Effects of minocycline add-on treatment on brain morphometry and cerebral perfusion in recent-onset schizophrenia

Chaves, Carolina de Andrade Lima; Marque, Cristiane Reberte de; Maia‐de‐Oliveira, João Paulo; Wichert‐Ana, Lauro; Ferrari, Thiago Borduqui; Santos, Antônio Carlos dos; Araújo, David; Machado‐de‐Sousa, João Paulo; Bressan, Rodrigo A.; Elkis, Hélio; Crippa, José Alexandre S; Guimarães, Francisco Silveira; Zuardi, Antônio Waldo; Baker, Glen B.; Dursun, Serdar; Hallak, Jaime Eduardo Cecílio

doi:10.1016/j.schres.2014.11.031

Cited by 36 publications

(32 citation statements)

References 46 publications

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“…In a recent meta-analysis, it was concluded that minocycline is superior to placebo for decreasing PANSS (positive and negative syndrome scale) total scores, PANSS negative subscale scores, and PANSS general subscale scores (Oya et al, 2014). In addition, two more recent randomized controlled trials produced results supporting the effectiveness of minocycline as an adjuvant treatment with antipsychotic drugs for treating negative symptoms of patients with schizophrenia (Chaves et al, 2015;Ghanizadeh et al, 2014). Regarding NSAIDs, a recent meta-analysis concluded that celecoxib augmentation could be a potentially useful strategy to reduce symptom severity in schizophrenia (Sommer et al, 2012), although further studies are needed before a definite conclusion can be accepted.…”

Section: Discussionmentioning

confidence: 99%

Quetiapine mitigates the neuroinflammation and oligodendrocyte loss in the brain of C57BL/6 mouse following cuprizone exposure for one week

Shao

Peng

Huang

et al. 2015

European Journal of Pharmacology

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Section: Discussionmentioning

confidence: 99%

Quetiapine mitigates the neuroinflammation and oligodendrocyte loss in the brain of C57BL/6 mouse following cuprizone exposure for one week

Shao

Peng

Huang

et al. 2015

European Journal of Pharmacology

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“…In cuprizone-fed C57BL/6 mice, minocycline reduced microglial activation and demyelination in the brain and prevented disturbances in motor coordination (Pasquini et al, 2007;Skripuletz et al, 2010;Tanaka et al, 2013). Furthermore, minocycline in combination with an antipsychotic such as risperidone, olanzapine, quetiapine, or clozapine significantly improved positive, negative, and cognitive symptoms in recent-onset or chronic schizophrenia patients (Levkovitz et al, 2010;Ghanizadeh et al, 2014;Chaves et al, 2015;Kelly et al, 2015). From these results, it is likely that application of minocycline can dampen M1 signaling, subsequently resulting in skewing of M2a microglia that reduce proinflammatory signaling and increase production of anti-inflammatory cytokines.…”

Section: Pharmacological Approach To Neuroinflammation In Asd and Schmentioning

confidence: 99%

Involvement of Neuroinflammation during Brain Development in Social Cognitive Deficits in Autism Spectrum Disorder and Schizophrenia

Nakagawa¹,

Chiba²

2016

Journal of Pharmacology and Experimental Therapeutics

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Development of social cognition, a unique and high-order function, depends on brain maturation from childhood to adulthood in humans. Autism spectrum disorder (ASD) and schizophrenia have similar social cognitive deficits, although age of onset in each disorder is different. Pathogenesis of these disorders is complex and contains several features, including genetic risk factors, environmental risk factors, and sites of abnormalities in the brain. Although several hypotheses have been postulated, they seem to be insufficient to explain how brain alterations associated with symptoms in these disorders develop at distinct developmental stages. Development of ASD appears to be related to cerebellar dysfunction and subsequent thalamic hyperactivation in early childhood. By contrast, schizophrenia seems to be triggered by thalamic hyperactivation in late adolescence, whereas hippocampal aberration has been possibly initiated in childhood. One of the possible culprits is metal homeostasis disturbances that can induce dysfunction of blood-cerebrospinal fluid barrier. Thalamic hyperactivation is thought to be induced by microglia-mediated neuroinflammation and abnormalities of intracerebral environment. Consequently, it is likely that the thalamic hyperactivation triggers dysregulation of the dorsolateral prefrontal cortex for lower brain regions related to social cognition. In this review, we summarize the brain aberration in ASD and schizophrenia and provide a possible mechanism underlying social cognitive deficits in these disorders based on their distinct ages of onset.

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“…Furthermore, a later meta-analysis including two of RCTs 149,150 published after the first meta-analysis, concluded that minocycline was superior to placebo for decreasing PANSS total scores, PANSS negative subscale scores and PANSS general subscale scores 151 . In line with the above conclusion, two more recent RCTs produced results supporting the effectiveness of minocycline, as an adjuvant treatment with antipsychotic drugs for treating negative symptoms of patients with schizophrenia 152,153 . In addition to significantly reducing positive and negative symptoms, when compared with placebo, add-on of minocycline ameliorated the gray matter volume decrease in the mid-posterior cingulate cortex and in the precentral gyrus shown in the patients in the placebo group, suggesting that minocycline may protect against gray matter loss and modulate fronto-temporal areas involved in the pathophysiology of schizophrenia 153 .…”

Section: Minocyclinementioning

confidence: 64%

Neuroinflammation in Schizophrenia Focused on the Pharmacological and Therapeutic Evidence

Xu¹

2015

Pharmacologia

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Background: Schizophrenia is a heterogeneous mental disorder with a variety of symptoms. Although, there are no pathognomonic abnormalities in brains of schizophrenia patients, recent years have witnessed research progresses in revealing pathologic changes in cellular and molecular levels. Objective: This article reviewed recent human studies showing neuroimmune alterations in schizophrenia patients and offered explanations for roles of neuroinflammation in the pathogenesis of schizophrenia by citing some of experimental data from non-human studies. The focus of this review was put on pharmacological and therapeutic evidence pointing to a recommendation of anti-inflammatory treatment for patients with schizophrenia. Particularly, it provided compelling evidence supporting an anti-inflammatory effect of antipsychotics by reviewing a relatively large body of studies in the categories of in vitro, animals and humans. Conclusion: Then, it reviewed recent clinical trials with minocycline, a second-generation tetracycline, or the selective COX-2 inhibitor celecoxib. Most of these clinical trials provided promising results of superior beneficial treatment effects as the consequence of co-administration of standard antipsychotic drugs and anti-inflammatory compounds, compared with antipsychotic drugs alone.

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Effects of minocycline add-on treatment on brain morphometry and cerebral perfusion in recent-onset schizophrenia

Cited by 36 publications

References 46 publications

Quetiapine mitigates the neuroinflammation and oligodendrocyte loss in the brain of C57BL/6 mouse following cuprizone exposure for one week

Quetiapine mitigates the neuroinflammation and oligodendrocyte loss in the brain of C57BL/6 mouse following cuprizone exposure for one week

Involvement of Neuroinflammation during Brain Development in Social Cognitive Deficits in Autism Spectrum Disorder and Schizophrenia

Neuroinflammation in Schizophrenia Focused on the Pharmacological and Therapeutic Evidence

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