Brain-derived neurotrophic factor serum and plasma levels in the treatment of acute schizophrenia with olanzapine or risperidone: 6-week prospective study

Mikulic, Suzan Kudlek; Mihaljević-Peleš, Alma; Šagud, Marina; Janović, Maja Bajs; Ganoci, Lana; Grubišin, Jasmina; Rojnic, Martina; Ćusa, Bjanka Vuksan; Bradaš, Zoran; Božina, Nada

doi:10.1080/08039488.2017.1340518

Cited by 18 publications

(9 citation statements)

References 56 publications

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“…Remarkably, drug treatment that is effective in controlling disease progression in schizophrenic patients can have diverse effects on peripheral BDNF protein levels [ 126 – 128 ]. In addition, some studies suggest that baseline BDNF levels in schizophrenia patients might reflect the susceptibility towards available drug therapies [ 129 , 130 ].…”

Section: Bdnf In Psychiatric Disordersmentioning

confidence: 99%

Brain-Derived Neurotrophic Factor in Brain Disorders: Focus on Neuroinflammation

et al. 2018

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Brain-derived neurotrophic factor (BDNF) is one of the most studied neurotrophins in the healthy and diseased brain. As a result, there is a large body of evidence that associates BDNF with neuronal maintenance, neuronal survival, plasticity, and neurotransmitter regulation. Patients with psychiatric and neurodegenerative disorders often have reduced BDNF concentrations in their blood and brain. A current hypothesis suggests that these abnormal BDNF levels might be due to the chronic inflammatory state of the brain in certain disorders, as neuroinflammation is known to affect several BDNF-related signaling pathways. Activation of glia cells can induce an increase in the levels of pro- and antiinflammatory cytokines and reactive oxygen species, which can lead to the modulation of neuronal function and neurotoxicity observed in several brain pathologies. Understanding how neuroinflammation is involved in disorders of the brain, especially in the disease onset and progression, can be crucial for the development of new strategies of treatment. Despite the increasing evidence for the involvement of BDNF and neuroinflammation in brain disorders, there is scarce evidence that addresses the interaction between the neurotrophin and neuroinflammation in psychiatric and neurodegenerative diseases. This review focuses on the effect of acute and chronic inflammation on BDNF levels in the most common psychiatric and neurodegenerative disorders and aims to shed some light on the possible biological mechanisms that may influence this effect. In addition, this review will address the effect of behavior and pharmacological interventions on BDNF levels in these disorders.

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Section: Bdnf In Psychiatric Disordersmentioning

confidence: 99%

Brain-Derived Neurotrophic Factor in Brain Disorders: Focus on Neuroinflammation

et al. 2018

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“…The studies of changes in BDNF levels during treatment are controversial; only relapse schizophrenic males patients showed elevated BDNF after 4 weeks of risperidone consumption (3-6 mg/day), a result that suggests gender should be considered when choosing the pharmacological treatment (167)(168)(169). However, other studies reported no alteration whatsoever after risperidone consumption (170,171).…”

Section: Risperidonementioning

confidence: 99%

Immunoendocrine Peripheral Effects Induced by Atypical Antipsychotics

et al. 2020

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Atypical antipsychotics (AAP) or second-generation antipsychotics are the clinical option for schizophrenia treatment during acute psychoses, but they are also indicated for maintenance during lifetime, even though they are being used for other psychiatric conditions in clinical practice such as affective disorders and autism spectrum disorder, among others. These drugs are differentiated from typical antipsychotics based on their clinical profile and are a better choice because they cause fewer side effects regarding extrapyramidal symptoms (EPS). Even though they provide clear therapeutic benefits, AAP induce peripheral effects that trigger phenotypic, functional, and systemic changes outside the Central Nervous System (CNS). Metabolic disease is frequently associated with AAP and significantly impacts the patient's quality of life. However, other peripheral changes of clinical relevance are present during AAP treatment, such as alterations in the immune and endocrine systems as well as the intestinal microbiome. These less studied alterations also have a significant impact in the patient's health status. This manuscript aims to revise the peripheral immunological, endocrine, and intestinal microbiome changes induced by AAP consumption recommended in the clinical guidelines for schizophrenia and other psychiatric disorders.

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“…Olanzapine did not increase plasma BDNF in a 6‐week prospective study of schizophrenic patients (n = 50) (Kudlek Mikulic et al, ). A study of ethnically homogenous schizophrenic patients correlated olanzapine treatment with shortened leukocyte telomere length and advanced metabolic age (Monroy‐Jaramillo et al, ).…”

Section: Resultsmentioning

confidence: 99%

“…Olanzapine did not increase plasma BDNF in a 6-week prospective study of schizophrenic patients (n = 50) (Kudlek Mikulic et al, 2017).…”

Section: Olanzapinementioning

confidence: 86%

Putative neuroprotective pharmacotherapies to target the staged progression of mental illness

Robertson

Coronado

Sethi

et al. 2019

Early Intervention Psych

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Aim: Neuropsychiatric disorders including depression, bipolar and schizophrenia frequently exhibit a neuroprogressive course from prodrome to chronicity. There are a range of agents exhibiting capacity to attenuate biological mechanisms associated with neuroprogression. This review will update the evidence for putative neuroprotective agents including clinical efficacy, mechanisms of action and limitations in current assessment tools, and identify novel agents with neuroprotective potential.Method: Data for this review were sourced from online databases PUBMED, Embase and Web of Science. Only data published since 2012 were included in this review, no data were excluded based on language or publication origin.Results: Each of the agents reviewed inhibit one or multiple pathways of neuroprogression including: inflammatory gene expression and cytokine release, oxidative and nitrosative stress, mitochondrial dysfunction, neurotrophin dysregulation and apoptotic signalling. Some demonstrate clinical efficacy in preventing neural damage or loss, relapse or cognitive/functional decline. Agents include: the psychotropic medications lithium, second generation antipsychotics and antidepressants; other pharmacological agents such as minocycline, aspirin, cyclooxygenase-2 inhibitors, statins, ketamine and alpha-2-delta ligands; and others such as erythropoietin, oestrogen, leptin, N-acetylcysteine, curcumin, melatonin and ebselen.Conclusions: Signals of evidence of clinical neuroprotection are evident for a number of candidate agents. Adjunctive use of multiple agents may present a viable avenue to clinical realization of neuroprotection. Definitive prospective studies of neuroprotection with multimodal assessment tools are required.

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Brain-derived neurotrophic factor serum and plasma levels in the treatment of acute schizophrenia with olanzapine or risperidone: 6-week prospective study

Cited by 18 publications

References 56 publications

Brain-Derived Neurotrophic Factor in Brain Disorders: Focus on Neuroinflammation

Brain-Derived Neurotrophic Factor in Brain Disorders: Focus on Neuroinflammation

Immunoendocrine Peripheral Effects Induced by Atypical Antipsychotics

Putative neuroprotective pharmacotherapies to target the staged progression of mental illness

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