Linking the cytokine and neurocircuitry hypotheses of depression: A translational framework for discovery and development of novel anti-depressants

Piser, Timothy M.

doi:10.1016/j.bbi.2010.02.006

Cited by 39 publications

(28 citation statements)

References 111 publications

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“…Moreover, frontal cortical regions that mediate action planning and executive function are hypometabolic in depressed individuals in the resting state (Piser 2010;Drevets et al 2008;Drevets 2007). Subjects with overweight/ obesity show evidence of reduced metabolic activity in the prefrontal lobe as well as atrophy of the superior, middle, inferior frontal, and orbitofrontal gyri (Volkow et al 2009).…”

Section: Cns Structure and Functionmentioning

confidence: 97%

“…Hypermetabolism of the subgenual anterior cingulate cortex corresponding to Brodmann's area 25 (Cg25) is a prominent abnormality in major depressive disorder (MDD) (Mayberg et al 2005;Seminowicz et al 2004;Mayberg 2003). The anterior cingulate cortex is a point of convergence where subcortical processing of motivational and affective information is integrated to guide decision-making (Piser 2010;Floresco et al 2008;Talmi et al 2009). …”

Section: Cns Structure and Functionmentioning

confidence: 98%

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Mood Disorders and Obesity: Understanding Inflammation as a Pathophysiological Nexus

et al. 2010

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The aim of this review is to evaluate the evidentiary base supporting the hypothesis that the increased hazard for obesity in mood disorder populations (and vice versa) is a consequence of shared pathophysiological pathways. We conducted a PubMed search of all English-language articles with the following search terms: obesity, inflammation, hypothalamic-pituitary-adrenal axis, insulin, cognition, CNS, and neurotransmitters, cross-referenced with major depressive disorder and bipolar disorder. The frequent co-occurrence of mood disorders and obesity may be characterized by interconnected pathophysiology. Both conditions are marked by structural and functional abnormalities in multiple cortical and subcortical brain regions that subserve cognitive and/or affective processing. Abnormalities in several interacting biological networks (e.g. immuno-inflammatory, insulin signaling, and counterregulatory hormones) contribute to the co-occurence of mood disorders and obesity. Unequivocal evidence now indicates that obesity and mood disorders are chronic low-grade pro-inflammatory states that result in a gradual accumulation of allostatic load. Abnormalities in key effector proteins of the pro-inflammatory cascade include, but are not limited to, cytokines/adipokines such as adiponectin, leptin, and resistin as well as tumor necrosis factor alpha and interleukin-6. Taken together, the bidirectional relationship between obesity and mood disorders may represent an exophenotypic manifestation of aberrant neural and inflammatory networks. The clinical implications of these observations are that, practitioners should screen individuals with obesity for the presence of clinically significant depressive symptoms (and vice versa). This clinical recommendation is amplified in individuals presenting with biochemical indicators of insulin resistance and other concurrent conditions associated with abnormal inflammatory signaling (e.g. cardiovascular disease).

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Section: Cns Structure and Functionmentioning

confidence: 97%

Section: Cns Structure and Functionmentioning

confidence: 98%

Mood Disorders and Obesity: Understanding Inflammation as a Pathophysiological Nexus

et al. 2010

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“…The NPI is a carer-based interview that assesses 10 behavioral disturbances in the subject. Based on animal and human clinical studies, [13][14][15][16][17] we identified 3 core symptoms from the NPI as being a priori compatible with the concept of sickness behavior (i.e., increased depression/ dysphoria, increased anxiety, and increased apathy). The main caregiver was revisited at 4 and 6 months with the NPI reassessed in an identical manner to that at 2 months.…”

Section: Methods Study Designmentioning

confidence: 99%

Proinflammatory cytokines, sickness behavior, and Alzheimer disease

Holmes¹,

Cunningham²,

Zotova³

et al. 2011

Neurology

198

158

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“…As we already know, inflammatory mechanisms play a role in the cause of major depressive disorders (Raedler, 2011). According to the cytokine hypothesis of depression, inflammatory cytokines act on neural circuits to evoke the behavioral and physiological changes observed in depression (Piser, 2010). The elevated systemic levels of TNF-a, IL-1b, and IL-6 were found to be reversed by antidepressants (Berton & Nestler, 2006).…”

Section: Introductionmentioning

confidence: 92%

Antidepressant-like effects of magnesium lithospermate B in a rat model of chronic unpredictable stress

Quan

Liu

Zhang

et al. 2015

Pharmaceutical Biology

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Materials and methods: Sprague-Dawley rats were subjected to the chronic unpredictable stress (CUS) protocol. Rats in the control group received no CUS during the whole experiment. In the model group, rats were exposed to CUS for 7 weeks. From the beginning of the 5th week, model group rats were randomly grouped and subjected to different treatments. In the experiment, control and model group rats were intraperitoneally (i.p.) injected with saline. MLB was dissolved in saline to give a final concentration, and the rats were injected (i.p.) with 15, 30, or 60 mg/kg MLB once a day for 3 weeks. Results: MLB administration significantly reduced: (1) the immobility time in the forced swimming test (19 s, p50.05); (2) the immobility time in the tail suspension test (76.3 s, p50.05); (3) the corticosterone (CORT) concentrations in the serum (21.7 nmol/L, p40.05); (4) the pro-inflammatory cytokine levels in the serum -TNF-a (92.1 pg/ml, p50.05), IL-1b (86.9 pg/ ml, p50.05), and IL-6 (93.8 pg/ml, p50.05); (5) pro-inflammatory cytokine levels in tissue -TNF-a (3.2 pg/mg protein, p50.05), IL-1b (1.5 pg/mg protein, p40.05), and IL-6 (6.3 pg/mg protein, p50.05); and (6) phospho-NF-kB (1.6, p50.05) and phospho-IkB-a (0.4, p50.05) expression in tissue. Discussion and conclusion: The results suggested that MLB might exert therapeutic actions on depression-like behavior and the HPA axis hyperactivity in CUS rats, and the mechanisms underlying the antidepressant-like effects of MLB might be mediated by regulation of the expression of NF-kB and IkB-a in rats.

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Linking the cytokine and neurocircuitry hypotheses of depression: A translational framework for discovery and development of novel anti-depressants

Cited by 39 publications

References 111 publications

Mood Disorders and Obesity: Understanding Inflammation as a Pathophysiological Nexus

Mood Disorders and Obesity: Understanding Inflammation as a Pathophysiological Nexus

Proinflammatory cytokines, sickness behavior, and Alzheimer disease

Antidepressant-like effects of magnesium lithospermate B in a rat model of chronic unpredictable stress

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