Expression of inflammatory markers in a genetic rodent model of depression

Strenn, Nina; Suchankova, Petra; Nilsson, Staffan; Fischer, Christina Weide; Wegener, Gregers; Mathé, Aleksander A.; Ekman, Agneta

doi:10.1016/j.bbr.2014.09.025

Cited by 23 publications

(15 citation statements)

References 60 publications

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“…The first hours after the traumatic event might represent a special "window of opportunity" for an intervention to prevent the development of a full-blown disorder (Zohar et al, 2009). Immunological alterations are a key finding in anxiety disorders and depression (Leonard and Song, 1996;Rosenblat et al, 2014;Young et al, 2014) and are supported by observations from animal model research such as the Flinders Sensitive line genetic model of depression (Carboni et al, 2010;Strenn et al, 2014). While endocrine changes associated with PTSD have been extensively researched, work from the last decade suggests alternations in the immune system are also strongly linked to PTSD.…”

Section: Introductionmentioning

confidence: 93%

Early post-stressor intervention with minocycline, a second-generation tetracycline, attenuates post-traumatic stress response in an animal model of PTSD

Levkovitz¹,

Fenchel²,

Kaplan³

et al. 2015

European Neuropsychopharmacology

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Section: Introductionmentioning

confidence: 93%

Early post-stressor intervention with minocycline, a second-generation tetracycline, attenuates post-traumatic stress response in an animal model of PTSD

Levkovitz¹,

Fenchel²,

Kaplan³

et al. 2015

European Neuropsychopharmacology

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“…; Strenn et al . ), while also in this case data obtained from the hippocampus are conflicting (Gos et al . ; Schroeter et al .…”

Section: S100b As An Active Factor In Neural Injurymentioning

confidence: 99%

“…From the bulk of data on patients and animal models of depression and, more in general, mood disorders, the indications currently emerging are of a down-regulation of the protein in the frontal cortex (Dean et al 2006;Strenn et al 2015), while also in this case data obtained from the hippocampus are conflicting (Gos et al 2013;Schroeter et al 2014). It may be relevant in this respect that the antidepressant fluoxetine has been shown to increase hippocampal and CSF levels of both the protein and its receptor in rats exposed to chronic mild stress, reversing the decrease induced by stress treatment (Rong et al 2010).…”

Section: Psychiatric Disordersmentioning

confidence: 99%

The S100B story: from biomarker to active factor in neural injury

Michetti

D’Ambrosi

Toesca

et al. 2018

Journal of Neurochemistry

273

238

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S100B is a Ca -binding protein mainly concentrated in astrocytes. Its levels in biological fluids (cerebrospinal fluid, peripheral and cord blood, urine, saliva, amniotic fluid) are recognized as a reliable biomarker of active neural distress. Although the wide spectrum of diseases in which the protein is involved (acute brain injury, neurodegenerative diseases, congenital/perinatal disorders, psychiatric disorders) reduces its specificity, its levels remain an important aid in monitoring the trend of the disorder. Mounting evidence now points to S100B as a Damage-Associated Molecular Pattern molecule which, when released at high concentration, through its Receptor for Advanced Glycation Endproducts, triggers tissue reaction to damage in a series of different neural disorders. This review addresses this novel scenario, presenting data indicating that S100B levels and/or distribution in the nervous tissue of patients and/or experimental models of different neural disorders, for which the protein is used as a biomarker, are directly related to the progress of the disease: acute brain injury (ischemic/hemorrhagic stroke, traumatic injury), neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, multiple sclerosis), congenital/perinatal disorders (Down syndrome, spinocerebellar ataxia-1), psychiatric disorders (schizophrenia, mood disorders), inflammatory bowel disease. In many cases, over-expression/administration of the protein induces worsening of the disease, whereas its deletion/inactivation produces amelioration. This review points out that the pivotal role of the protein resulting from these data, opens the perspective that S100B may be regarded as a therapeutic target for these different diseases, which appear to share some common features reasonably attributable to neuroinflammation, regardless their origin.

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“…Accordingly, astrocytic gene expression such as structural glial-fibrillary-acidic-protein (GFAP) is markedly decreased in PFC samples of postmortem tissue from depressed patients (Nagy et al, 2014) (Figure 2). In rats, GFAP protein expression is reduced following maternal deprivation (Leventopoulos et al, 2007) or a 5-week social defeat paradigm (Araya-Callis et al, 2012), while S100β mRNA, a marker of astrocytes and oligodendrocytes, is decreased in a genetic model of depression (Strenn et al, 2015). Astrocytes can be classified into three types according to their morphology and spatial organization: 1) first radial astrocytes have long unbranched processes and surround blood vessels, 2) protoplasmic astrocytes are present mostly in gray matter and display highly branched short processes and finally 3) fibrous astrocytes have a classic stellar shape and are enriched in the white matter (Chen and Swanson, 2003).…”

Section: Validity For Human Disordersmentioning

confidence: 99%

Pathogenesis of depression: Insights from human and rodent studies

2016

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Major depressive disorder (MDD) will affect one out of every five people in their lifetime and is the leading cause of disability worldwide. Nevertheless, mechanisms associated with the pathogenesis of MDD have yet to be completely understood and current treatments remain ineffective in a large subset of patients. In this review, we summarize the most recent discoveries and insights for which parallel findings have been obtained in human depressed subjects and rodent models of mood disorders in order to examine the potential etiology of depression. These mechanisms range from synaptic plasticity mechanisms to epigenetics and the immune system where there is strong evidence to support a functional role in the development of specific depression symptomology. Ultimately we conclude by discussing how novel therapeutic strategies targeting central and peripheral processes might ultimately aid in the development of effective new treatments for MDD and related stress disorders.

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Expression of inflammatory markers in a genetic rodent model of depression

Cited by 23 publications

References 60 publications

Early post-stressor intervention with minocycline, a second-generation tetracycline, attenuates post-traumatic stress response in an animal model of PTSD

Early post-stressor intervention with minocycline, a second-generation tetracycline, attenuates post-traumatic stress response in an animal model of PTSD

The S100B story: from biomarker to active factor in neural injury

Pathogenesis of depression: Insights from human and rodent studies

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