Ultrastructural alterations of oligodendrocytes in prefrontal white matter in schizophrenia: A post-mortem morphometric study

Vikhreva, Olga; Rakhmanova, V. I.; Orlovskaya, D.D.; Na, Uranova

doi:10.1016/j.schres.2016.04.023

Cited by 70 publications

(44 citation statements)

References 54 publications

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“…Symmetric axospinous synapses in deep cortical layers originate in part from dopamine connections (Kubota et al, 2016). In other ultrastructural studies, Uranova and Aganova (1989) have shown layer specific abnormalities such as fewer synapses in the ACC, and fewer mitochondria in oligodendrocytes in both gray and white matter (Uranova et al, 2007; Vikhreva et al, 2016). The latter observation suggests that oligodendrocytes need or have less energy, which may have an impact on proper myelination.…”

Section: Mitochondrial Abnormalities In Schizophreniamentioning

confidence: 94%

“…The production of ATP and calcium buffering are essential in maintaining synaptic strength and abnormalities in these processes could lead to decreased metabolism and defective synaptic activity (Ben-Shachar and Laifenfeld, 2004; Chang and Reynolds, 2006; Duchen et al, 2008). Many of our electron microscopic studies and those of Uranova and colleagues (Kolomeets and Uranova, 2009; Uranova et al, 1996, 2001, 2007; Vikhreva et al, 2016) have examined mitochondrial size, number, location, structural integrity and markers of viability in various brain regions implicated in schizophrenia. Ultrastructural studies are possible with well-preserved tissue with short postmortem intervals (Figure 2).…”

Section: Mitochondrial Abnormalities In Schizophreniamentioning

confidence: 99%

“…mtDNA, mitochondrial DNA. 1) Roberts et al, 2015; 2) Barksdale, et al, 2014; 3) Wang et al, 1999; 4) Reid et al, 2010; 5) Uranova et al, 2007, Vikhreva et al, 2016; 6) Mamdani et al, 2014; 7) Somerville et al, 2011; 8) Somerville et al, 2012; 9) Maurer et al, 2001; Ben-Shakar & Karry, 2008; 10) Cavalier et al, 1995; Prince et al, 1999, 2000; 11) Uranova et al, 1996, 2001; 12) Kung & Roberts, 1999; 13) McCollum et al, 2015; 14) Kolomeets & Uranova, 1999; 15) Walker & Roberts, 2016; 16) Rice et al, 2014.…”

Section: Figureunclassified

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Postmortem studies on mitochondria in schizophrenia

Roberts

2017

Schizophrenia Research

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The aim of this paper is to provide a brief review of mitochondrial structure as it relates to function and then present abnormalities in mitochondria in postmortem schizophrenia with a focus on ultrastructure. Function, morphology, fusion, fission, motility, ΔΨmem, ATP production, mitochondrial derived vesicles, and mitochondria-associated ER membranes will be briefly covered. Pathology in mitochondria has long been implicated in schizophrenia, as shown by genetic, proteomic, enzymatic and anatomical abnormalities. The cortex and basal ganglia will be reviewed. In the anterior cingulate cortex, the number of mitochondria per neuronal somata in layers 5/6 in schizophrenia is decreased by 43%. There are also fewer mitochondria in terminals forming axospinous synapses. In the caudate and putamen the number of mitochondria is abnormal in both glial cells and neurons in schizophrenia subjects, the extent of which depends on treatment, response and predominant lifetime symptoms. Treatment-responsive schizophrenia subjects had about a 40% decrease in the number of mitochondria per synapse in the caudate nucleus and putamen, while treatment resistant cases had normal values. A decrease in mitochondrial density in the neuropil distinguishes paranoid from undifferentiated schizophrenia. The appearance, size and density of mitochondria were normal in the nucleus accumbens. In the substantia nigra, COX subunits were affected in rostral regions. Mitochondrial hyperplasia occurs within axon terminals that synapse onto dopamine neurons, but mitochondria in dopamine neuronal somata are similar in size and number. In schizophrenia, mitochondria are differentially affected depending on the brain region, cell type, subcellular location, treatment status, treatment response and symptoms.

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Section: Mitochondrial Abnormalities In Schizophreniamentioning

confidence: 94%

Section: Mitochondrial Abnormalities In Schizophreniamentioning

confidence: 99%

Section: Figureunclassified

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Postmortem studies on mitochondria in schizophrenia

Roberts

2017

Schizophrenia Research

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“…По нашему мнению, одной из важных причин более выраженной ультраструктурной патологии МВ при приступообразой шизофрении могут быть особенности активации микроглии, в частности ее большая степень по сравнению с непрерывнотекущей шизофренией. Ультраструктурные признаки активации микроглии, тесно контактирующей с измененными по дистрофическому и деструктивному типам олигодендроцитами и с МВ, были описаны нами в гиппокампе [3] и белом веществе под префронтальной корой [23]. Наше предположение о связи более выраженной активации микроглии при приступообразной шизофрении по сравнению с непрерывнотекущей согласуется с предположением J. Steiner и соавт.…”

Section: Discussionunclassified

Ultrastructural changes of myelinated fibers in the brain in continuous and attack-like paranoid schizophrenia

Uranova¹,

Kolomeets²,

Vikhreva³

et al. 2017

Z. nevrol. psikhiatr. im. S.S. Korsakova

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“…ОЛ, как показал электронно-микроскопический анализ образцов аутопсийного мозга, являются при шизофрении наиболее измененными клетками мозга [34,35]. Снижение численной плотности ОЛ в аутопсийном мозге пациентов выявлено в ряде областей мозга, значимых для патогенеза заболевания и наиболее часто демонстрирующих изменения по данным ДТВ, таких как серое и прилежащее белое вещество префронтальной и теменной коры [36,37], гиппокамп [38].…”

Section: нарушения дифференцировки олигодендроцитов при шизофренииunclassified

Disturbance of oligodendrocyte differentiation in schizophrenia in relation to main hypothesis of the disease

Kolomeets

2017

Z. nevrol. psikhiatr. im. S.S. Korsakova

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Increasing evidence coming from neuroimaging, molecular genetic and post-mortem studies have implicated oligodendrocyte abnormalities and compromised myelin integrity in schizophrenia. Activity-dependent myelination in adult brain is considered to be an important mechanism of neural circuit's plasticity due to the presence of a large population of oligodendrocyte progenitor cells (OPC) in the adult CNS. Growing evidence for impairment of oligodendrocyte differentiation has been reported in the brain of schizophrenia subjects. OPC are very vulnerable inflammation, oxidative stress, and elevated glutamate levels leading to excitotoxicity. The mechanisms of prolonged suppression of oligodendrocyte differentiation caused by prenatal maternal infection or preterm birth are discussed in view of increased risk of schizophrenia, neurodevelopmental and inflammation hypotheses of the disease. The data that some neuroleptics stimulate OPC differentiation and ameliorate myelin alterations support the notion that impairment in the differentiation of OPCs contributes to oligodendrocyte abnormalities and to the pathophysiology of schizophrenia.

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Ultrastructural alterations of oligodendrocytes in prefrontal white matter in schizophrenia: A post-mortem morphometric study

Cited by 70 publications

References 54 publications

Postmortem studies on mitochondria in schizophrenia

Postmortem studies on mitochondria in schizophrenia

Ultrastructural changes of myelinated fibers in the brain in continuous and attack-like paranoid schizophrenia

Disturbance of oligodendrocyte differentiation in schizophrenia in relation to main hypothesis of the disease

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