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Fw: reelin: gene or environment?

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-----Original Message-----From: Holly Bortfeld

Listmates,Two interesting abstracts here on reelin. The second suggests that viralinfection in pregnancy may reduce reelin production in post-natal braindevelopment. It's quite interesting to consider the role that reelin mightplay in ASD brains and how that role might be triggered. It's not at allclear that a genetic defect mediates the role reelin would play: rather acertain variant might predispose toward vulnerability to certain insults, oreven without the variant, that reelin disruptions from environmental sourcescould cause problems.So again, let's treat the research seriously as a clue to what's going on inautism; let's also not jump to the conclusion that this proves a dominantrole for genetic influences. MarkMol Psychiatry 2000 Nov;5(6):654-63, 571 Reduction in Reelin immunoreactivity in hippocampus of subjects withschizophrenia, bipolar disorder and major depression.Fatemi SH, Earle JA, McMenomy TDepartment of Psychiatry, University of Minnesota Medical School,Minneapolis55455, USA. fatem002@...Accumulation of neurobiological knowledge points to neurodevelopmentaloriginsfor certain psychotic and mood disorders. Recent landmark postmortem reportsimplicate Reelin, a secretory glycoprotein responsible for normal laminationofbrain, in the pathology of schizophrenia and bipolar disorders. We employedquantitative immunocytochemistry to measure levels of Reelin protein invariouscompartments of hippocampal formation in subjects diagnosed withschizophrenia,bipolar disorder and major depression compared to normal controls.Significantreductions were observed in Reelin-positive adjusted cell densities in thedentate molecular layer (ANOVA, P < 0.001), CA4 area (ANOVA, P < 0.001),totalhippocampal area (ANOVA, P < 0.038) and in Reelin-positive cell counts inCA4(ANOVA, P < 0.042) of schizophrenics vs controls. Adjusted Reelin-positivecelldensities were also reduced in CA4 areas of subjects with bipolar disorder(ANOVA, P < 0.001) and nonsignificantly in those with major depression. CA4areas were also significantly reduced in schizophrenic (ANOVA, P < 0.009)patients. No significant effects of confounding variables were found. Theexception was that family history of psychiatric illness correlated stronglywith Reelin reductions in several areas of hippocampus (CA4, adjusted celldensity, F = 13.77, P = 0.001). We present new immunocytochemical evidenceshowing reductions in Reelin expression in hippocampus of subjects withschizophrenia, bipolar disorder and major depression and confirm recentreportsdocumenting a similar deficit involving Reelin expression in brains ofsubjectswith schizophrenia and bipolar disorder.PMID: 11126396, UI: 21012503----------Mol Psychiatry 1999 Mar;4(2):145-54 Defective corticogenesis and reduction in Reelin immunoreactivity in cortexandhippocampus of prenatally infected neonatal mice.Fatemi SH, Emamian ES, Kist D, Sidwell RW, Nakajima K, Akhter P, Shier A,Sheikh S, KDepartment of Psychiatry, University of Minnesota Medical School,Minneapolis55455, USA. fatem002@...Recent reports indicate an association between second trimester humaninfluenzaviral infection and later development of schizophrenia. Postmortem humanbrainstudies also provide evidence for reduction in Reelin mRNA (an importantsecretory protein responsible for normal lamination of the brain) inschizophrenic brains. We hypothesized that human influenza infection in day9pregnant mice would alter the expression of reelin in day 0 neonatal brains.Prenatally-infected murine brains from postnatal day 0 showed significantreductions in reelin-positive cell counts in layer I of neocortex and othercortical and hippocampal layers when compared to controls. Whereas layer ICajal-Retzius cells produced significantly less Reelin in infected animals,thesame cells showed normal production of calretinin and nNOS when compared tocontrol brains. Moreover, prenatal viral infection caused decreases inneocortical and hippocampal thickness. These results implicate a potentialroleof prenatal viral infection in causation of neuronal migration abnormalitiesvia reduction in Reelin production in neonatal brains.PMID: 10208446, UI: 99223145----------Visit the ARN Homepage! http://www.geocities.com/ARNFL

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