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sábado, 5 de febrero de 2011

Tratamiento crónico de melatonina: Efecto en la neurogenesis

 Sobre el buen dormir y la melatonina:

Chronic treatment with melatonin stimulates dendrite maturation and complexity in adult hippocampal neurogenesis of mice

J. Pineal Res. 2011; 50:29–37
Gerardo Ramirez-Rodriguez, Leonardo Ortíz-López, Aline Domínguez-Alonso, Gloria A. Benítez-King and Gerd Kempermann

1Laboratory of Neurogenesis, Department of Neuropharmacology, National Institute of  Psychiatry. Mexico D.F., Mexico; 2Department of Neuropharmacology, National Institute of Psychiatry, Mexico D.F., Mexico; 3CRTD –Center for Regenerative Therapies Dresden,
Dresden, Germany

Fig. 6. Schematic representation of melatonin effects altering dendrite complexity of new neurons. Chronic melatonin treatment (8 mg/kg) for 14 days increases dendrite complexity of new neurons identified by doublecortin staining (imagen de abajo) , while in mice treated with vehicle the number of immature neurons and neurons with more complex dendrites are lower than that in melatonin-treated mice (imagen de arriba). Draw box shows the events corresponding to the cell survival and dendrite maturation of the neurogenic process in which melatonin plays a role.

Abstract: In the course of adult hippocampal neurogenesis, the postmitotic maturation and survival phase is associated with dendrite maturation. Melatonin modulates the survival of new neurons with relative specificityDuring this phase, the new neurons express microtubule-associated protein doublecortin (DCX). Here, we show that the entire population of cells expressing DCX is increased after 14 days of treatment with melatonin. As melatonin also affects microtubule polymerization which is important for neuritogenesis and dendritogenesis, we studied the consequences of chronic melatonin administration on dendrite maturation of DCX-positive cells. Treatment with melatonin increased the number of DCX-positive immature neurons with more complex dendrites. Sholl analysis revealed that melatonin treatment lead to greater complexity of the dendritic tree. In addition, melatonin increased the total volume of the granular cell layer. Besides its survival-promoting effect, melatonin thus also increases dendritic maturation in adult neurogenesis. This might open the opportunity of using melatonin as an adjuvant in attempts to extrinsically stimulate adult hippocampal neurogenesis in neuropsychiatric disease, dementia or cognitive ageing.

Saludos cordiales/Gustavo

miércoles, 2 de febrero de 2011


Electroconvulsive seizure and VEGF increase the proliferation of neural stem-like cells in rat hippocampus

Eri Segi-Nishida, Jennifer L. Warner-Schmidt, and Ronald S. Duman*
Laboratory of Molecular Psychiatry, Department of Psychiatry and Pharmacology, Yale University School of Medicine, New Haven, CT 06508
Edited by Fred H. Gage, Salk Institute for Biological Studies, San Diego, CA, and approved May 7, 2008 (received for review November 15, 2007)

All classes of antidepressants increase hippocampal cell proliferation and neurogenesis, which contributes, in part, to the behavioral actions of these treatments. Among antidepressant treatments, electroconvulsive seizure (ECS) is the most robust stimulator of hippocampal cell proliferation and the most efficacious treatment for depression, but the cellular mechanisms underlying the actions of ECS are unknown. To address this question, we investigated the effect of ECS on proliferation of neural stem-like and/or progenitor cells in the subgranular zone of rat dentate gyrus. We define the neural differentiation cascade from stem-like cells to early neural progenitors (also referred to as quiescent and amplifying neural progenitors, respectively) by coexpression of selective cellular and mitotic activity markers. We find that at an early mitotic phase ECS increases the proliferation of quiescent progenitors and then at a later phase increases the proliferation of amplifying progenitors. We further demonstrate that vascular endothelial growth factor (VEGF) signaling is necessary for ECS induction of quiescent neural progenitor cell proliferation and is sufficient to produce this effect. These findings demonstrate that ECS and subsequent induction of VEGF stimulates the proliferation of neural stem-like cells and neural progenitor cells, thereby accounting for the superior neurogenic actions of ECS compared with chemical antidepressants.

saludos cordiales/Gustavo

martes, 1 de febrero de 2011

Altered hippocampal morphology in unmedicated patients with major depressive illness

Altered hippocampal morphology in unmedicated patients with major depressive illness

Bearden CE, Thompson PM, Avedissian C, Klunder AD, Nicoletti M, Dierschke N, Brambilla P and Soares JC (2009) Altered
hippocampal morphology in unmedicated patients with major depressive illness. ASN NEURO 1(4):art:e00020.doi:10.1042/AN20090026

Despite converging evidence that major depressive illness is associated with both memory impairment and hippocampal pathology, findings vary widely across studies and it is not known whether these changes are regionally specific.
In the present study we acquired brain MRIs (magnetic resonance images) from 31 unmedicated patients with MDD (major depressive disorder; mean age 39.2 + -11.9 years; 77% female) and 31 demographically comparable controls. Three-dimensional parametric mesh models were created to examine localized alterations of hippocampal morphology. Although global volumes did not differ between groups, statistical mapping results revealed that in MDD patients, more severe depressive symptoms were associated with greater left hippocampal atrophy, particularly in CA1 (cornu ammonis 1) subfields and the subiculum. However, previous treatment with atypical antipsychotics was associated with a trend towards larger left hippocampal volume. Our findings suggest effects of illness severity on hippocampal size, as well as a possible effect of past history of atypical antipsychotic treatment, which may reflect prolonged neuroprotective effects. This possibility awaits confirmation in longitudinal studies.

Key words: antipsychotic, brain mapping, hippocampus,
mood disorder, neuroimaging, subiculum, unipolar depression.

saludos cordiales/Gustavo

lunes, 31 de enero de 2011

NATALIZUMAB: Algunas Revisiones y artìculos relevantes

PMC Results
Items 1 - 20 of 367

Effects of Natalizumab Treatment on Foxp3+ T Regulatory Cells
Max-Philipp Stenner, Anne Waschbisch, Dorothea Buck, Sebastian Doerck, Hermann Einsele, Klaus V. Toyka, and Heinz Wiendl
PLoS ONE. 2008; 3(10): e3319. Published online 2008 October 6. doi: 10.1371/journal.pone.0003319.
PMCID: PMC2553177

Effect of plasma exchange in accelerating natalizumab clearance and restoring leukocyte function
B O. Khatri, S Man, G Giovannoni, A P. Koo, J-C Lee, B Tucky, F Lynn, S Jurgensen, J Woodworth, S Goelz, P W. Duda, M A. Panzara, R M. Ransohoff, and R J. Fox
Neurology. 2009 February 3; 72(5): 402–409. doi: 10.1212/01.wnl.0000341766.59028.9d.
PMCID: PMC2677532

Natalizumab for the treatment of relapsing multiple sclerosis
Richard A Rudick and Michael A Panzara
Biologics. 2008 June; 2(2): 189–199. Published online 2008 June.
PMCID: PMC2721353

Natalizumab in the Treatment of Multiple Sclerosis
Özgür Yaldizli and Norman Putzki
Ther Adv Neurol Disord. 2009 March; 2(2): 115–128. doi: 10.1177/1756285608101861.
PMCID: PMC3002624

Natalizumab: A new treatment for relapsing remitting multiple sclerosis
Michael Hutchinson
Ther Clin Risk Manag. 2007 June; 3(2): 259–268. Published online 2007 June.
PMCID: PMC1936307

Natalizumab treatment is associated with peripheral sequestration of proinflammatory T cells
P Kivisäkk, B C. Healy, V Viglietta, F J. Quintana, M A. Hootstein, H L. Weiner, and S J. Khoury
Neurology. 2009 June 2; 72(22): 1922–1930. doi: 10.1212/WNL.0b013e3181a8266f.
PMCID: PMC2690969

Reactivation of Human Herpesvirus-6 in Natalizumab Treated Multiple Sclerosis Patients
Karen Yao, Susan Gagnon, Nahid Akhyani, Elizabeth Williams, Julie Fotheringham, Elliot Frohman, Olaf Stuve, Nancy Monson, Michael K. Racke, and Steven Jacobson
PLoS ONE. 2008; 3(4): e2028. Published online 2008 April 30. doi: 10.1371/journal.pone.0002028.
PMCID: PMC2323568

Natalizumab in the treatment of multiple sclerosis
Brandon A Brown
Ther Clin Risk Manag. 2009; 5: 585–594. Published online 2009 August 3.
PMCID: PMC2724189

Immunologic, clinical, and radiologic status 14 months after cessation of natalizumab therapy
O Stüve, P D. Cravens, E M. Frohman, J T. Phillips, G M. Remington, G von Geldern, S Cepok, M P. Singh, J W. Cohen Tervaert, M De Baets, D MacManus, D H. Miller, E W. Radü, E M. Cameron, N L. Monson, S Zhang, R Kim, B Hemmer, and M K. Racke
Neurology. 2009 February 3; 72(5): 396–401. doi: 10.1212/01.wnl.0000327341.89587.76.
PMCID: PMC2677530

Natalizumab in the treatment of Crohn's disease
Danila Guagnozzi and Renzo Caprilli
Biologics. 2008 June; 2(2): 275–284. Published online 2008 June.
PMCID: PMC2721358

Increased numbers of circulating hematopoietic stem/progenitor cells are chronically maintained in patients treated with the CD49d blocking antibody natalizumab
Halvard Bonig, Annette Wundes, Kai-Hsin Chang, Sylvia Lucas, and Thalia Papayannopoulou
Blood. 2008 April 1; 111(7): 3439–3441. Prepublished online 2008 January 14. doi: 10.1182/blood-2007-09-112052.
PMCID: PMC2275012

An evidence-based review of natalizumab therapy in the management of Crohn's disease
Raja GR Edula and Michael F Picco
Ther Clin Risk Manag. 2009; 5: 935–942. Published online 2009 November 29.
PMCID: PMC2789688

Treatment of refractory epilepsy with natalizumab in a patient with multiple sclerosis. Case report
Stefano Sotgiu, Maria R Murrighile, and Gabriela Constantin
BMC Neurol. 2010; 10: 84. Published online 2010 September 23. doi: 10.1186/1471-2377-10-84.
PMCID: PMC2954970

Anti-adhesion molecule therapy for inflammatory bowel disease
Subrata Ghosh and Remo Panaccione
Therap Adv Gastroenterol. 2010 July; 3(4): 239–258. doi: 10.1177/1756283X10373176.
PMCID: PMC3002582

Natalizumab in pediatric multiple sclerosis patients
E. Ann Yeh and Bianca Weinstock-Guttman
Ther Adv Neurol Disord. 2010 September; 3(5): 293–299. doi: 10.1177/1756285610381526.
PMCID: PMC3002661

Quantitative risk-benefit analysis of natalizumab
J P. Thompson, K Noyes, E R. Dorsey, S R. Schwid, and R G. Holloway
Neurology. 2008 July 29; 71(5): 357–364. doi: 10.1212/01.wnl.0000319648.65173.7a.
PMCID: PMC2676947

Evaluation of Patients Treated with Natalizumab for Progressive Multifocal Leukoencephalopathy
Tarek A. Yousry, Eugene O. Major, Caroline Ryschkewitsch, Gary Fahle, Steven Fischer, Jean Hou, Blanche Curfman, Katherine Miszkiel, Nicole Mueller-Lenke, Esther Sanchez, Frederik Barkhof, Ernst-Wilhelm Radue, Hans R. Jäger, and David B. Clifford
N Engl J Med. Author manuscript; available in PMC 2007 July 30.
PMCID: PMC1934511
Published in final edited form as: N Engl J Med. 2006 March 2; 354(9): 924–933. doi: 10.1056/NEJMoa054693.
Manuscript: | Abstract | Full Text | PDF–104K |

Remitting–relapsing multiple sclerosis patient refractory to conventional treatments and bone marrow transplantation who responded to natalizumab
Athanasia Mouzaki, Maria Koutsokera, Zoe Dervilli, Maria Rodi, Dimitra Kalavrizioti, Nikolaos Dimisianos, Ioannis Matsoukas, and Panagiotis Papathanasopoulos
Int J Gen Med. 2010; 3: 313–320. Published online 2010 October 5. doi: 10.2147/IJGM.S13648.
PMCID: PMC2962327

GLANCE: Results of a phase 2, randomized, double-blind, placebo-controlled study
A D. Goodman, H Rossman, A Bar-Or, A Miller, D H. Miller, K Schmierer, F Lublin, O Khan, N M. Bormann, M Yang, M A. Panzara, A W. Sandrock, and For the GLANCE Investigators
Neurology. 2009 March 3; 72(9): 806–812. doi: 10.1212/01.wnl.0000343880.13764.69.
PMCID: PMC2821836

Bruising following natalizumab infusion for relapsing-remitting multiple sclerosis: a case report
Stylianos Gatzonis and Anna Siatouni
J Med Case Reports. 2009; 3: 8955. Published online 2009 August 27. doi: 10.4076/1752-1947-3-8955.
PMCID: PMC2827173

domingo, 30 de enero de 2011