The ratio and interaction between neurotrophin and immune signaling during electroconvulsive therapy in late-life depression

Loef, Dore; Vansteelandt, Kristof; Oudega, Mardien L.; Eijndhoven, Philip van; Carlier, Angela; Exel, Eric van; Rhebergen, Didi; Sienaert, Pascal; Vandenbulcke, Mathieu; Bouckaert, Filip; Dols, Annemiek

doi:10.1016/j.bbih.2021.100389

Cited by 7 publications

(5 citation statements)

References 28 publications

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“…Moreover, microglia-derived IL-1β can inhibit the expression of EAAT, reduce the transfer of Glu from the synaptic cleft to astrocytes, and aggravate the hyperexcited stimulation of postsynaptic neurons by Glu. In addition, astrocytes absorb less Glu, transform and generate less Gln, and transport less Gln to glutamatergic neurons, a process that would balance Glu release from glutamatergic neurons to a certain extent 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 TNFα, 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].…”

Section: Bdnf Deficiency and Dysfunctionmentioning

confidence: 84%

“…Given its importance, BDNF will be used as a representative neurotrophic factor to discuss the effects and mechanisms of inflammatory factors on neural activities mediated by neurotrophic factors. 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 ].…”

Section: Neurological Impairments Caused By Immune Imbalancementioning

confidence: 86%

“…In conclusion, a significant decrease in estrogen levels disrupts immune homeostasis, particularly the levels of the immune factors TNF-α, IL-1β, IL-4, IL-6, IL-10 and IL-18 through the ERα/ERβ/GPER-associated NLRP3/NF-κB signaling pathway, which involves many signaling molecules, such as TLR2, TLR4, P2X7R, SIRT1, CREB, MS-KIF18A, PI3K, AKT, Gs, cAMP, PKA, PJA1, Serpina3n, Src, and MMP-9 [ 19 – 24 , 41 , 43 , 44 , 47 – 49 , 52 , 54 – 56 , 58 ]. Subsequently, the increase of inflammatory cytokine levels causes BBB destruction [ 25 , 62 – 74 , 165 ], the dysfunction of neurotransmitters such as 5-HT [ 80 – 85 ], DA [ 86 – 97 ], NE [ 98 – 105 ], GABA [ 29 , 30 , 106 – 113 ] and Glu [ 79 , 114 – 121 ], BDNF deficiency and dysfunction [ 26 , 128 – 135 ], and attenuation of neuroplasticity [ 136 – 146 ], which are key factors in the onset and progression of depression (Fig. 10 ).…”

Section: Discussionmentioning

confidence: 99%

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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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Section: Bdnf Deficiency and Dysfunctionmentioning

confidence: 84%

Section: Neurological Impairments Caused By Immune Imbalancementioning

confidence: 86%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Estrogen-immuno-neuromodulation disorders in menopausal depression

Zhang,

Tan,

Tang

2024

J Neuroinflammation

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“…It is important to note that BDNF has been argued to be regulated by various factors such as stress hormones, monoamines, glutamatergic system, and inflammatory cytokines (Şahin et al ., 2015). The level of BDNF and its relationship with cytokines (including TNF-α) is different in various cognitive disorders and their different stages (Loef et al ., 2021; Yap et al ., 2021). Saha et al .…”

Section: Discussionmentioning

confidence: 99%

Effect of l-Dopa in acute temozolomide-induced cognitive impairment in male mice: a possible antineuroinflammatory role

Salarinejad¹,

Esmaeilpour²,

Shabani³

et al. 2023

Behavioural Pharmacology

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Temozolomide is used commonly in the treatment of some types of cancers, but it may also result in cognitive impairments such as memory deficits. l-Dopa, a well known medicine for the central nervous system, has been shown to have positive effects on some cognitive disorders. Here we sought to investigate the effect of l-Dopa on temozolomide-induced cognitive impairments. BALB/c mice were subjected to 3-days temozolomide and 6-days concomitant l-Dopa/benserazide administration in six groups (control, l-Dopa 25 mg/kg, l-Dopa 75 mg/kg, temozolomide, temozolomide + l-Dopa 25 mg/kg, and temozolomide + l-Dopa 75 mg/kg). Open field test, object location recognition, novel object recognition test, and shuttle-box test were carried out to determine the locomotor, anxiety-like behavior, and memory function of subjects. TNF-α and brain-derived neurotrophic factor (BDNF) gene expression in the hippocampus was measured by real-time PCR. Mice treated with temozolomide showed recognition memory impairment, along with hippocampal TNF-α and BDNF mRNA expression level raise, and detection of histological insults in hematoxylin and eosin hippocampal slides. Mice that received temozolomide + l-Dopa showed normal behavioral function and lower TNF-α and BDNF hippocampal mRNA expression levels, and histologically normal hippocampal CA1 region in comparison with mice in the temozolomide group. Our results provide evidence that l-Dopa prevents temozolomide-induced recognition memory deficit in mice at the acute phase probably via l-Dopa antineuroinflammatory effects.

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“…Given the inverse relationship between cortisol exposition and hippocampal volumes in both animal and human studies [ 29 ], the reduction of inflammatory processes by ECT may also contribute to increased hippocampal volumes after ECT [ 30 ] in addition to more direct neurotrophic effects. There is some evidence from ECT research that inflammatory activity can influence the relationship between BDNF and ECT treatment outcomes [ 31 ]. However, it may be that neuroplastic effects of ECT are necessary but not sufficient for a response.…”

Section: Patient Findingsmentioning

confidence: 99%