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Reduced Volumes (reduced + volume)
Selected AbstractsTime course and nature of brain atrophy in the MRL mouse model of central nervous system lupusARTHRITIS & RHEUMATISM, Issue 6 2009John G. Sled Objective Similar to patients with systemic lupus erythematosus, autoimmune MRL/lpr mice spontaneously develop behavioral deficits and pathologic changes in the brain. Given that the disease-associated brain atrophy in this model is not well understood, the present study was undertaken to determine the time course of morphometric changes in major brain structures of autoimmune MRL/lpr mice. Methods Computerized planimetry and high-resolution magnetic resonance imaging (MRI) were used to compare the areas and volumes of brain structures in cohorts of mice that differ in severity of lupus-like disease. Results A thinner cerebral cortex and smaller cerebellum were observed in the MRL/lpr substrain, even before severe autoimmunity developed. With progression of the disease, the brain area of coronal sections became smaller and the growth of the hippocampus was retarded, which likely contributed to the increase in the ventricle area:brain area ratio. MRI revealed reduced volume across different brain regions, with the structures in the vicinity of the ventricular system particularly affected. The superior colliculus, periaqueductal gray matter, pons, and midbrain were among the regions most affected, whereas the volumes of the parietal-temporal lobe, parts of the cerebellum, and lateral ventricles in autoimmune MRL/lpr mice were comparable with values in congenic controls. Conclusion These results suggest that morphologic alterations in the brains of MRL/lpr mice are a consequence of several factors, including spontaneous development of lupus-like disease. A periventricular pattern of parenchymal damage is consistent with the cerebrospinal fluid neurotoxicity, limbic system pathologic features, and deficits in emotional reactivity previously documented in this model. [source] The role of BDNF and its receptors in depression and antidepressant drug action: Reactivation of developmental plasticityDEVELOPMENTAL NEUROBIOLOGY, Issue 5 2010Eero Castrén Abstract Recent evidence suggests that neuronal plasticity plays an important role in the recovery from depression. Antidepressant drugs and electroconvulsive shock treatment increase the expression of several molecules, which are associated with neuronal plasticity, in particular the neurotrophin BDNF and its receptor TrkB. Furthermore, these treatments increase neurogenesis and synaptic numbers in several brain areas. Conversely, depression, at least in its severe form, is associated with reduced volumes of the hippocampus and prefrontal cortex and in at least some cases these neurodegenerative signs can be attenuated by successful treatment. Such observations suggest a central role for neuronal plasticity in depression and the antidepressant effect, and also implicate BDNF signaling as a mediator of this plasticity. The antidepressant fluoxetine can reactivate developmental-like neuronal plasticity in the adult visual cortex, which, under appropriate environmental guidance, leads to the rewiring of a developmentally dysfunctional neural network. These observations suggest that the simple form of the neurotrophic hypothesis of depression, namely, that deficient levels of neurotrophic support underlies mood disorders and increases in these neurotrophic factors to normal levels brings about mood recovery, may not sufficiently explain the complex process of recovery from depression. This review discusses recent data on the role of BDNF and its receptors in depression and the antidepressant response and suggests a model whereby the effects of antidepressant treatments could be explained by a reactivation of activity-dependent and BDNF-mediated cortical plasticity, which in turn leads to the adjustment of neuronal networks to better adapt to environmental challenges. © 2010 Wiley Periodicals, Inc. Develop Neurobiol 2010 [source] Studies on the effects of gentamicin on rat metanephric development in vitroNEPHROLOGY, Issue 1-2 2000Luise A Cullen SUMMARY: Reduced nephron endowment has been associated with increased risk of developing essential hypertension and chronic renal failure. Both in vivo and in vitro exposure of developing rat metanephroi to gentamicin has been reported to inhibit metanephric development resulting in reduced nephron endowment. The aim of the present study was to confirm that gentamicin results in reduced nephron endowment in vitro, and to extend understanding of the mechanisms responsible for this reduced endowment. Embryonic day 14 (E14) rat metanephroi were cultured for up to 4 days in serum-free medium with or without 50 ,g/mL gentamicin. Metanephroi cultured in the presence of gentamicin were 25% smaller than control metanephroi after 2 days culture and 30% smaller after 4 days (P < 0.001). This decrease in total metanephric volume was reflected in reduced volumes of ureteric duct epithelium, mesenchyme/interstitium and nephron epithelia. The reduced volume of ureteric duct epithelium in gentamicin-treated metanephroi was associated with a 30% reduction in the number of ureteric duct branch points at 2 days. Metanephroi cultured with gentamicin contained 20% fewer glomeruli than control metanephroi (P < 0.005) at 4 days. These glomeruli were 30% smaller than control glomeruli (P < 0.05). Qualitative observations of Pax-2 immunostained mesenchymal condensates indicated no difference in condensate size, location or morphology. These results confirm that in vitro exposure of developing rat metanephroi to gentamicin results in reduced nephron endowment. The defect in nephrogenesis centres around the inhibition of ureteric duct branching. [source] Cerebellar morphology in Tourette syndrome and obsessive-compulsive disorderANNALS OF NEUROLOGY, Issue 4 2010Russell H. Tobe MD Objective Neuroanatomical and functional imaging studies have identified the cerebellum as an integral component of motor and language control. Few studies, however, have investigated the role of the cerebellum in Tourette syndrome (TS), a condition defined by the presence of semi-involuntary movements and sounds. Methods Magnetic resonance imaging was conducted in 163 persons with TS and 147 control participants. Multivariate linear regression models were used to explore effects on cerebellar surface morphology and underlying volumes for the main diagnosis effects of TS as well as comorbid obsessive-compulsive disorder (OCD) and attention-deficit/hyperactivity disorder. Additionally, the correlations of symptom severity with cerebellar morphology were also assessed. Results The TS group demonstrated reduced volumes of the cerebellar hemispheres bilaterally that derived primarily from reduced gray matter in crus I and lobules VI, VIIB, and VIIIA. These decreased regional volumes accompanied increasing tic symptom severity and motoric disinhibition as demonstrated by a finger tapping test. Males had reduced volumes of these same regions compared with females, irrespective of diagnosis. Comorbid OCD was associated with relative enlargement of these regions in proportion to the increasing severity of OCD symptoms. Interpretation The cerebellum is involved in the pathogenesis of TS and tic-related OCD. Baseline gender differences in cerebellar morphology may in part account for the more prevalent expression of TS in males. ANN NEUROL 2010;67:479,487 [source] Preliminary evidence for persistent abnormalities in amygdala volumes in adolescents and young adults with bipolar disorderBIPOLAR DISORDERS, Issue 6 2005Hilary P Blumberg Objectives:, Abnormalities in volumes of the amygdala have been reported previously in adolescents and adults with bipolar disorder (BD). Several studies have reported reduced volumes in adolescents with BD; however, both decreases and increases in volumes have been reported in adults with BD. Understanding of potential developmental contributions to these disturbances in morphology of the amygdala has been limited by the absence of longitudinal data in persons with BD. Here we use a within-subject longitudinal design to investigate whether amygdala volume abnormalities persist in adolescents and young adults with BD over a time interval of approximately 2 years. Methods:, Participants included 18 adolescents and young adults: 10 participants with BD I and 8 healthy comparison participants. Amygdala volumes were measured on high-resolution magnetic resonance imaging scans acquired twice for each subject over intervals of approximately 2 years. Amygdala volumes were the dependent measures in a mixed-model statistical analysis to compare amygdala volumes between groups over time while covarying for total brain volume. Results:, Amygdala volumes were significantly smaller in adolescents and young adults with BD compared with healthy participants (p = 0.018). The effect of time was not significant. Conclusions:, Although the sample size is modest, this study provides preliminary evidence to support the presence of decreased amygdala volumes in adolescents and young adults with BD that persist during this developmental epoch. [source] | ||||||||||