147–156)

      Yong Gu, Guoqing Zheng, Mingjing Xu, Yue Li, Xingmiao Chen, Wenzong Zhu, Yao Tong, Sookja K. Chung, Ke Jian Liu and Jiangang Shen

      Article first published online: 17 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07542.x

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      A novel explanation for blood-brain barrier breakdown. Mechanisms of blood–brain barrier (BBB) breakdown are unclear. This study highlighted the roles of caveolin-1 in regulating BBB permeability via inhibiting matrix metalloproteinases (MMPs) and protecting tight junction proteins in microvascular endothelial cells. Nitric oxide mediated MMPs activation is partly through down-regulation of caveolin-1 during cerebral ischemia-reperfusion injury. The study provides a novel explanation for BBB disruption in ischemic stroke.

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      Neuroglobin attenuates Alzheimer-like tau hyperphosphorylation by activating Akt signaling (pages 157–164)

      Li-Ming Chen, Yan-Si Xiong, Fan-Li Kong, Min Qu, Qun Wang, Xiao-Qian Chen, Jian-Zhi Wang and Ling-Qiang Zhu

      Article first published online: 13 MAY 2011 | DOI: 10.1111/j.1471-4159.2011.07275.x

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      Neuroglobin as a potential therapeutic target for Alzheimer’s disease. Neuroglobin (Ngb) can protect neural cells from beta-amyloid-induced toxicity in Alzheimer’s disease (AD). Here, it is reported that the level of Ngb was negatively correlated with tau phosphorylation in a mouse model for Alzheimer’s disease. This study indicates that Ngb may attenuate tau hyperphosphorylation through activating the Akt signaling pathway, implying a therapeutic target for AD.

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      Phosphorylation of microtubule-associated protein tau by AMPK-related kinases (pages 165–176)

      Hirotaka Yoshida and Michel Goedert

      Article first published online: 11 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07523.x

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      Microtubule-associated protein tau is abnormally hyperphosphorylated in the filamentous inclusions of human tauopathies. Phosphorylation of S262/S356 is known to regulate microtubule dynamics and transport. We show that AMPK-related kinases are involved in the phosphorylation of S262/S356, implying their possible role in the hyperphosphorylation of tau.

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      Prion protein polymerisation triggered by manganese-generated prion protein seeds (pages 177–189)

      Shirley Hesketh, Andrew R. Thompsett and David R. Brown

      Article first published online: 11 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07540.x

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      The Seedy side of PrionsThis study was undertaken to better identify the catalytic mechanism of seeded prion protein aggregation using a novel polymerisation assay for PrP, which does not require denaturants, but relies on the generation of prion seeds by reaction with manganese. Our findings suggest that the polymerisation process and possibly the infection process are dependent on unique key characteristics of both the substrate and the seed within this reaction. The kinetics involved suggests that seed formation must be an ongoing process during the disease and the disruption of this process might prove a possible avenue to prevent disease progression.

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      Cell adhesion molecules contribute to Alzheimer’s disease: multiple pathway analyses of two genome-wide association studies (pages 190–198)

      Guiyou Liu, Yongshuai Jiang, Ping Wang, Rennan Feng, Nan Jiang, Xiaoyun Chen, Hui Song and Zugen Chen

      Article first published online: 17 NOV 2011 | DOI: 10.1111/j.1471-4159.2011.07547.x

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      Cell adhesion molecules contribute to Alzheimer’s disease The findings of this study corroborate the link between cell adhesion molecules pathway and susceptibility to Alzheimer’s disease, paving the way for genetic analysis of AD and possible development of therapeutic strategies.

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