Inflammatory mechanisms contribute to microembolism-induced anxiety-like and depressive-like behaviors

Nemeth, Christina L.; Miller, Andrew H.; Tansey, Malú G.; Neigh, Gretchen N.

doi:10.1016/j.bbr.2016.01.057

Cited by 12 publications

(11 citation statements)

References 69 publications

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“…The neuroplastic hypothesis of depression suggests that alterations in the plasticity of neural networks are a relevant factor in mood disorders including depression [26], and FLX restores structural plasticity [27]. The cytokine hypothesis of depression implicates the immune system in the development of depression, and suggests that anti-depressant drugs prevent microembolism-induced changes in inflammation and behavior [28,29].…”

Section: Discussionmentioning

confidence: 99%

3,5,6,7,8,3′,4′-Heptamethoxyflavone, a Citrus Flavonoid, Ameliorates Corticosterone-Induced Depression-like Behavior and Restores Brain-Derived Neurotrophic Factor Expression, Neurogenesis, and Neuroplasticity in the Hippocampus

et al. 2016

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Abstract:We previously reported that the citrus flavonoid 3,5,6,7,8,3 1 ,4 1 -heptamethoxyflavone (HMF) increased the expression of brain-derived neurotrophic factor (BDNF) in the hippocampus of a transient global ischemia mouse model. Since the BDNF hypothesis of depression postulates that a reduction in BDNF is directly involved in the pathophysiology of depression, we evaluated the anti-depressive effects of HMF in mice with subcutaneously administered corticosterone at a dose of 20 mg/kg/day for 25 days. We demonstrated that the HMF treatment ameliorated (1) corticosterone-induced body weight loss, (2) corticosterone-induced depression-like behavior, and (3) corticosterone-induced reductions in BDNF production in the hippocampus. We also showed that the HMF treatment restored (4) corticosterone-induced reductions in neurogenesis in the dentate gyrus subgranular zone and (5) corticosterone-induced reductions in the expression levels of phosphorylated calcium-calmodulin-dependent protein kinase II and extracellular signal-regulated kinase1/2. These results suggest that HMF exerts its effects as an anti-depressant drug by inducing the expression of BDNF.

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Section: Discussionmentioning

confidence: 99%

3,5,6,7,8,3′,4′-Heptamethoxyflavone, a Citrus Flavonoid, Ameliorates Corticosterone-Induced Depression-like Behavior and Restores Brain-Derived Neurotrophic Factor Expression, Neurogenesis, and Neuroplasticity in the Hippocampus

et al. 2016

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“…In addition, a wide range of behavioral actions have been associated with NSAID inhibition of COX. 34,119,128,160 Data have been compiled on NSAID classified by chemical structure, COX selectivity, and putative mechanism of action. Any data on COX inhibitors must be carefully evaluated, since COX selectivity is almost always based on in vitro determinations using human cells, varies depending on the type of assay employed, and may not translate from human to animal cells or from one species to another.…”

Section: Local Anestheticsmentioning

confidence: 99%

A Review of the Effects of Pain and Analgesia on Immune System Function and Inflammation: Relevance for Preclinical Studies

DeMarco

Nunamaker

2019

comp med

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One of the most significant challenges facing investigators, laboratory animal veterinarians, and IACUCs, is how to balance appropriate analgesic use, animal welfare, and analgesic impact on experimental results. This is particularly true for in vivo studies on immune system function and inflammatory disease. Often times the effects of analgesic drugs on a particular immune function or model are incomplete or don't exist. Further complicating the picture is evidence of the very tight integration and bidirectional functionality between the immune system and branches of the nervous system involved in nociception and pain. These relationships have advanced the concept of understanding pain as a protective neuroimmune function and recognizing pathologic pain as a neuroimmune disease. This review strives to summarize extant literature on the effects of pain and analgesia on immune system function and inflammation in the context of preclinical in vivo studies. The authors hope this work will help to guide selection of analgesics for preclinical studies of inflammatory disease and immune system function.

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“…As the mechanistic pathway between apathy and dementia is unknown, clarifying the biological correlates of apathy will be important to develop novel treatment targets. A preponderance of studies has established a positive association between proinflammatory cytokines (including C-Reactive Protein (CRP), Interleukin-1 (IL-1), and Interleukin-6 (IL-6)) and depression, of which apathy is an important component [ 7 , 8 , 9 , 10 , 11 , 12 ]. Growing evidence suggests that apathy symptoms may mediate the previously described relationship between depression and cognitive decline [ 13 , 14 ].…”

Section: Introductionmentioning

confidence: 99%

Mediation Analyses of the Role of Apathy on Motoric Cognitive Outcomes

Ceïde

Eguchi

Ayers

et al. 2022

IJERPH

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Recent literature indicates that apathy is associated with poor cognitive and functional outcomes in older adults, including motoric cognitive risk syndrome (MCR), a predementia syndrome. However, the underlying biological pathway is unknown. The objectives of this study were to (1) examine the cross-sectional associations between inflammatory cytokines (Interleukin 6 (IL-6) and C-Reactive Protein (CRP)) and apathy and (2) explore the direct and indirect relationships of apathy and motoric cognitive outcomes as it relates to important cognitive risk factors. N = 347 older adults (≥65 years old) enrolled in the Central Control of Mobility in Aging Study (CCMA). Linear and logic regression models showed that IL-6, but not CRP was significantly associated with apathy adjusted for age, gender, and years of education (β = 0.037, 95% CI: 0.002–0.072, p = 0.04). Apathy was associated with a slower gait velocity (β = −14.45, 95% CI: −24.89–4.01, p = 0.01). Mediation analyses demonstrated that IL-6 modestly mediates the relationship between apathy and gait velocity, while apathy mediated the relationships between dysphoria and multimorbidity and gait velocity. Overall, our findings indicate that apathy may be an early predictor of motoric cognitive decline. Inflammation plays a modest role, but the underlying biology of apathy warrants further investigation.

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Inflammatory mechanisms contribute to microembolism-induced anxiety-like and depressive-like behaviors

Cited by 12 publications

References 69 publications

3,5,6,7,8,3′,4′-Heptamethoxyflavone, a Citrus Flavonoid, Ameliorates Corticosterone-Induced Depression-like Behavior and Restores Brain-Derived Neurotrophic Factor Expression, Neurogenesis, and Neuroplasticity in the Hippocampus

3,5,6,7,8,3′,4′-Heptamethoxyflavone, a Citrus Flavonoid, Ameliorates Corticosterone-Induced Depression-like Behavior and Restores Brain-Derived Neurotrophic Factor Expression, Neurogenesis, and Neuroplasticity in the Hippocampus

A Review of the Effects of Pain and Analgesia on Immune System Function and Inflammation: Relevance for Preclinical Studies

Mediation Analyses of the Role of Apathy on Motoric Cognitive Outcomes

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