Increased susceptibility to apoptosis in cultured fibroblasts from antipsychotic-naïve first-episode schizophrenia patients

Gassó, Patricia; Mas, Sergi; Molina, Oriol; Lafuente, Amàlia; Bernardo, Miquel; Parellada, Eduard

doi:10.1016/j.jpsychires.2013.09.017

Cited by 44 publications

(39 citation statements)

References 52 publications

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“…Another study shows that antipsychotics like haloperidol, eticlopride, raclopride, chlorpromazine and risperidone protect neuronal cells against cell death (50). Caspase-3 activity has been found to be higher in antipsychotic-naïve fi rst episode schizophrenia patients (32). Antipsychotics can be a confounding factor in this study.…”

Section: Discussionmentioning

confidence: 56%

“…Even though apoptosis is frequently determined in schizophrenia and other neurodegenerative diseases, nucleosome measurements have not been widely used. In a recent study, a susceptibility to apoptosis in antipsychotic-naive schizophrenia patients has been found (32). Another study showed an increased apoptosis in euthymic bipolar disorder patients (33).…”

Section: Discussionmentioning

confidence: 94%

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Elevated nucleosome level and oxidative stress in schizophrenia patients

Bahçeci¹,

Mh²,

Us³

et al. 2015

BLL

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AIM: The aim of this study was to investigate the effect of oxidative stress on nucleosome levels and its relation with the clinical features in schizophrenia patients. MATERIAL AND METHOD: Thirty schizophrenia patients and 30 healthy controls were enrolled in this study. Patients were diagnosed with schizophrenia according to the 4th edition of the Diagnostic and Statistical Manual for Mental Disorders (DSM-IV). The control group consisted of 30 healthy subjects matched to the patients with regard to age and gender and who had no history of any psychiatric disorder. The severity of schizophrenia symptoms in the patients was evaluated using the Positive and Negative Syndrome Scale (PANSS) and the Clinical Global Impression Severity Scale (CGI-S). Physical and neurological examinations were performed in each of the patients and controls. RESULTS: Nucleosome, total oxidant levels and OSI values were higher in schizophrenia patients than in controls (p < 0.05). There was no signifi cant difference in the total antioxidant levels. There was a positive correlation between the nucleosome level and PANSS positive subscale (p = 0.028, r = 0.402). There was a positive correlation between TAS and age (p = 0.025, r = 0.289), PANSS total (p < 0.001, r = 0.604). There was a negative correlation between OSI and PANSS total (p = 0.019, r = -0.427), PANSS positive subscale (p = 0.043, r = -0.372). There was a negative correlation between TOS and PANS total (p = 0.028, r = -0.402). CONCLUSION: In this study we found a correlation between nucleosome level and PANSS positive subscale. To our knowledge, this is the fi rst study that evaluates oxidative stress and nucleosomes released from apoptotic cells together (Tab. 2, Ref. 50). Text in PDF www.elis.sk.

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Section: Discussionmentioning

confidence: 56%

Section: Discussionmentioning

confidence: 94%

Elevated nucleosome level and oxidative stress in schizophrenia patients

Bahçeci¹,

Mh²,

Us³

et al. 2015

BLL

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“…There is evidence that oxidative stress leads to apoptosis in some cell types (Aizenman et al, 2000;Esteve et al, 1999;Kagan et al, 2002). In a recent study, a susceptibility to apoptosis in antipsychotic-naive schizophrenia patients has been found (Gasso et al, 2014). Apoptotic neurons have been shown in some neurodegenerative disorders like Alzheimer's and Huntington's diseases, and bipolar disorder (Bredesen, 1995;Dragunow et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

Increased oxidative stress and oxidative DNA damage in non-remission schizophrenia patients

Çöpoğlu

Virit

Kokaçya

et al. 2015

Psychiatry Research

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“…Sirtuin 1 (SIRT1) serves as a deacetylase for proteins involved in multiple cellular pathways, including stress response and apoptosis, and has a protective role in neurodegenerative disorders (Godoy et al 2014). First-episode schizophrenic patients present an increased susceptibility for apoptosis (i.e., fibroblast culture) which possibly affects onset and progression of this disorder (Gassó et al 2014). The NAD-dependent deacetylase, involved in oxidative stress and aging processes, increases in antioxidant capacity following moderate/prolonged exercise in aged rat hearts (Ferrara et al 2008;Lai et al 2014;Lin et al 2014); physical exercise promotes further the downstream pathways of SIRT1 (Suchankova et al 2009).…”

Section: Exercise Alleviation Of Apoptosis Underlying Schizophreniamentioning

confidence: 99%

“…Thus, the emergent developmental dysregulation (perinatal and adolescent) relates to the consequent evolution of neuropsychiatric presymptoms/symptoms in early adulthood, presumably via induction of inflammatory processes, oxidative and nitrosative stress pathways, mitochondrial dysfunction, apoptosis, and epigenetic dysregulation (Archer et al 2014b;Debnath et al 2014;Faizi et al 2014;Pietersen et al 2014). Schizophrenia spectrum disorders, arising from disrupted neurodevelopment and accelerated neurodegeneration, are linked to alterations of apoptotic mechanisms originating from two processes: (i) epigenetic, with polymorphisms in genes related to cell survival and apoptosis (Benedetti et al 2010;Spangaro et al 2012), and (ii) low Bcl-2 and GSK3 levels and increased Bax/Bcl-2 ratios, contributing to increased apoptotic susceptibility in schizophrenic patients (Gassó et al 2014). High ratios of Bax, a pro-apoptotic protein, relative to Bcl-2, an antiapoptotic protein, accelerate apoptosis, whereas the reverse, low Bax relative to Bcl-2, suppressed apoptosis ; accelerated apoptosis is implicated in cognitive symptoms of schizophrenia .…”

Section: Exercise Alleviation Of Apoptosis Underlying Schizophreniamentioning

confidence: 99%

Physical Exercise Alleviates Health Defects, Symptoms, and Biomarkers in Schizophrenia Spectrum Disorder

Archer

Kostrzewa

2015

Neurotox Res

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Schizophrenia spectrum disorders are characterized by symptom profiles consisting of positive and negative symptoms, cognitive impairment, and a plethora of genetic, epigenetic, and phenotypic biomarkers. Assorted animal models of these disorders and clinical neurodevelopmental indicators have implicated neurodegeneration as an element in the underlying pathophysiology. Physical exercise or activity regimes--whether aerobic, resistance, or endurance--ameliorate regional brain and functional deficits not only in affected individuals but also in animal models of the disorder. Cognitive deficits, often linked to regional deficits, were alleviated by exercise, as were quality-of-life, independent of disorder staging and risk level. Apoptotic processes intricate to the etiopathogenesis of schizophrenia were likewise attenuated by physical exercise. There is also evidence of manifest benefits endowed by physical exercise in preserving telomere length and integrity. Not least, exercise improves overall health and quality-of-life. The notion of scaffolding as the outcome of physical exercise implies the "buttressing" of regional network circuits, neurocognitive domains, anti-inflammatory defenses, maintenance of telomeric integrity, and neuro-reparative and regenerative processes.

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Increased susceptibility to apoptosis in cultured fibroblasts from antipsychotic-naïve first-episode schizophrenia patients

Cited by 44 publications

References 52 publications

Elevated nucleosome level and oxidative stress in schizophrenia patients

Elevated nucleosome level and oxidative stress in schizophrenia patients

Increased oxidative stress and oxidative DNA damage in non-remission schizophrenia patients

Physical Exercise Alleviates Health Defects, Symptoms, and Biomarkers in Schizophrenia Spectrum Disorder

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