Neuroinflammation, memory, and depression: new approaches to hippocampal neurogenesis

Wu, Anbiao; Zhang, Jiyan

doi:10.1186/s12974-023-02964-x

Cited by 39 publications

(4 citation statements)

References 274 publications

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“…It is postulated that damage produced by over-expression of cytokines dysregulates neuroplasticity by disrupting BDNF and leads to a variety of neurological and/or neuropsychiatric conditions including MDD [265]. This hypothesis was verified recently by the findings that neuroinflammation leads to dysregulated neurogenesis, particularly in the DG of the hippocampus [266].…”

Section: Microbiota-neurotrophic Factors-neuroinflammationmentioning

confidence: 95%

Role of Glial Cells in Neuronal Function, Mood Disorders, and Drug Addiction

Tizabi,

Getachew,

Hauser

et al. 2024

Brain Sciences

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Mood disorders and substance use disorder (SUD) are of immense medical and social concern. Although significant progress on neuronal involvement in mood and reward circuitries has been achieved, it is only relatively recently that the role of glia in these disorders has attracted attention. Detailed understanding of the glial functions in these devastating diseases could offer novel interventions. Here, following a brief review of circuitries involved in mood regulation and reward perception, the specific contributions of neurotrophic factors, neuroinflammation, and gut microbiota to these diseases are highlighted. In this context, the role of specific glial cells (e.g., microglia, astroglia, oligodendrocytes, and synantocytes) on phenotypic manifestation of mood disorders or SUD are emphasized. In addition, use of this knowledge in the potential development of novel therapeutics is touched upon.

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Section: Microbiota-neurotrophic Factors-neuroinflammationmentioning

confidence: 95%

Role of Glial Cells in Neuronal Function, Mood Disorders, and Drug Addiction

Tizabi,

Getachew,

Hauser

et al. 2024

Brain Sciences

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show abstract

“…It is postulated that damage produced by over-expression of the cytokines, dysregulates neuroplasticity by disrupting BDNF and leads to a variety of neurological and/or neuropsychiatric conditions including MDD [227]. This hypothesis was verified recently by the findings that neuroinflammation leads to dysregulated neurogenesis, particularly in the DG of the hippocampus [228].…”

Section: Microbiota-neurotrophic Factors-neuroinflammationmentioning

confidence: 96%

Role of Glial Cells in Depression and Drug Addiction

Tizabi,

Getachew,

Hauser

et al. 2024

Preprint

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Major depressive disorder (MDD) and substance use disorder (SUD) are of immense medical and social concerns. Although significant progress on neuronal involvement in mood and reward circuitries has been achieved, only relatively recently the role of glia in these disorders have attracted attention. Detail understanding of the glial function in these devastating diseases could offer novel interventions. Here, following a brief review of circuitries involved in mood regulation and reward perception, specific contribution of the neurotrophic factors, neuroinflammation and gut microbiota to these diseases are highlighted. In this context, the role of specific glial cells (e.g., microglia, astroglia, oligodendrocytes and synantocytes) on phenotypic manifestation of MDD or SUD are emphasized. In addition, potential use of this knowledge in developing novel therapeutics is touched upon.

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“…Recently, significantly abnormal proportions of T-cell subsets, activation of microglia, and elevated levels of inflammatory cytokines in the central nervous system and peripheral blood were detected during the onset of menopausal depression [ 15 – 17 ], and these immune disorders increase the activity of the estrogen-immuno-neuromodulation system, which may be the key to resolving neuronal dysfunction in menopausal depression. However, due to the involvement of multiple ERs [ 18 – 21 ], immune responses and regulatory factors [ 19 – 27 ] and nerve signaling molecules [ 26 – 30 ], the disturbance of signaling pathways in this complex system remains unclear and has not been comprehensively reviewed in menopausal depression.…”

Section: Introductionmentioning

confidence: 99%

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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Neuroinflammation, memory, and depression: new approaches to hippocampal neurogenesis

Cited by 39 publications

References 274 publications

Role of Glial Cells in Neuronal Function, Mood Disorders, and Drug Addiction

Role of Glial Cells in Neuronal Function, Mood Disorders, and Drug Addiction

Role of Glial Cells in Depression and Drug Addiction

Estrogen-immuno-neuromodulation disorders in menopausal depression

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