Sleep deprivation aggravates lipopolysaccharide-induced anxiety, depression and cognitive impairment: The role of pro-inflammatory cytokines and synaptic plasticity-associated proteins

Zhang, Yue-Ming; Wei, Ru-Meng; Feng, Yi-Zhou; Zhang, Kai-Xuan; Ge, Yi-Jun; Kong, Xiao-Yi; Li, Xue-Yan; Chen, Gui-Hai

doi:10.1016/j.jneuroim.2023.578252

Cited by 7 publications

(1 citation statement)

References 60 publications

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“…Blood samples and depression scale scores from elderly patients with depression show that the levels of TNF-α and BDNF are negatively correlated, and the ratio of TNF-α to BDNF is consistent with the Montgomery-Asberg Depression Rating Scale (MADRS) [ 128 ]. Other studies have confirmed that TNF-α, IL-1β and IL-6 reduce the expression of BDNF in the brain [ 129 , 130 ], which further attenuates the activation of PI3K/Akt and MAPK P38, downstream signaling molecules of TrkB (transmembrane receptor of BDNF on neurons), leading to structural damage and dysfunction of neurons [ 26 , 131 , 132 ]. These results suggest that inflammatory cytokines can induce BDNF deficiency and dysfunction.…”

Section: Neurological Impairments Caused By Immune Imbalancementioning

confidence: 97%

Estrogen-immuno-neuromodulation disorders in menopausal depression

Zhang,

Tan,

Tang

2024

J Neuroinflammation

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A significant decrease in estrogen levels puts menopausal women at high risk for major depression, which remains difficult to cure despite its relatively clear etiology. With the discovery of abnormally elevated inflammation in menopausal depressed women, immune imbalance has become a novel focus in the study of menopausal depression. In this paper, we examined the characteristics and possible mechanisms of immune imbalance caused by decreased estrogen levels during menopause and found that estrogen deficiency disrupted immune homeostasis, especially the levels of inflammatory cytokines through the ERα/ERβ/GPER-associated NLRP3/NF-κB signaling pathways. We also analyzed the destruction of the blood-brain barrier, dysfunction of neurotransmitters, blockade of BDNF synthesis, and attenuation of neuroplasticity caused by inflammatory cytokine activity, and investigated estrogen-immuno-neuromodulation disorders in menopausal depression. Current research suggests that drugs targeting inflammatory cytokines and NLRP3/NF-κB signaling molecules are promising for restoring homeostasis of the estrogen-immuno-neuromodulation system and may play a positive role in the intervention and treatment of menopausal depression.

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