Ultrastructural alterations of synaptic contacts and astrocytes in postmortem caudate nucleus of schizophrenic patients

Uranova, N.A.; Casanova, Manuel F.; DeVaughn, Nathan M.; Orlovskaya, D.D.; Денисов, Д. В.

doi:10.1016/0920-9964(96)00059-x

Cited by 58 publications

(31 citation statements)

References 5 publications

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“…White blood cells from patients with schizophrenia have shown mitochondrial swelling [Naneishvili and Zurabashvili, 1976;Inuwa et al, 2005] and fewer mitochondria in cases compared to controls [Inuwa et al, 2005]. Early studies on post-mortem tissue revealed decreased numbers of mitochondria in oligodendrocytes from the striatum in schizophrenia [Uranova et al, 1996[Uranova et al, , 2001Kung and Roberts, 1999] and mitochondrial hyperplasia [Kolomeets and Uranova, 1999]. More recent studies have failed to identify changes in the number of mitochondria in the neuropil, dendrites, or terminals of neuronal processes in the striatum [Somerville et al, 2011a,b].…”

Section: Evidence For Mitochondrial Abnormalities and Dysfunction In mentioning

confidence: 98%

The mitochondrial genome and psychiatric illness

Anglin

Mazurek

Tarnopolsky

et al. 2012

American J of Med Genetics Pt B

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Psychiatric disorders are a leading cause of morbidity and mortality, yet their underlying pathophysiology remains unclear. Searches for a genetic cause of bipolar disorder, schizophrenia, and major depressive disorder have yielded inconclusive results. There is increasing interest in the possibility that defects in the mitochondrial genome may play an important role in psychiatric illness. We undertook a review of the literature investigating mitochondria and adult psychiatric disorders. MEDLINE, PsycINFO, and EMBASE were searched from their inception through September 2011, and the reference lists of identified articles were reviewed for additional studies. While multiple lines of evidence, including clinical, genetic, ultrastructural, and biochemical studies, support the involvement of mitochondria in the pathophysiology of psychiatric illness, many studies have methodological limitations and their findings have not been replicated. Clinical studies suggest that psychiatric features can be prominent, and the presenting features of mitochondrial disorders. There is limited but inconsistent evidence for the involvement of mitochondrial DNA haplogroups and mitochondria-related nuclear gene polymorphisms, and for mitochondrial ultrastructural and biochemical abnormalities in psychiatric illness. The current literature suggests that mitochondrial dysfunction and mitochondrial genetic variations may play an important role in psychiatric disorders, but additional methodologically rigorous and adequately powered studies are needed before definitive conclusions can be drawn.

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Section: Evidence For Mitochondrial Abnormalities and Dysfunction In mentioning

confidence: 98%

The mitochondrial genome and psychiatric illness

Anglin

Mazurek

Tarnopolsky

et al. 2012

American J of Med Genetics Pt B

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“…On the other hand, increased oxidative stress may be a result of pathological processes [3,[18][19][20]. The studies examining the relationship between schizophrenia and total oxidant-antioxidant levels are scarce [21,22]. To our knowledge, there is only one study that analyzed TOL and OSI as well as TAL in schizophrenia [23].…”

Section: Introductionmentioning

confidence: 95%

Oxidative metabolism may be associated with negative symptoms in schizophrenia

Güneş

Altındağ

Bulut

et al. 2017

Psychiatry and Clinical Psychopharmacology

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Objective: In the present study, we aimed to examine the relationship between the oxidative metabolism with disease severity, sociodemographic, and clinical characteristics in the patients with schizophrenia. Methods: Seventy-one patients with schizophrenia and 76 healthy volunteers were included in the study. Plasma total antioxidant level (TAL) and total oxidant level (TOL) were analyzed, and oxidative stress index (OSI) was calculated.Results: There was a statistically significant increase in TOL and OSI and decrease in TAL in the patients with schizophrenia compared to the controls (p < .05). There were positive, mild, statistically significant correlations between TOL, OSI, and Positive and Negative Syndrome Scale-Total scores (p = .01, p = .01, respectively), Positive and Negative Syndrome ScaleNegative scores (p = .002, p = .001, respectively), Positive and Negative Syndrome Scale Global Psychopathology scores (p = .03, p = .03, respectively), and Clinical Global ImpressionSeverity Scale scores (p = .008, p = .009 respectively). OSI levels were significantly lower in the patients who were on treatment with atypical antipsychotics (AAP) compared to the patients who were on typical antipsychotics (TAP) and combined antipsychotic (CAP) agents (p = .032). Conclusions: Oxidative stress was higher in schizophrenia patients. The increased severity of negative symptoms was in line with the disruption in oxidative balance. Oxidative stress is quite lower in AAP users compared to the TAP and CAP users. One of the mechanisms underlying the fact that AAPs are more effective on negative symptoms than typical agents may be the positive effect on the oxidative stress.ARTICLE HISTORY

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“…Снижение числа митохондрий в астроцитах может быть объяснено преимущественно уменьшением разме-ров цитоплазмы клеток, однако имеющаяся тенденция к существенному (на 17%) уменьшению их объемной фрак-ции может свидетельствовать об истинном дефиците ми-тохондрий в астроцитах при воздействии на культуру СК пациентов по сравнению с контролем. Следует отметить впервые установленное сходство изменений астроцитов в культуре ткани под влиянием СК больных шизофренией с результатами исследований аутопсийного материала, при которых были выявлены дистрофические изменения астроцитов в мозге больных шизофренией: уменьшение числа и объемной фракции митохондрий, появление ли-пофусциноподобных включений в их цитоплазме [22][23][24][25]. Кроме того, результаты молекулярно-генетических и биохимических исследований свидетельствуют о дис-функции астроцитов и нарушении их энергетического, глутаматного и кинуренинового метаболизма в мозге при шизофрении [19][20][21].…”

Section: Discussionunclassified

“…С дру-гой стороны, дисфункция астроцитов может быть суще-ственным звеном патогенеза шизофрении, так как имеет прямое отношение к нарушениям энергетического, глута-матного и кинуренинового метаболизма в мозге пациен-тов [19][20][21]. К тому же в аутопсийном мозге больных ши-зофренией были выявлены нарушения ультраструктуры астроцитов дистрофического типа в префронтальной ко-ре, гиппокампе и хвостатом ядре мозга [22][23][24][25]. Однако причины и механизмы этих изменений остаются малоиз-ученными.…”

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Effects of schizophrenic blood serum on astrocytes in human fetal brain organotypic culture: a morphometric study

Kolomeets

Vostrikov

2015

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

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Ultrastructural alterations of synaptic contacts and astrocytes in postmortem caudate nucleus of schizophrenic patients

Cited by 58 publications

References 5 publications

The mitochondrial genome and psychiatric illness

The mitochondrial genome and psychiatric illness

Oxidative metabolism may be associated with negative symptoms in schizophrenia

Effects of schizophrenic blood serum on astrocytes in human fetal brain organotypic culture: a morphometric study

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