scholarly journals Age-Related Increase in the Number of Oligodendrocytes Is Dysregulated in Schizophrenia and Mood Disorders

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Victor Vostrikov ◽  
Natalya Uranova

The postnatal maturation of the human prefrontal cortex is associated with substantial increase of number of oligodendrocytes. Previously, we reported decreased numerical density of oligodendrocytes in the prefrontal cortex in schizophrenia and mood disorders. To gain further understanding of the role oligodendrocytes in pathogenesis of schizophrenia and mood disorders, we examined the effect of the age on the number of oligodendrocytes in the prefrontal cortex in schizophrenia, bipolar disorder, and major depressive disorder. We revealed the age-related increase in numerical density of oligodendrocytes in layer VI and adjacent white matter of BA10 and BA 9 in normal controls but not in schizophrenia, bipolar disorder, and major depressive disorder. The absence of normal increase in the number of oligodendrocytes in gray and white matter with age in schizophrenia and mood disorders suggests that age-related process of oligodendrocyte increase is dysregulated in schizophrenia and mood disorders.

Author(s):  
Brianne Disabato ◽  
Isabelle E. Bauer ◽  
Jair C. Soares ◽  
Yvette Sheline

Unipolar major depressive disorder (MDD) and bipolar disorder (BD) are among the world’s leading causes of disability. This chapter highlights the importance of neuroimaging in understanding their neural mechanisms. Depression affects limbic-corticostriatopallidothalamic regions. Structurally, depressed subjects showed increased volume of lesions in white matter (WMH) and decreased gray matter in prefrontal-striatum, orbitofrontal, anterior cingulate cortices, and hippocampus. Functionally, depressed subjects showed abnormal activation in amygdala and medial prefrontal cortex and dsyconnectivity in executive and emotional networks. BD was associated with frontocingulate, limbic-striatal, and hippocampus abnormalities. Specifically, BD subjects showed increased WMH in frontocortical and subcortical areas and altered microstructure in limbic-striatal, cingulate, thalamus, corpus callosum, and prefrontal regions. Functionally, abnormal activations in dorsolateral prefrontal and ventrolimbic regions, hypoconnectivity in the cinguloinsularopercular, mesoparalimbic, and cerebellar networks, and hyperconnectivity in affective and executive networks were also observed. These studies show congruence. Full integration of them would allow better understanding of mood disorders.


2017 ◽  
Vol 39 ◽  
pp. 51-56 ◽  
Author(s):  
K. Hamazaki ◽  
M. Maekawa ◽  
T. Toyota ◽  
B. Dean ◽  
T. Hamazaki ◽  
...  

AbstractBackgroundStudies investigating the relationship between n-3 polyunsaturated fatty acid (PUFA) levels and psychiatric disorders have thus far focused mainly on analyzing gray matter, rather than white matter, in the postmortem brain. In this study, we investigated whether PUFA levels showed abnormalities in the corpus callosum, the largest area of white matter, in the postmortem brain tissue of patients with schizophrenia, bipolar disorder, or major depressive disorder.MethodsFatty acids in the phospholipids of the postmortem corpus callosum were evaluated by thin-layer chromatography and gas chromatography. Specimens were evaluated for patients with schizophrenia (n = 15), bipolar disorder (n = 15), or major depressive disorder (n = 15) and compared with unaffected controls (n = 15).ResultsIn contrast to some previous studies, no significant differences were found in the levels of PUFAs or other fatty acids in the corpus callosum between patients and controls. A subanalysis by sex gave the same results. No significant differences were found in any PUFAs between suicide completers and non-suicide cases regardless of psychiatric disorder diagnosis.ConclusionsPatients with psychiatric disorders did not exhibit n-3 PUFAs deficits in the postmortem corpus callosum relative to the unaffected controls, and the corpus callosum might not be involved in abnormalities of PUFA metabolism. This area of research is still at an early stage and requires further investigation.


Symmetry ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 2414
Author(s):  
Chiara Spironelli ◽  
Francesca Fusina ◽  
Marco Bortolomasi ◽  
Alessandro Angrilli

In the last few decades, the incidence of mood disorders skyrocketed worldwide and has brought an increasing human and economic burden. Depending on the main symptoms and their evolution across time, they can be classified in several clinical subgroups. A few psychobiological indices have been extensively investigated as promising markers of mood disorders. Among these, frontal asymmetry measured at rest with quantitative EEG has represented the main available marker in recent years. Only a few studies so far attempted to distinguish the features and differences among diagnostic types of mood disorders by using this index. The present study measured frontal EEG asymmetry during a 5-min resting state in three samples of patients with bipolar disorder in a Euthymic phase (EBD, n = 17), major depressive disorder (MDD, n = 25) and persistent depressive disorder (PDD, n = 21), once termed dysthymia. We aimed to test the hypothesis that MDD and PDD lack the typical leftward asymmetry exhibited by normal as well as EBD patients, and that PDD shows greater clinical and neurophysiological impairments than MDD. Clinical scales revealed no symptoms in EBD, and significant larger anxiety and depression scores in PDD than in MDD patients. Relative beta (i.e., beta/alpha ratio) EEG asymmetry was measured from lateral frontal sites and results revealed the typical greater left than right frontal beta activity in EBD, as well as a lack of asymmetry in both MDD and PDD. The last two groups also had lower bilateral frontal beta activity in comparison with the EBD group. Results concerning group differences were interpreted by taking into account both the clinical and the neurophysiological domains.


2018 ◽  
Author(s):  
Jonathan R. I. Coleman ◽  
Héléna A. Gaspar ◽  
Julien Bryois ◽  
Gerome Breen ◽  
◽  
...  

AbstractBackgroundMood disorders (including major depressive disorder and bipolar disorder) affect 10-20% of the population. They range from brief, mild episodes to severe, incapacitating conditions that markedly impact lives. Despite their diagnostic distinction, multiple approaches have shown considerable sharing of risk factors across the mood disorders.MethodsTo clarify their shared molecular genetic basis, and to highlight disorder-specific associations, we meta-analysed data from the latest Psychiatric Genomics Consortium (PGC) genome-wide association studies of major depression (including data from 23andMe) and bipolar disorder, and an additional major depressive disorder cohort from UK Biobank (total: 185,285 cases, 439,741 controls; non-overlapping N = 609,424).ResultsSeventy-three loci reached genome-wide significance in the meta-analysis, including 15 that are novel for mood disorders. More genome-wide significant loci from the PGC analysis of major depression than bipolar disorder reached genome-wide significance. Genetic correlations revealed that type 2 bipolar disorder correlates strongly with recurrent and single episode major depressive disorder. Systems biology analyses highlight both similarities and differences between the mood disorders, particularly in the mouse brain cell types implicated by the expression patterns of associated genes. The mood disorders also differ in their genetic correlation with educational attainment – positive in bipolar disorder but negative in major depressive disorder.ConclusionsThe mood disorders share several genetic associations, and can be combined effectively to increase variant discovery. However, we demonstrate several differences between these disorders. Analysing subtypes of major depressive disorder and bipolar disorder provides evidence for a genetic mood disorders spectrum.


Sign in / Sign up

Export Citation Format

Share Document