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[PMID]: 27180142
[Au] Autor:Canavero S; Ren X; Kim CY; Rosati E
[Ad] Address:Turin Advanced Neuromodulation Group, Turin, Italy. Electronic address: sercan@inwind.it....
[Ti] Title:Neurologic foundations of spinal cord fusion (GEMINI).
[So] Source:Surgery;160(1):11-9, 2016 Jul.
[Is] ISSN:1532-7361
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Cephalosomatic anastomosis has been carried out in both monkeys and mice with preservation of brain function. Nonetheless the spinal cord was not reconstructed, leaving the animals unable to move voluntarily. Here we review the details of the GEMINI spinal cord fusion protocol, which aims at restoring electrophysiologic conduction across an acutely transected spinal cord. The existence of the cortico-truncoreticulo-propriospinal pathway, a little-known anatomic entity, is described, and its importance concerning spinal cord fusion emphasized. The use of fusogens and electrical stimulation as adjuvants for nerve fusion is addressed. The possibility of achieving cephalosomatic anastomosis in humans has become reality in principle.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1606
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review

  2 / 1352174 MEDLINE  
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[PMID]: 27143608
[Au] Autor:Ren X; Orlova EV; Maevsky EI; Bonicalzi V; Canavero S
[Ad] Address:Hand and Microsurgical Center, the Second Affiliated Hospital of Harbin Medical University, Harbin, China; State-Province Key Laboratories of Biomedicine-Pharmaceutics, Harbin Medical University, Harbin, China; Department of Molecular Pharmacology and Therapeutics, Stritch School of Medicine, Loyola...
[Ti] Title:Brain protection during cephalosomatic anastomosis.
[So] Source:Surgery;160(1):5-10, 2016 Jul.
[Is] ISSN:1532-7361
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Cephalosomatic anastomosis requires neuroprotective techniques, such as deep hypothermia, to preserve brain activity. Despite the failure of pharmacologic neuroprotection, new strategies, including ischemic pre- and postconitioning and the use of Perftoran, have to be explored to complement hypothermia. This article summarizes the field of brain protection during CSA and these promising strategies.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1606
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review

  3 / 1352174 MEDLINE  
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[PMID]: 26827626
[Au] Autor:Sivukhina EV; Jirikowski GF
[Ad] Address:Institute of Anatomy II, Jena University Hospital, Jena, Germany.
[Ti] Title:Magnocellular hypothalamic system and its interaction with the hypothalamo-pituitary-adrenal axis.
[So] Source:Steroids;111:21-8, 2016 Jul.
[Is] ISSN:1878-5867
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The hypothalamo-neurohypophyseal system plays a key role in maintaining homeostasis and in regulation of numerous adaptive reactions, e.g., endocrine stress response. Nonapeptides vasopressin and oxytocin are the major hormones of this system. They are synthesized by magnocellular neurons of the paraventricular and supraoptic hypothalamic nuclei. Magnocellular vasopressin is known to be one of the main physiological regulators of water-electrolyte balance. Its importance for control of the hypothalamo-pituitary-adrenal axis has been widely described. Magnocellular oxytocin is secreted predominantly during lactation and parturition. The complex actions of oxytocin within the brain include control of reproductive behavior and its involvement in central stress response to different stimuli. It's neuroendocrine basis is activation of the hypothalamo-pituitary-adrenal axis: corticotropin-releasing hormone is synthesized in parvocellular neurons of the paraventricular hypothalamic nuclei. The transitory coexpression of vasopressin in these cells upon stress has been described. Glucocorticoids, the end products of the hypothalamo-pituitary-adrenal axis have both central and peripheral actions. Their availability to target tissues is mainly dependent on systemic levels of corticosteroid-binding globulin. Intrinsic expression of this protein in different brain regions in neurons and glial cells has been recently demonstrated. Regulation of the hypothalamo-pituitary-adrenal axis and hypothalamo-neurohypophyseal system is highly complex. The role of both systems in the pathogenesis of various chronic ailments in humans has extensively been studied. Their disturbed functioning seems to be linked to various psychiatric, autoimmune and cardiovascular pathologies.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1606
[Js] Journal subset:IM
[St] Status:In-Data-Review

  4 / 1352174 MEDLINE  
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[PMID]: 26980143
[Au] Autor:Georgiev D; Yoshihara T; Kawabata R; Matsubara T; Tsubomoto M; Minabe Y; Lewis DA; Hashimoto T
[Ad] Address:Department of Psychiatry and Neurobiology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan;...
[Ti] Title:Cortical Gene Expression After a Conditional Knockout of 67 kDa Glutamic Acid Decarboxylase in Parvalbumin Neurons.
[So] Source:Schizophr Bull;42(4):992-1002, 2016 Jul.
[Is] ISSN:1745-1701
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:In the cortex of subjects with schizophrenia, expression of glutamic acid decarboxylase 67 (GAD67), the enzyme primarily responsible for cortical GABA synthesis, is reduced in the subset of GABA neurons that express parvalbumin (PV). This GAD67 deficit is accompanied by lower cortical levels of other GABA-associated transcripts, including GABA transporter-1, PV, brain-derived neurotrophic factor (BDNF), tropomyosin receptor kinase B, somatostatin, GABAA receptor α1 subunit, and KCNS3 potassium channel subunit mRNAs. In contrast, messenger RNA (mRNA) levels for glutamic acid decarboxylase 65 (GAD65), another enzyme for GABA synthesis, are not altered. We tested the hypothesis that this pattern of GABA-associated transcript levels is secondary to the GAD67 deficit in PV neurons by analyzing cortical levels of these GABA-associated mRNAs in mice with a PV neuron-specific GAD67 knockout. Using in situ hybridization, we found that none of the examined GABA-associated transcripts had lower cortical expression in the knockout mice. In contrast, PV, BDNF, KCNS3, and GAD65 mRNA levels were higher in the homozygous mice. In addition, our behavioral test battery failed to detect a change in sensorimotor gating or working memory, although the homozygous mice exhibited increased spontaneous activities. These findings suggest that reduced GAD67 expression in PV neurons is not an upstream cause of the lower levels of GABA-associated transcripts, or of the characteristic behaviors, in schizophrenia. In PV neuron-specific GAD67 knockout mice, increased levels of PV, BDNF, and KCNS3 mRNAs might be the consequence of increased neuronal activity secondary to lower GABA synthesis, whereas increased GAD65 mRNA might represent a compensatory response to increase GABA synthesis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1606
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1093/schbul/sbw022

  5 / 1352174 MEDLINE  
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[PMID]: 26712857
[Au] Autor:Voineskos AN; Felsky D; Wheeler AL; Rotenberg DJ; Levesque M; Patel S; Szeszko PR; Kennedy JL; Lencz T; Malhotra AK
[Ad] Address:Campbell Family Mental Health Institute, Centre for Addiction and Mental Health, Toronto, Ontario, Canada; Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada; These authors contributed equally to the article. Aristotle.Voineskos@camh.ca....
[Ti] Title:Limited Evidence for Association of Genome-Wide Schizophrenia Risk Variants on Cortical Neuroimaging Phenotypes.
[So] Source:Schizophr Bull;42(4):1027-36, 2016 Jul.
[Is] ISSN:1745-1701
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: There are now over 100 established genetic risk variants for schizophrenia; however, their influence on brain structure and circuitry across the human lifespan are not known. METHODS: We examined healthy individuals 8-86 years of age, from the Centre for Addiction and Mental Health, the Zucker Hillside Hospital, and the Philadelphia Neurodevelopmental Cohort. Following thorough quality control procedures, we investigated associations of established genetic risk variants with heritable neuroimaging phenotypes relevant to schizophrenia, namely thickness of frontal and temporal cortical regions (n = 565) and frontotemporal and interhemispheric white matter tract fractional anisotropy (FA) (n = 530). RESULTS: There was little evidence for association of risk variants with imaging phenotypes. No association with cortical thickness of any region was present. Only rs12148337, near a long noncoding RNA region, was associated with white matter FA (splenium of corpus callosum) following multiple comparison correction (corrected p = .012); this single nucleotide polymorphism was also associated with genu FA and superior longitudinal fasciculus FA at p <.005 (uncorrected). There was no association of polygenic risk score with white matter FA or cortical thickness. CONCLUSIONS: In sum, our findings provide limited evidence for association of schizophrenia risk variants with cortical thickness or diffusion imaging white matter phenotypes. When taken with recent lack of association of these variants with subcortical brain volumes, our results either suggest that structural neuroimaging approaches at current resolution are not sufficiently sensitive to detect effects of these risk variants or that multiple comparison correction in correlated phenotypes is too stringent, potentially "eliminating" biologically important signals.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1606
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1093/schbul/sbv180

  6 / 1352174 MEDLINE  
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[PMID]: 26656881
[Au] Autor:van den Oord EJ; Clark SL; Xie LY; Shabalin AA; Dozmorov MG; Kumar G; Vladimirov VI; Magnusson PK; Aberg KA; Swedish Schizophrenia Consortium
[Ad] Address:Center for Biomarker Research and Precision Medicine, Virginia Commonwealth University, Richmond, VA; ejvandenoord@vcu.edu....
[Ti] Title:A Whole Methylome CpG-SNP Association Study of Psychosis in Blood and Brain Tissue.
[So] Source:Schizophr Bull;42(4):1018-26, 2016 Jul.
[Is] ISSN:1745-1701
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Mutated CpG sites (CpG-SNPs) are potential hotspots for human diseases because in addition to the sequence variation they may show individual differences in DNA methylation. We performed methylome-wide association studies (MWAS) to test whether methylation differences at those sites were associated with schizophrenia. We assayed all common CpG-SNPs with methyl-CpG binding domain protein-enriched genome sequencing (MBD-seq) using DNA extracted from 1408 blood samples and 66 postmortem brain samples (BA10) of schizophrenia cases and controls. Seven CpG-SNPs passed our FDR threshold of 0.1 in the blood MWAS. Of the CpG-SNPs methylated in brain, 94% were also methylated in blood. This significantly exceeded the 46.2% overlap expected by chance (P-value < 1.0×10(-8)) and justified replicating findings from blood in brain tissue. CpG-SNP rs3796293 in IL1RAP replicated (P-value = .003) with the same direction of effects. This site was further validated through targeted bisulfite pyrosequencing in 736 independent case-control blood samples (P-value < 9.5×10(-4)). Our top result in the brain MWAS (P-value = 8.8×10(-7)) was CpG-SNP rs16872141 located in the potential promoter of ENC1. Overall, our results suggested that CpG-SNP methylation may reflect effects of environmental insults and can provide biomarkers in blood that could potentially improve disease management.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1606
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1093/schbul/sbv182

  7 / 1352174 MEDLINE  
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[PMID]: 27288826
[Au] Autor:Han JC
[Ad] Address:Department of Pediatrics, University of Tennessee Health Science Center and Children's Foundation Research Institute, Le Bonheur Children's Hospital, Memphis, TN, United States of America. Electronic address: jhan14@uthsc.edu.
[Ti] Title:Rare Syndromes and Common Variants of the Brain-Derived Neurotrophic Factor Gene in Human Obesity.
[So] Source:Prog Mol Biol Transl Sci;140:75-95, 2016.
[Is] ISSN:1878-0814
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Rare genetic disorders that cause BDNF haploinsufficiency, such as WAGR syndrome, 11p deletion, and 11p inversion, serve as models for understanding the role of BDNF in human energy balance and neurocognition. Patients with BDNF haploinsufficiency or inactivating mutations of the BDNF receptor exhibit hyperphagia, childhood-onset obesity, intellectual disability, and impaired nociception. Prader-Willi, Smith-Magenis, and ROHHAD syndromes are separate genetic disorders that do not directly affect the BDNF locus but share many similar clinical features with BDNF haploinsufficiency, and BDNF insufficiency is believed to possibly contribute to the pathophysiology of each of these conditions. In the general population, common variants of BDNF that affect BDNF gene expression or BDNF protein processing have also been associated with modest alterations in energy balance and cognitive functioning. Thus, variable degrees of BDNF insufficiency appear to contribute to a spectrum of excess weight gain and cognitive impairment that ranges in phenotypic severity. In this modern era of precision medicine, genotype-specific therapies aimed at increasing BDNF signaling in patients with rare and common disorders associated with BDNF insufficiency could serve as useful approaches for treating obesity and neurodevelopmental disorders.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1606
[Js] Journal subset:IM
[St] Status:In-Data-Review

  8 / 1352174 MEDLINE  
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[PMID]: 27155457
[Au] Autor:Wong VS; Langley B
[Ad] Address:Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, United States.
[Ti] Title:Epigenetic changes following traumatic brain injury and their implications for outcome, recovery and therapy.
[So] Source:Neurosci Lett;625:26-33, 2016 Jun 20.
[Is] ISSN:1872-7972
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:Traumatic brain injury (TBI) contributes to nearly a third of all injury-related deaths in the United States. For survivors of TBI, depending on severity, patients can be left with devastating neurological disabilities that include impaired cognition or memory, movement, sensation, or emotional function. Despite the efforts to identify novel therapeutics, the only strategy to combat TBI is risk reduction (helmets, seatbelts, removal of fall hazards, etc.). Enormous heterogeneity exists within TBI, and it depends on the severity, the location, and whether the injury was focal or diffuse. Evidence from recent studies support the involvement of epigenetic mechanisms such as DNA methylation, chromatin post-translational modification, and miRNA regulation of gene expression in the post-injured brain. In this review, we discuss studies that have assessed epigenetic changes and mechanisms following TBI, how epigenetic changes might not only be limited to the nucleus but also impact the mitochondria, and the implications of these changes with regard to TBI recovery.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1606
[Js] Journal subset:IM
[St] Status:In-Data-Review

  9 / 1352174 MEDLINE  
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[PMID]: 26876477
[Au] Autor:Devall M; Roubroeks J; Mill J; Weedon M; Lunnon K
[Ad] Address:Institute of Clinical and Biomedical Science, University of Exeter Medical School, University of Exeter, Devon, UK....
[Ti] Title:Epigenetic regulation of mitochondrial function in neurodegenerative disease: New insights from advances in genomic technologies.
[So] Source:Neurosci Lett;625:47-55, 2016 Jun 20.
[Is] ISSN:1872-7972
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:The field of mitochondrial epigenetics has received increased attention in recent years and changes in mitochondrial DNA (mtDNA) methylation has been implicated in a number of diseases, including neurodegenerative diseases such as amyotrophic lateral sclerosis. However, current publications have been limited by the use of global or targeted methods of measuring DNA methylation. In this review, we discuss current findings in mitochondrial epigenetics as well as its potential role as a regulator of mitochondria within the brain. Finally, we summarize the current technologies best suited to capturing mtDNA methylation, and how a move towards whole epigenome sequencing of mtDNA may help to advance our current understanding of the field.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1606
[Js] Journal subset:IM
[St] Status:In-Data-Review

  10 / 1352174 MEDLINE  
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[PMID]: 26868600
[Au] Autor:Bourassa MW; Alim I; Bultman SJ; Ratan RR
[Ad] Address:Sperling Center for Hemorrhagic Stroke Recovery, Burke Medical Research Institute, 785 Mamaroneck Ave, White Plains, NY 10605, USA; Brain and Mind Research Institute, Weill Medical College of Cornell University, 1300 York Ave. Box 65, New York, NY 10065, USA....
[Ti] Title:Butyrate, neuroepigenetics and the gut microbiome: Can a high fiber diet improve brain health?
[So] Source:Neurosci Lett;625:56-63, 2016 Jun 20.
[Is] ISSN:1872-7972
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:As interest in the gut microbiome has grown in recent years, attention has turned to the impact of our diet on our brain. The benefits of a high fiber diet in the colon have been well documented in epidemiological studies, but its potential impact on the brain has largely been understudied. Here, we will review evidence that butyrate, a short-chain fatty acid (SCFA) produced by bacterial fermentation of fiber in the colon, can improve brain health. Butyrate has been extensively studied as a histone deacetylase (HDAC) inhibitor but also functions as a ligand for a subset of G protein-coupled receptors and as an energy metabolite. These diverse modes of action make it well suited for solving the wide array of imbalances frequently encountered in neurological disorders. In this review, we will integrate evidence from the disparate fields of gastroenterology and neuroscience to hypothesize that the metabolism of a high fiber diet in the gut can alter gene expression in the brain to prevent neurodegeneration and promote regeneration.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1606
[Js] Journal subset:IM
[St] Status:In-Data-Review


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