P.362 Antipsychotic treatment for the maintenance phase of schizophrenia: An updated systematic review of the guidelines and algorithms

Shimomura, Yuka; Kikuchi, Yudai; Takefumi, S.; H, Uchida; Mimura, M.; Takeuchi, H.

doi:10.1016/j.euroneuro.2019.09.380

Cited by 2 publications

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“…In addition, DNA oxidative damage, e.g., 8-hydroxydeoxyguanosine, can interfere with gene transcription and affect promoter function, which can lead to impaired transcription of essential genes, i.e., suppressor genes, p53 gene, ras gene, and further mutations. In turn, RNA oxidative damage can damage protein translation, which leads to reduced expression of proteins and loss of their physiological functions (Table 2) [18,36,37].…”

Section: Oxidative Nitrosative and Sulfuric Stress In Schizophreniamentioning

confidence: 99%

“…Pharmacotherapy of schizophrenia faces some problems including polypragmasia resulting from the lack of standards for the use of polypharmacotherapy [36]. According to the new recommendations of the American Psychiatric Association of 2020, schizophrenia therapy, especially in younger people experiencing the first psychotic episode, should be started with atypical drugs, initially at a low dose, with observation of the response to treatment and side effects [37]. Olanzapine is one of the often chosen drugs with minor side effects from the extrapyramidal system (in contrast to classical neuroleptics).…”

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confidence: 99%

“…In addition, it is important that the complication of the assessment of risk related to cardiometabolic syndrome is due to some FEP patients showing impaired glucose metabolism preceding the use of antipsychotic treatment [42]. This should be taken into account at the stage of qualifying patients for treatment and during atypical antipsychotics pharmacotherapy based on recommended dose reduction ("doses must be reduced gradually at a rate of approximately 20% every 6 months") [43] as a risk-benefit strategy prior to treatment [37].…”

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confidence: 99%

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Oxidative-Antioxidant Imbalance and Impaired Glucose Metabolism in Schizophrenia

et al. 2020

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Schizophrenia is a neurodevelopmental disorder featuring chronic, complex neuropsychiatric features. The etiology and pathogenesis of schizophrenia are not fully understood. Oxidative-antioxidant imbalance is a potential determinant of schizophrenia. Oxidative, nitrosative, or sulfuric damage to enzymes of glycolysis and tricarboxylic acid cycle, as well as calcium transport and ATP biosynthesis might cause impaired bioenergetics function in the brain. This could explain the initial symptoms, such as the first psychotic episode and mild cognitive impairment. Another concept of the etiopathogenesis of schizophrenia is associated with impaired glucose metabolism and insulin resistance with the activation of the mTOR mitochondrial pathway, which may contribute to impaired neuronal development. Consequently, cognitive processes requiring ATP are compromised and dysfunctions in synaptic transmission lead to neuronal death, preceding changes in key brain areas. This review summarizes the role and mutual interactions of oxidative damage and impaired glucose metabolism as key factors affecting metabolic complications in schizophrenia. These observations may be a premise for novel potential therapeutic targets that will delay not only the onset of first symptoms but also the progression of schizophrenia and its complications.

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Section: Oxidative Nitrosative and Sulfuric Stress In Schizophreniamentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Oxidative-Antioxidant Imbalance and Impaired Glucose Metabolism in Schizophrenia

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Histone Deacetylase Inhibitors as Cognitive Enhancers and Modifiers of Mood and Behavior

Pal

Sukocheva

Sahu

et al. 2023

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Background: Epigenetic regulation of gene signalling is one of the fundamental molecular mechanisms for the generation and maintenance of cellular memory. Histone acetylation is a common epigenetic mechanism associated with increased gene transcription in the central nervous system (CNS). Stimulation of gene transcription by histone acetylation is important for the development of CNS-based long-term memory. Histone acetylation is a target for cognitive enhancement via the application of histone deacetylase (HDAC) inhibitors. The promising potential of HDAC inhibitors has been observed in the treatment of several neurodevelopmental and neurodegenerative diseases, Objective: This study assessed the current state of HDAC inhibition as an approach to cognitive enhancement and treatment of neurodegenerative diseases. Our analysis provides insights into the mechanism of action of HDAC inhibitors, associated epigenetic priming, and describes the therapeutic success and potential complications after unsupervised use of the inhibitors. Results and Conclusion: Several chromatin-modifying enzymes play key roles in the regulation of cognitive processes. The importance of HDAC signaling in the brain is highlighted in this review. Recent advancements in the field of cognitive epigenetics are supported by the successful development of various HDAC inhibitors, demonstrating effective treatment of mood-associated disorders. The current review discusses the therapeutic potential of HDAC inhibition and observed complications after mood and cognitive enhancement therapies.

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P.362 Antipsychotic treatment for the maintenance phase of schizophrenia: An updated systematic review of the guidelines and algorithms

Cited by 2 publications

References 0 publications

Oxidative-Antioxidant Imbalance and Impaired Glucose Metabolism in Schizophrenia

Oxidative-Antioxidant Imbalance and Impaired Glucose Metabolism in Schizophrenia

Histone Deacetylase Inhibitors as Cognitive Enhancers and Modifiers of Mood and Behavior

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