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Journal of Neurochemistry

Cover image for Vol. 120 Issue 6

March 2012

Volume 120, Issue 6

Pages 851–1144

  1. EDITORIAL HIGHLIGHT

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW ARTICLES
    4. ORIGINAL ARTICLES
    5. OBITUARY
    6. RETRACTION
    7. ACKNOWLEDGEMENT OF REVIEWERS
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      Where did the ventricles go? (pages 851–852)

      Richard F. Keep, Jianming Xiang and Anuska V. Andjelkovic

      Version of Record online: 6 MAR 2012 | DOI: 10.1111/j.1471-4159.2011.07585.x

  2. REVIEW ARTICLES

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW ARTICLES
    4. ORIGINAL ARTICLES
    5. OBITUARY
    6. RETRACTION
    7. ACKNOWLEDGEMENT OF REVIEWERS
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      β-Site APP-cleaving enzyme 1 trafficking and Alzheimer’s disease pathogenesis (pages 869–880)

      Jiangli Tan and Geneviève Evin

      Version of Record online: 23 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07623.x

  3. ORIGINAL ARTICLES

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW ARTICLES
    4. ORIGINAL ARTICLES
    5. OBITUARY
    6. RETRACTION
    7. ACKNOWLEDGEMENT OF REVIEWERS
    1. Gene Regulation & Genetics

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      Serine hydroxymethyltransferase 1 and 2: gene sequence variation and functional genomic characterization (pages 881–890)

      Scott J. Hebbring, Yubo Chai, Yuan Ji, Ryan P. Abo, Gregory D. Jenkins, Brooke Fridley, Jianping Zhang, Bruce W. Eckloff, Eric D. Wieben and Richard M. Weinshilboum

      Version of Record online: 6 FEB 2012 | DOI: 10.1111/j.1471-4159.2012.07646.x

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      Serine hydroxymethyltransferase (SHMT) genomics and functional genomics. SHMT1 and SHMT2 are enzymes in the ‘Folate Cycle’– a cycle that plays an important role in neural development and function. In this study, we resequenced the SHMT1 and SHMT2 genes and performed functional genomic studies which identified SNPs that were highly correlated with expression of both mRNA and protein.

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      Epigenetic dysregulation of the dopamine system in diet-induced obesity (pages 891–898)

      Zivjena Vucetic, Jesse Lea Carlin, Kathy Totoki and Teresa M. Reyes

      Version of Record online: 6 FEB 2012 | DOI: 10.1111/j.1471-4159.2012.07649.x

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      Chronic consumption of a high-fat diet can alter the expression of dopamine-related genes; however, the mechanism that drives this response remains unclear. This work identifies differential DNA methylation as a potential link between high-fat diet and altered gene expression in the brain. A better understanding of the CNS adaptations that occur during the development of obesity will prove critical in designing both better behavioral and pharmacological therapeutics for obesity.

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      An astrocyte-specific enhancer of the aquaporin-4 gene functions through a consensus sequence of POU transcription factors in concert with multiple upstream elements (pages 899–912)

      Yoichiro Abe, Hiroko Ikeshima-Kataoka, Wakami Goda, Takako Niikura and Masato Yasui

      Version of Record online: 2 FEB 2012 | DOI: 10.1111/j.1471-4159.2012.07652.x

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      Aquaporin-4 is a water channel specifically expressed in astrocytes in the brain. In this study, a 286-bp region in the 5′-flanking region of the mouse aquaporin-4 gene was found to enhance promoter activity specifically in astrocytes. Clustered five cis-elements, including a consensus sequence of POU transcription factors, are cooperatively involved in the transcription. This study demonstrates a novel mechanism for transcriptional regulation in astrocytes.

      Corrected by:

      Corrigendum: Corrigendum

      Vol. 138, Issue 4, 640–641, Version of Record online: 24 JUN 2016

    4. Brain Development & Cell Differentiation

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      Molecular heterogeneity in the choroid plexus epithelium: the 22-member γ-protocadherin family is differentially expressed, apically localized, and implicated in CSF regulation (pages 913–927)

      Mark A. Lobas, Lindsey Helsper, Claire G. Vernon, Dietmar Schreiner, Yong Zhang, Michael J. Holtzman, Daniel R. Thedens and Joshua A. Weiner

      Version of Record online: 7 DEC 2011 | DOI: 10.1111/j.1471-4159.2011.07587.x

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      Not just for neurons anymore: brain epithelial cells show protocadherin specificity tooThe γ-protocadherins (γ-Pcdhs) are a family of 22 cadherin-like adhesion molecules, differentially expressed among neurons, that are critical for neural circuit formation and neuronal survival. We found that these proteins are highly expressed in the choroid plexus (CP), epithelial cells that produce cerebrospinal fluid (CSF), suggesting a role in this tissue.We found that, like neurons, each CP epithelial cell expresses distinct subsets of γ-Pcdhs, and localizes the proteins to their apical surface. Mice lacking the γ-Pcdhs only in the CP exhibit small ventricles, suggesting a role for this protein family in CSF dynamics.This work uncovers a surprising molecular diversity of CP epithelial cells, and implicates this diversity in the control of brain metabolism.

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      Dystroglycan promotes filopodial formation and process branching in differentiating oligodendroglia (pages 928–947)

      Christopher Eyermann, Kevin Czaplinski and Holly Colognato

      Version of Record online: 4 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07600.x

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      Legend: Dystroglycan (green) and F-actin (red) enriched filopodia extending from the leading edge of an oligodendroglial process. Methods: Oligodendrocyte precursor cells were transfected (Amaxa) with a full-length dystroglycan construct expressing GFP (DG-GFP), differentiated for 48 h, and fixed with 4% PFA. Cells were incubated with rabbit anti-GFP (Molecular Probes, Eugene, OR, USA) in 1% BSA, followed by DyLight 488 anti-rabbit secondary (Jackson Immuno-Research). Cells were co-stained with Texas Red phalloidin (Invitrogen) to visualize F-actin. Non-muscle dystroglycan: how oligodendroglia “shape” up We report that the extracellular matrix receptor dystroglycan is necessary for laminin enhancement of filopodial formation, process outgrowth, and process branching in differentiating oligodendroglia. Dystroglycan-blocking antibodies reduced filopodia formation in newly differentiating oligodendroglia, whereas dystroglycan depletion via siRNA decreased the process branching complexity of pre-myelinating oligodendroglia. These results suggest that dystroglycan–laminin interactions influence oligodendroglia process dynamics and may regulate the myelination capacity of individual oligodendroglia.

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      Sex differences in microglial colonization of the developing rat brain (pages 948–963)

      Jaclyn M. Schwarz, Paige W. Sholar and Staci D. Bilbo

      Version of Record online: 9 FEB 2012 | DOI: 10.1111/j.1471-4159.2011.07630.x

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      Colonization of Microglia in Cognitive Brain Regions: Sex Differences Neonatal male rats have significantly more amoeboid microglia than females within the hippocampus, cortex and amygdala. Before adolescence and into adulthood, females have significantly more microglia with long, branched processes than males in these same brain regions. These data may lend valuable insight into distinct windows of vulnerability between the sexes following an immune challenge.

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      Exposure of foetal neural progenitor cells to IL-1β impairs their proliferation and alters their differentiation – a role for maternal inflammation? (pages 964–973)

      Sean J. Crampton, Louise M. Collins, Andre Toulouse, Yvonne M. Nolan and Gerard W. O’Keeffe

      Version of Record online: 9 FEB 2012 | DOI: 10.1111/j.1471-4159.2011.07634.x

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      A role for maternal inflammation in neural progenitor cell development? Inflammatory cytokines have the potential to affect the developing brain. Here, we report that IL-1β can inhibit the growth and alter the differentiation of foetal neural progenitor cells. This study necessitates an examination of the consequences that maternal immune system activation during pregnancy has on the cellular architecture of the developing brain

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      Group IVA phospholipase A2 is necessary for growth cone repulsion and collapse (pages 974–984)

      Staci D. Sanford, Bo Goen Yun, Christina C. Leslie, Robert C. Murphy and Karl H. Pfenninger

      Version of Record online: 6 FEB 2012 | DOI: 10.1111/j.1471-4159.2012.07651.x

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      Critical Role for Phospholipase A2 in Growth Cone Repulsion. The goal is to advance our understanding of the molecular mechanism that triggers growth cone detachment during repellent-induced turning and collapse. We report that semaphorin 3A stimulation of Group IVA phospholipase A2 (GIVA PLA2) is necessary for growth cone turning and collapse. The data introduce GIVA PLA2 and the generation of arachidonic acid into the semaphorin 3A-activated signaling pathway that regulates growth cone adhesion.

    9. Bioenergetics & Metabolism

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      Dietary n-6 polyunsaturated fatty acid deprivation increases docosahexaenoic acid metabolism in rat brain (pages 985–997)

      Miki Igarashi, Hyung-Wook Kim, Lisa Chang, Kaizong Ma and Stanley I. Rapoport

      Version of Record online: 23 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07597.x

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      Dietary n-6 polyunsaturated fatty acid (PUFA) deprivation increases docosahexaenoic acid (DHA) content and DHA-selective Ca2+-independent iPLA2 expression in rat brain. In this study, we report that these changes are accompanied by up-regulated DHA incorporation from plasma and DHA turnover in brain phospholipids. Increased DHA metabolism following dietary n-6 PUFA deprivation may increase antiinflammatory DHA metabolites in brain and promote neuroprotection.

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      Tacrine and its analogues impair mitochondrial function and bioenergetics: a lipidomic analysis in rat brain (pages 998–1013)

      Tânia Melo, Romeu A. Videira, Sónia André, Elisabete Maciel, Carla S. Francisco, Ana M. Oliveira-Campos, Lígia M. Rodrigues, Maria R.M. Domingues, Francisco Peixoto and M. Manuel Oliveira

      Version of Record online: 10 FEB 2012 | DOI: 10.1111/j.1471-4159.2011.07636.x

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      Understanding the brain activity of tacrine and related compounds is important to design drugs that improve their therapeutic efficiency for Alzheimer’s disease. We report that tacrine and two tacrine analogues decrease mitochondrial cardiolipin content and increase phosphatidylserines oxidation, which are linked with the loss of respiratory energy control. Although their inhibition on acetylcholinesterase activity might be considered therapeutic, they could also worsen the disease by damaging neural cell respiration.

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      Ca2+ signals of astrocytes are modulated by the NAD+/NADH redox state (pages 1014–1025)

      Robert P. Requardt, Petra G. Hirrlinger, Franziska Wilhelm, Ulrike Winkler, Stefanie Besser and Johannes Hirrlinger

      Version of Record online: 2 FEB 2012 | DOI: 10.1111/j.1471-4159.2012.07645.x

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      The adjustment of signaling and energy metabolism is a crucial task for the brain and the NAD+/NADH redox state is of central importance for cellular energy metabolism. Here, we show that the NAD+/NADH redox state modulates dopamine-induced Ca2+-signals in cortical astrocytes. This modulation most likely contributes to coordinating the metabolic status and Ca2+-signals in the context of cortical dopaminergic signaling.

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      Enzymatic transamination of d-kynurenine generates kynurenic acid in rat and human brain (pages 1026–1035)

      Veronica Pérez-de la Cruz, Laura Amori, Korrapati V. Sathyasaikumar, Xiao-Dan Wang, Francesca M. Notarangelo, Hui-Qiu Wu and Robert Schwarcz

      Version of Record online: 2 FEB 2012 | DOI: 10.1111/j.1471-4159.2012.07653.x

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      Transamination of D-kynurenine generates kynurenic acid in rat and human brainLike the natural tryptophan metabolite l-kynurenine, d-kynurenine might be transaminated to kynurenic acid (KYNA), an astrocyte-derived neuromodulator with possible links to human brain diseases. This KYNA synthesis route was demonstrated using brain and liver tissue homogenate from rats and humans, and confirmed in the rat striatum in vivo. Endogenous d-kynurenine, perhaps stemming from microorganisms, might constitute an alternate source of KYNA in the mammalian brain.

    13. Neuroinflammation & Neuroimmunology

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      Activation of transient receptor potential ankyrin 1 evokes nociception through substance P release from primary sensory neurons (pages 1036–1047)

      Yoki Nakamura, Yujiro Une, Kanako Miyano, Hiromi Abe, Kazue Hisaoka, Norimitsu Morioka and Yoshihiro Nakata

      Version of Record online: 6 FEB 2012 | DOI: 10.1111/j.1471-4159.2011.07628.x

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      How does activation of TRPA1 induce nociceptive behaviors and inflammatory responses? Activation of peripheral TRPA1 leads to phosphorylation of intracellular p38 MAP kinase and substance P release from both central and peripheral terminals of primary sensory neurons. Hence, substance P mediates TRPA1-induced responses and modulation of TRPA1 could be a potent therapeutic approach.

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      Obovatol improves cognitive functions in animal models for Alzheimer’s disease (pages 1048–1059)

      Dong-Young Choi, Jae Woong Lee, Jin Peng, Young Jung Lee, Jin-Yi Han, Yeon Hee Lee, Im Seop Choi, Sang Bae Han, Jae Kyung Jung, Woong Soo Lee, Seung-Ho Lee, Byoung-Mog Kwon, Ki-Wan Oh and Jin Tae Hong

      Version of Record online: 10 FEB 2012 | DOI: 10.1111/j.1471-4159.2011.07642.x

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      Anti-neuroinflammation and improved cognitive function by obovatol. Neuroinflammation and deposition of amyloid-beta are implicated in pathogenesis of Alzheimer’s disease. Here, we demonstrated that obovatol, a natural anti-neuroinflammatory compound attenuated cognitive impairments in Alzheimer’s disease model and the effects were related to suppression of NF-κB pathway. These results suggest that obovatol could be a therapeutic intervention of Alzheimer’s disease pathogenesis

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      Saturated long-chain fatty acids activate inflammatory signaling in astrocytes (pages 1060–1071)

      Sunita Gupta, Alecia G. Knight, Shruti Gupta, Jeffrey N. Keller and Annadora J. Bruce-Keller

      Version of Record online: 6 FEB 2012 | DOI: 10.1111/j.1471-4159.2012.07660.x

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      The good fat, the bad fat, and the brain Obesity and metabolic syndrome detrimentally affect the brain through unknown mechanisms. This paper demonstrates the ability of saturated fatty acids to trigger cytokine release from cultured astrocytes, and the ability of ω-3 unsaturated fatty acids to block cytokine release. These data suggest that circulating saturated fatty acids could cause brain inflammation and thus participate in the adverse neurologic consequences of metabolic syndrome

    16. Neuronal Plasticity & Behavior

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      Harpagoside attenuates MPTP/MPP+ induced dopaminergic neurodegeneration and movement disorder via elevating glial cell line-derived neurotrophic factor (pages 1072–1083)

      Xiaoyu Sun, Zhongkui Xiong, Yongfang Zhang, Ya Meng, Gang Xu, Zhiming Xia, Jiamei Li, Rui Zhang, Zunji Ke, Zongqin Xia and Yaer Hu

      Version of Record online: 6 FEB 2012 | DOI: 10.1111/j.1471-4159.2011.07635.x

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      Harpagoside attenuates dopaminergic degeneration via elevating glial cell line-derived neurotrophic factorNew therapeutic approaches targeting the dopaminergic neurodegenerative process are under active investigations. In this study, we report that harpagoside, an iridoid purified from the Chinese medicinal herb Scrophularia ningpoensis, significantly prevents and rescues the MPP+/MPTP-induced dopaminergic neurodegeneration and movement disorder, mainly through elevating glial cell line-derived neurotrophic factor (GDNF). Thus, we provide brand-new basic evidence for clinical researches.

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      Minimal essential length of Clostridium botulinum C3 peptides to enhance neuronal regenerative growth and connectivity in a non-enzymatic mode (pages 1084–1096)

      Peter Loske, Francesco Boato, Sven Hendrix, Johannes Piepgras, Ingo Just, Gudrun Ahnert-Hilger and Markus Höltje

      Version of Record online: 6 FEB 2012 | DOI: 10.1111/j.1471-4159.2012.07657.x

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      Short cut to regeneration: small C3bot peptides help neurons to regrow The current study was undertaken to determine the shortest peptide fragment derived from Clostridium botulinum C3 transferase to foster neuronal regenerative growth. Here, we show that short enzyme-deficient C3 peptides, especially a 26 amino acid fragment, can act to improve neuronal outgrowth and to enhance motor regeneration after spinal cord injury. Therefore, we consider treatment with C3 peptides as a very promising strategy for future goals to improve recovery from devastating neuronal injuries including damage to the spinal cord. This seems to be all the more important since no specific neuronal treatment regimes exist so far. Cross-section of mouse spinal cord at darkfield illumination. Graph shows results of C3bot 26mer on motor recovery following spinal cord injury. Small micrograph depicts serotonergic boutons contacting spinal motoneurons.

    18. Molecular Basis of Disease

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      Mephedrone, an abused psychoactive component of ‘bath salts’ and methamphetamine congener, does not cause neurotoxicity to dopamine nerve endings of the striatum (pages 1097–1107)

      Mariana Angoa-Pérez, Michael J. Kane, Dina M. Francescutti, Katherine E. Sykes, Mrudang M. Shah, Abiy M. Mohammed, David M. Thomas and Donald M. Kuhn

      Version of Record online: 9 FEB 2012 | DOI: 10.1111/j.1471-4159.2011.07632.x

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      “Meow meow” turns out to be a kitten and not a lion Mephedrone, a psychoactive component of “bath salts”, is being abused increasingly throughout the US and Europe but it is not known if this agent is neurotoxic like its close structural congener methamphetamine. Mice treated with a binge-like dosing regimen of mephedrone did not show signs of damage to dopamine nerve terminals despite developing significant hyperthermia and hyper-locomotion, indices of increased synaptic dopamine. It appears that the addition to methamphetamine of a β-keto group and a 4-methyl substituent on the ring to yield mephedrone obviates the neurotoxicity caused by methamphetamine ingestion.

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      Nicotine stimulates secretion of corticosterone via both CRH and AVP receptors (pages 1108–1116)

      Kabirullah Lutfy, Otaren Aimiuwu, Michael Mangubat, Chang-Sung Shin, Namiko Nerio, Richard Gomez, Yanjun Liu and Theodore C. Friedman

      Version of Record online: 23 JAN 2012 | DOI: 10.1111/j.1471-4159.2011.07633.x

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      How does nicotine activate the stress response? The study was performed to determine which CRH receptor is involved in the nicotine-stimulated secretion of corticosterone. The nicotine-induced stimulation of the hypothalamic-pituitary adrenal axis (HPA) is mediated by both the CRH-R and the AVP V1b receptor and when the CRH receptor is blocked, nicotine may utilize the AVP V1b receptor to mediate secretion of corticosterone. The use of specific antagonists that block both AVP and CRH receptors may be needed to decrease the pleasurable component of nicotine, which may be mediated by corticosterone.

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      Myosin II activity regulates neurite outgrowth and guidance in response to chondroitin sulfate proteoglycans (pages 1117–1128)

      Panpan Yu, Lizzie Y. Santiago, Yasuhiro Katagiri and Herbert M. Geller

      Version of Record online: 6 FEB 2012 | DOI: 10.1111/j.1471-4159.2011.07638.x

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      Chondroitin sulfate proteoglycans (CSPGs) play a negative role in axon guidance and regeneration. We demonstrate that these actions of CSPGs are dependent upon myosin II activity as CSPGs increase the phosphorylation of myosin light chains and inhibition of myosin II activity promotes growth on CSPGs. These results extend our knowledge of the role of cytoskeletal motor proteins in response to inhibitory axon guidance molecules.

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      Control of BACE1 degradation and APP processing by ubiquitin carboxyl-terminal hydrolase L1 (pages 1129–1138)

      Mingming Zhang, Yu Deng, Yawen Luo, Shuting Zhang, Haiyan Zou, Fang Cai, Keiji Wada and Weihong Song

      Version of Record online: 10 FEB 2012 | DOI: 10.1111/j.1471-4159.2011.07644.x

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      BACE1 is essential for generating Aβ, a central component of neuritic plaques in AD brains. Previously we demonstrated that BACE1 is ubiquitinated and the degradation of BACE1 is mediated by the ubiquitin-proteasome pathway. Ubiquitin carboxyl-terminal hydrolase L1 (UCHL1) is a deubiquitinating enzyme that regulates ubiquitin-dependent protein degradation. This study aimed to define the role of UCHL1 in the proteasomal degradation of BACE1. We found that overexpression of UCHL1 accelerates BACE1degradation and decreases APP C99 and Aβ generation in the stable cells, and disruption of Uchl1 gene significantly elevates levels of endogenous BACE1, C99 and Aβ in the Uchl1-null gad mice. The study demonstrated that UCHL1 affects BACE1 degradation, APP processing and Aβ production both in vitro and in vivo. The results suggest that potentiation of UCHL1 might be able to reduce the level of BACE1 and Aβ in brains, which makes it a novel target for AD drug development.

  4. OBITUARY

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW ARTICLES
    4. ORIGINAL ARTICLES
    5. OBITUARY
    6. RETRACTION
    7. ACKNOWLEDGEMENT OF REVIEWERS
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      Mark A. Smith: neurocytochemistry innovator (pages 1139–1140)

      Xiongwei Zhu, Rudy J. Castellani, Nicholas P. Ziats, Robert B. Petersen, Hyoung gon Lee and George Perry

      Version of Record online: 23 JAN 2012 | DOI: 10.1111/j.1471-4159.2012.07656.x

  5. RETRACTION

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW ARTICLES
    4. ORIGINAL ARTICLES
    5. OBITUARY
    6. RETRACTION
    7. ACKNOWLEDGEMENT OF REVIEWERS
    1. You have free access to this content
  6. ACKNOWLEDGEMENT OF REVIEWERS

    1. Top of page
    2. EDITORIAL HIGHLIGHT
    3. REVIEW ARTICLES
    4. ORIGINAL ARTICLES
    5. OBITUARY
    6. RETRACTION
    7. ACKNOWLEDGEMENT OF REVIEWERS
    1. You have free access to this content
      Acknowledgement of Reviewers (pages 1142–1144)

      Version of Record online: 6 MAR 2012 | DOI: 10.1111/j.1471-4159.2012.07672.x

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