scholarly journals Associations of immunometabolic risk factors with symptoms of depression and anxiety: The role of cardiac vagal activity

2018 ◽  
Vol 73 ◽  
pp. 493-503 ◽  
Author(s):  
Mandy X. Hu ◽  
Brenda W.J.H. Penninx ◽  
Eco J.C. de Geus ◽  
Femke Lamers ◽  
Dora C.-H. Kuan ◽  
...  
2020 ◽  
Vol 8 (4) ◽  
pp. 641-656
Author(s):  
Meghan Vinograd ◽  
Alexander Williams ◽  
Michael Sun ◽  
Lyuba Bobova ◽  
Kate B. Wolitzky-Taylor ◽  
...  

Neuroticism has been associated with depression and anxiety both cross-sectionally and longitudinally. Interpretive bias has been associated with depression and anxiety, primarily in cross-sectional and bias induction studies. The purpose of the current study was to examine the role of interpretive bias as a prospective risk factor and a mediator of the relation between neuroticism and depressive and anxious symptoms in young adults assessed longitudinally. Neuroticism significantly predicted a broad general-distress dimension but not intermediate fears and anhedonia-apprehension dimensions or a narrow social-fears dimension. Neuroticism also significantly predicted negative interpretive bias for social scenarios. Negative interpretive bias for social scenarios did not significantly predict dimension scores, nor did it mediate the relation between neuroticism and general distress or social fears. These results suggest that although neuroticism relates to negative interpretive bias, its risk for symptoms of depression and anxiety is at most weakly conferred through negative interpretive bias.


Author(s):  
Stefan Kindler ◽  
Marike Bredow-Zeden

Temporomandibular joint disorder (TMD) is a painful functional disorder of the temporomandibular joint, masticatory muscles, and associated musculoskeletal structures of the head and neck. TMD is a type of chronic pain and is widely used as a model for chronic pain. The etiology of TMD pain is multifactorial. Biological, behavioral, environmental, social, emotional, and cognitive factors can contribute to TMD. TMD can manifest with musculoskeletal facial pain complaints and with different forms of jaw dysfunction. Biobehavioral studies suggest an association between TMD pain and coexisting psychopathology, including depression and anxiety. This chapter presents practical clinical recommendations on how to treat patients with symptoms of depression, anxiety, and TMD pain. The authors underline the importance of considering depression and anxiety as risk factors for TMD.


2016 ◽  
Vol 97 (6) ◽  
pp. 919-928 ◽  
Author(s):  
Joyce A. Kootker ◽  
Maria L. van Mierlo ◽  
Jan C. Hendriks ◽  
Judith Sparidans ◽  
Sascha M. Rasquin ◽  
...  

2019 ◽  
Vol 48 (Supplement_1) ◽  
pp. i31-i31
Author(s):  
E V Backhouse ◽  
S D Shenkin ◽  
A McIntosh ◽  
I Deary ◽  
H Whalley ◽  
...  

2020 ◽  
Vol 11 ◽  
Author(s):  
Hinke M. Endedijk ◽  
Stefanie A. Nelemans ◽  
Remmelt R. Schür ◽  
Marco P. M. Boks ◽  
Pol van Lier ◽  
...  

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S95-S95
Author(s):  
Tal Frolinger ◽  
Umar Iqbal ◽  
Giulio M Pasinetti

Abstract This study investigates the role of microglia activity in stress-induced depression and anxiety and the mechanisms associated with the role of certain microbiome derived anti-inflammatory polyphenols in attenuating stress-induced microglia immune priming and symptoms of depression. We implemented a chronic unpredictable stress (CUS) paradigm to exhibit priming of microglia innate immunity in the context of the onset of depression and anxiety phenotypes. Mechanistic studies related to prophylactic treatment using dietary microbiome derived polyphenols were also investigated in this model. Depression and anxiety phenotypes, gene expression in microglia and protein expression in the cortex of mice were measured following a primary exposure to short-term unpredictable stress (US) followed by CUS. We examined the long-term, persistent CUS induced changes at 4-weeks of post-stress rest following a secondary US exposure. We found depression phenotypes resulted from US only following exposure to CUS. This was accompanied by an increase and persistent upregulation of toll-like receptor 4 (TLR4), RAGE, and HMGB1 gene expression in isolated cortical microglia. Priming by CUS also amplified gene expression of IL-1β in microglia and protein IL-1β in the cerebral cortex following US re-exposure. Increased activity of NF-kB was also noted in the period following CUS. Furthermore, polyphenol treatment prevented stress-induced phenotypes, upregulation of HMGB1, IL-1B, and TLR4 gene expression, as well as upregulation of IL-1β and NF-kB. The study suggests that latent activity of the TLR4-NFkB-IL1β pathway contributes to immune priming and increases susceptibility to depression-like behaviors. Anti-depressant effects of polyphenols may result from their ability to attenuate microglia priming.


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