A response to the commentary “Indolamine 2,3-dioxygenase regulation and neuropsychiatric symptoms” by Loftis, J.M. on “Serotonin and interleukin-6: The role of genetic polymorphisms in IFN-induced neuropsychiatric symptoms” by Udina, M., Moreno-España, J., Navinés, R., Gimenez, D., Langohr, K., Gratacòs, M., Capuron, L., de la Torre, R., Solà, R., Martin-Santos, R. http:\\dx.doi.org/10.1016/j.psyneuen.2013.03.007

2013 ◽  
Vol 38 (9) ◽  
pp. 1830-1831 ◽  
Author(s):  
Marc Udina ◽  
Ricard Navinés ◽  
Lucile Capuron ◽  
Rocío Martín-Santos
Keyword(s):  
Genetic Polymorphisms ◽  
Interleukin 6 ◽  
Neuropsychiatric Symptoms

Serotonin and interleukin-6: The role of genetic polymorphisms in IFN-induced neuropsychiatric symptoms

2013 ◽  
Vol 38 (9) ◽  
pp. 1803-1813 ◽  
Author(s):  
Marc Udina ◽  
José Moreno-España ◽  
Ricard Navinés ◽  
Dolors Giménez ◽  
Klaus Langohr ◽  
...  
Keyword(s):  
Genetic Polymorphisms ◽  
Interleukin 6 ◽  
Neuropsychiatric Symptoms

Prognostic role of genetic polymorphisms of the interleukin-6 signaling pathway in patients with severe heart failure

2019 ◽  
Vol 19 (5) ◽  
pp. 428-437 ◽  
Author(s):  
Peter R. Hansen ◽  
Karl Emil Nelveg-Kristensen ◽  
Henrik B. Rasmussen ◽  
Christian Torp-Pedersen ◽  
Lars Køber ◽  
...  
Keyword(s):  
Heart Failure ◽  
Signaling Pathway ◽  
Genetic Polymorphisms ◽  
Interleukin 6 ◽  
Severe Heart Failure ◽  
Prognostic Role

Role of interleukin-6 in the early and late fracture healing phase

2016 ◽  
Author(s):  
Katja Prystaz ◽  
Anna Kovtun ◽  
Kathrin Kaiser ◽  
Verena Heidler ◽  
Jochen Kroner ◽  
...  
Keyword(s):  
Fracture Healing ◽  
Interleukin 6 ◽  
Healing Phase

scholarly journals Monitoring and Modulating Inflammation-Associated Alterations in Synaptic Plasticity: Role of Brain Stimulation and the Blood–Brain Interface

Biomolecules ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 359
Author(s):  
Maximilian Lenz ◽  
Amelie Eichler ◽  
Andreas Vlachos
Keyword(s):  
Synaptic Plasticity ◽  
Brain Stimulation ◽  
Vascular Function ◽  
Neuropsychiatric Symptoms ◽  
Systemic Infection ◽  
Brain Functions ◽  
Blood Brain ◽  
Brain Interface ◽  
The Central Nervous System

Inflammation of the central nervous system can be triggered by endogenous and exogenous stimuli such as local or systemic infection, trauma, and stroke. In addition to neurodegeneration and cell death, alterations in physiological brain functions are often associated with neuroinflammation. Robust experimental evidence has demonstrated that inflammatory cytokines affect the ability of neurons to express plasticity. It has been well-established that inflammation-associated alterations in synaptic plasticity contribute to the development of neuropsychiatric symptoms. Nevertheless, diagnostic approaches and interventional strategies to restore inflammatory deficits in synaptic plasticity are limited. Here, we review recent findings on inflammation-associated alterations in synaptic plasticity and the potential role of the blood–brain interface, i.e., the blood–brain barrier, in modulating synaptic plasticity. Based on recent findings indicating that brain stimulation promotes plasticity and modulates vascular function, we argue that clinically employed non-invasive brain stimulation techniques, such as transcranial magnetic stimulation, could be used for monitoring and modulating inflammation-induced alterations in synaptic plasticity.

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