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1.
Front Psychiatry ; 11: 31, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32153434

RESUMO

Brain derived neurotrophic factor (BDNF) has been implicated in the pathophysiology of schizophrenia. As BDNF regulates axonal and dendritic growth, altered BDNF levels in schizophrenia patients might underlie changes in structural connectivity that have been identified by magnetic resonance imaging (MRI). We investigated a possible correlation between BDNF serum levels, fiber tract architecture, and regional grey matter volumes in 19 schizophrenia patients and a gender- and age-matched control group. Two patients had to be excluded due to abnormalities in their MRI scans. Serum samples were obtained to determine BDNF levels, and T1- as well as diffusion-weighted sequences were acquired. We, then, investigated correlations between BDNF serum levels with neuroimaging parameters, using Voxel-based Morphometry (VBM) and Tract-based Spatial Statistics (TBSS). We found a significant negative correlation between BDNF serum levels and FA values in the right inferior fronto-occipital fasciculus and the right superior longitudinal fasciculus. These regions also showed a decrease in AD values in schizophrenia patients. Grey matter volumes were reduced in patients but there was no correlation between regional grey matter volumes and BDNF. The right superior longitudinal fasciculus has been repeatedly identified to exhibit microstructural changes in schizophrenia patients. Our findings of a negative correlation between BDNF and FA values in patients might indicate that BDNF is upregulated to compensate decreased structural connectivity as it induces neural plasticity and shows increased levels in damaged tissue. These findings of our pilot study are encouraging leads for future research in larger samples.

2.
Front Psychiatry ; 10: 275, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31105606

RESUMO

Numerous neuroimaging studies have revealed structural brain abnormalities in schizophrenia patients. There is emerging evidence that dysfunctional nerve growth factor (NGF) signaling may contribute to structural brain alterations found in these patients. In this pilot study, we investigated whether there was a correlation between NGF serum levels and gray matter volume (GMV) in schizophrenia patients. Further, we investigated whether there was an overlap between the correlative findings and cross-sectional GMV differences between schizophrenia patients (n = 18) and healthy controls (n = 19). Serum NGF was significantly correlated to GMV in the left prefrontal lobe, the left midcingulate cortex, and the brainstem in schizophrenia patients. However, we did not find any correlations of NGF serum levels with GMV in healthy controls. Schizophrenia patients showed smaller GMV than healthy controls in brain regions located in the bilateral limbic system, bilateral parietal lobe, bilateral insula, bilateral primary auditory cortex, left frontal lobe, and bilateral occipital regions. In a conjunction analysis, GMV in the left midcingulate cortex (MCC) appears negatively correlated to NGF serum levels in the group of schizophrenia patients and also to be reduced compared to healthy controls. These results suggest an increased vulnerability of schizophrenia patients to changes in NGF levels compared to healthy controls and support a role for NGF signaling in the pathophysiology of schizophrenia. As our pilot study is exploratory in nature, further studies enrolling larger sample sizes will be needed to further corroborate our findings and to investigate the influence of additional covariates.

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