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Adult neurogenesis in the iNature hippocampal dentate gyrus is regulated by a specific microglia cell population and is functionally involved in the behavioral response to stress.
However, the role of microglia in hippocampal neurogenesis and stress resilience remains unclear.
On March 17, 2021, University of Electronic Science and Technology of China You Zili and Chen Huafu jointly published a research paper entitled "IL4-driven microglia modulate stress resilience through BDNF-dependent neurogenesis" in Science Advances.
The study found that interleukin 4 (IL4 ) Driven microglia are characterized by high expression of Arg1, which is essential for maintaining hippocampal neurogenesis and stress resistance.
By knocking down the microglia IL4R, reducing the Arg1 + microglia in the hippocampus can inhibit hippocampal neurogenesis and enhance the susceptibility to stress.
By enhancing the IL4 signaling pathway, increasing Arg1 + microglia in the hippocampus restores hippocampal neurogenesis and the ability to adapt to stress-induced depression.
It was found that brain-derived neurotrophic factor (BDNF) is necessary for the neurogenesis of IL4-driven microglia.
In summary, the results of this study indicate that IL4-driven microglia in the hippocampus triggers BDNF-dependent neurogenesis, which responds to chronic stress and helps prevent depression-like symptoms.
These findings confirm the regulation of specific microglia phenotypes as a treatment strategy for mood disorders.
In addition, on March 12, 2021, Liao Wei and Chen Huafu of the University of Electronic Science and Technology of China published a research paper entitled "Cortical structural differences in major depressive disorder correlate with cell type-specific transcriptional signatures" in Nature Communications.
Neuroimaging data and publicly available transcriptome data from two independent cohorts investigated the relationship between whole brain gene expression and morphological changes in MDD patients.
Morphological similarity network (MSN) analysis showed that compared with the control group, individuals with MDD can replicate differences in cortical structure.
Using human brain gene expression data, the study observed that the expression of MDD-related genes is spatially correlated with MSN differences.
Analysis of cell type-specific characteristic genes showed that microglia and neuron-specific transcriptional changes are most of the observations related to MDD-specific MSN differences.
In general, the findings of this study will link the molecular and structural changes associated with MDD (click to read).
As we all know, prolonged stress can cause a chain reaction in the inflammatory system and lead to neuropsychiatric diseases, such as depression and anxiety, which can affect neurogenesis.
In adulthood, new neurons are produced in two areas of the brain (the dentate gyrus (DG) of the hippocampus and the subventricular area).
Neural stem/progenitor cells (NSPC) undergo proliferation, differentiation, survival and maturation, form new neurons, and finally integrate into the neural network.
These processes are negatively affected by the stress experience, and treatment with antidepressants by altering the neurogenic microenvironment has a positive effect.
These adult-born neurons are essential for emotional control and behavioral output.
The change in the amplitude of the continuous production of new neurons is related to the pathophysiology of depression and the efficacy of antidepressants.
Microglia are the main immune cells in the brain and play a central role in immune surveillance and maintaining brain homeostasis.
Studies have shown that microglia can regulate neurogenesis by secreting various factors that regulate the neurogenic microenvironment.
Under stress or pathological conditions, microglia secrete inflammatory mediators, destroy neuronal functions and impair neurogenesis, increase vulnerability to stress and promote the occurrence and development of depression.
The role of microglia in neurogenesis depends on the balance of soluble factors released by microglia under different activation conditions.
Microglial cell-derived neurotrophic factor (BDNF) is an important mediator of communication between microglia and neurons, and promotes many aspects of brain function through its high-affinity receptor tropomyosin-related kinase B (TrkB).
Microglia BDNF may also be involved in neurobehavioral plasticity and neurogenesis, so it may be the pathophysiological basis of depression.
Interleukin 4 (IL4) is a multifunctional cytokine expressed in the brain and is involved in the regulation of inflammation and physiological processes in the central nervous system (CNS).
Lack of IL4 can weaken the flexibility to resist depression caused by stress, and increasing the level of IL4 can alleviate depression-like behaviors.
Studies have shown that IL4 can reprogram microglia to the Arg1+ phenotype to maintain brain homeostasis, neuroprotection and tissue repair.
However, little is known about the effects of IL4-induced Arg1 + microglia on neurogenesis and stress elasticity.
In view of the role of microglia in the pathogenesis of depression, it is hypothesized that promoting the neuroprotective phenotype of microglia will improve stress response and depressive behavior.
In line with this expectation, the study found that in mice exposed to chronic mild stress (CMS), overexpression of hippocampal IL4 promoted Arg1 + microglia to promote neurogenesis, thereby attenuating depression-like behavior.
Reference message: https://advances.
sciencemag.
org/content/7/12/eabb9888
However, the role of microglia in hippocampal neurogenesis and stress resilience remains unclear.
On March 17, 2021, University of Electronic Science and Technology of China You Zili and Chen Huafu jointly published a research paper entitled "IL4-driven microglia modulate stress resilience through BDNF-dependent neurogenesis" in Science Advances.
The study found that interleukin 4 (IL4 ) Driven microglia are characterized by high expression of Arg1, which is essential for maintaining hippocampal neurogenesis and stress resistance.
By knocking down the microglia IL4R, reducing the Arg1 + microglia in the hippocampus can inhibit hippocampal neurogenesis and enhance the susceptibility to stress.
By enhancing the IL4 signaling pathway, increasing Arg1 + microglia in the hippocampus restores hippocampal neurogenesis and the ability to adapt to stress-induced depression.
It was found that brain-derived neurotrophic factor (BDNF) is necessary for the neurogenesis of IL4-driven microglia.
In summary, the results of this study indicate that IL4-driven microglia in the hippocampus triggers BDNF-dependent neurogenesis, which responds to chronic stress and helps prevent depression-like symptoms.
These findings confirm the regulation of specific microglia phenotypes as a treatment strategy for mood disorders.
In addition, on March 12, 2021, Liao Wei and Chen Huafu of the University of Electronic Science and Technology of China published a research paper entitled "Cortical structural differences in major depressive disorder correlate with cell type-specific transcriptional signatures" in Nature Communications.
Neuroimaging data and publicly available transcriptome data from two independent cohorts investigated the relationship between whole brain gene expression and morphological changes in MDD patients.
Morphological similarity network (MSN) analysis showed that compared with the control group, individuals with MDD can replicate differences in cortical structure.
Using human brain gene expression data, the study observed that the expression of MDD-related genes is spatially correlated with MSN differences.
Analysis of cell type-specific characteristic genes showed that microglia and neuron-specific transcriptional changes are most of the observations related to MDD-specific MSN differences.
In general, the findings of this study will link the molecular and structural changes associated with MDD (click to read).
As we all know, prolonged stress can cause a chain reaction in the inflammatory system and lead to neuropsychiatric diseases, such as depression and anxiety, which can affect neurogenesis.
In adulthood, new neurons are produced in two areas of the brain (the dentate gyrus (DG) of the hippocampus and the subventricular area).
Neural stem/progenitor cells (NSPC) undergo proliferation, differentiation, survival and maturation, form new neurons, and finally integrate into the neural network.
These processes are negatively affected by the stress experience, and treatment with antidepressants by altering the neurogenic microenvironment has a positive effect.
These adult-born neurons are essential for emotional control and behavioral output.
The change in the amplitude of the continuous production of new neurons is related to the pathophysiology of depression and the efficacy of antidepressants.
Microglia are the main immune cells in the brain and play a central role in immune surveillance and maintaining brain homeostasis.
Studies have shown that microglia can regulate neurogenesis by secreting various factors that regulate the neurogenic microenvironment.
Under stress or pathological conditions, microglia secrete inflammatory mediators, destroy neuronal functions and impair neurogenesis, increase vulnerability to stress and promote the occurrence and development of depression.
The role of microglia in neurogenesis depends on the balance of soluble factors released by microglia under different activation conditions.
Microglial cell-derived neurotrophic factor (BDNF) is an important mediator of communication between microglia and neurons, and promotes many aspects of brain function through its high-affinity receptor tropomyosin-related kinase B (TrkB).
Microglia BDNF may also be involved in neurobehavioral plasticity and neurogenesis, so it may be the pathophysiological basis of depression.
Interleukin 4 (IL4) is a multifunctional cytokine expressed in the brain and is involved in the regulation of inflammation and physiological processes in the central nervous system (CNS).
Lack of IL4 can weaken the flexibility to resist depression caused by stress, and increasing the level of IL4 can alleviate depression-like behaviors.
Studies have shown that IL4 can reprogram microglia to the Arg1+ phenotype to maintain brain homeostasis, neuroprotection and tissue repair.
However, little is known about the effects of IL4-induced Arg1 + microglia on neurogenesis and stress elasticity.
In view of the role of microglia in the pathogenesis of depression, it is hypothesized that promoting the neuroprotective phenotype of microglia will improve stress response and depressive behavior.
In line with this expectation, the study found that in mice exposed to chronic mild stress (CMS), overexpression of hippocampal IL4 promoted Arg1 + microglia to promote neurogenesis, thereby attenuating depression-like behavior.
Reference message: https://advances.
sciencemag.
org/content/7/12/eabb9888
