Neuroimmunology of Behavioral Comorbidities Associated With Cancer and Cancer Treatments

Frontiers in Immunology, Journal Year: 2018, Volume and Issue: 9

Published: June 7, 2018

Behavioral comorbidities (depression, anxiety, fatigue, cognitive disturbances and neuropathic pain) are prevalent in cancer patients survivors. These mental neurological health issues reduce quality-of-life, which is a significant societal concern given the increasing rates of long-term survival after various cancers. Hypothesized causes behavioral with include tumor biology, stress associated experience treatments. A relatively recent leading mechanism by these contribute to changes neurobiology that underlie behavior inflammation. Indeed, both basic clinical research indicates peripheral inflammation leads central other illness contexts. Given limitations assessing neuroimmunology populations, this review primarily synthesizes evidence neuroimmune neuroinflammatory due two components (tumor biology treatments) altered affective-like or behaviors rodents. Specifically, alterations microglia, neuroinflammation, immune trafficking brain compiled models tumors, chemotherapy, and/or radiation. Evidence-based neuronal mechanisms may lead proposed. Finally, converging populations discussed.

Language: Английский

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A Tilted Axis: Maladaptive Inflammation and HPA Axis Dysfunction Contribute to Consequences of TBI

Frontiers in Neurology, Journal Year: 2019, Volume and Issue: 10

Published: April 24, 2019

Each year approximately 1.7 million people sustain a traumatic brain injury (TBI) in the US alone. Associated with these head injuries is high prevalence of neuropsychiatric symptoms including irritability, depression, and anxiety. Neuroinflammation, due part to microglia, can worsen or even cause disorders after TBI. For example, mounting evidence demonstrates that microglia become "primed" hyper-reactive an exaggerated pro-inflammatory phenotype following multiple immune challenges. Microglial priming occurs experimental TBI correlates emergence depressive-like behavior as well cognitive dysfunction. Critically, challenges are various include illness, aging, stress. The collective influence any combination shapes neuroimmune environment response stress reliably induces inflammation could therefore be gateway altered neuropathology behavioral decline Given increasing incidence stress-related psychiatric TBI, degree which affects outcome particular interest. This review aims highlight role hypothalamic-pituitary-adrenal (HPA) axis key mediator stress-immune pathway communication We will first describe maladaptive neuroinflammation how contributes through both anti- mechanisms. Clinical data describing HPA-axis dysfunction consequences responses discussed. Lastly, we common models used better elucidate relationship between HPA Together, studies described this suggest prevalent dynamic nature neuroinflammatory injury. Experimental stressors directly engage represent important areas for future research define pathways mediating

Language: Английский

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Resolution of inflammation-induced depression requires T lymphocytes and endogenous brain interleukin-10 signaling

Neuropsychopharmacology, Journal Year: 2018, Volume and Issue: 43(13), P. 2597 - 2605

Published: July 16, 2018

Language: Английский

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The Influence of Microglial Elimination and Repopulation on Stress Sensitization Induced by Repeated Social Defeat

Biological Psychiatry, Journal Year: 2018, Volume and Issue: 85(8), P. 667 - 678

Published: Oct. 25, 2018

Language: Английский

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Implications of the gut microbiota in vulnerability to the social avoidance effects of chronic social defeat in male mice

Brain Behavior and Immunity, Journal Year: 2017, Volume and Issue: 66, P. 45 - 55

Published: June 19, 2017

Language: Английский

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