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The article offers information related to microglia, its role in the immune system and its inflammatory processes in Alzheimer's disease. It is evident that recent insights about microglia have suggested potential new therapies for the disease, which is the leading cause of dementia worldwide. It also analyzes genetic regions and genes that appear to influence disease risk and genetic trail that leads to Alzheimer's.

• The innovative decellularization method via freeze-thaw cycles and detergent-enzymatic cycles endowed the decellularized brain with extremely few cellular immunogenic components and abundant ECM constituents. • The MSCs-encapsulated decellularized brain ECM (dBECM)-based hydrogel can effectively promote neuron compensation and neural recovery in TBI mice, owing to the capacity to up-regulate the neural-related genes and promote the neural differentiation of MSCs into NSCs and neurons. • The MSCs-encapsulated dBECM-based hydrogel can potentially regulate the neuroinflammation after TBI, since the hydrogel works synergistically with MSCs to stimulate the M1-to-M2 polarization and down-regulate the pro-inflammatory cytokines of microglia. Damaged neurons and harsh microenvironments contribute to the injury cascades following traumatic brain injury (TBI). Mesenchymal stem cell (MSC) therapy is considered a viable choice for brain injury treatment; however, its clinical use is hindered by limited engraftment, low survival ratio, and uncontrolled differentiation. Herein, the decellularized brain extracellular matrix (dBECM) was prepared through a new method as a delivery system for MSCs. dBECM-based hydrogel with favorable biochemical and biomechanical features provides a microenvironment for MSCs in nerve repair. The MSCs-encapsulated dBECM-based hydrogel is shown to improve neuron compensation and structural regeneration, alleviate neuroinflammation, and promote M1-to-M2 polarization of microglia. Our results first demonstrate that the combination of dBECM and MSCs is a critical vehicle to promote TBI repair from neurogenesis and immunoregulation, showing promise for the physiological recovery of neurogenic diseases and injuries. [ABSTRACT FROM AUTHOR]

Researchers from Nanjing Medical University have discovered that ganglion cell-derived LysoPS induces retinal neovascularisation by activating the microglial GPR34-PI3K-AKT-NINJ1 axis. This process plays a crucial role in the pathogenesis of retinopathy, particularly in patients with proliferative diabetic retinopathy. The study highlights the complex interaction between dysfunctional ganglion cells, microglia, and vascular endothelial cells in the development of retinal neovascularisation. By inhibiting the GPR34-PI3K-AKT-NINJ1 axis, researchers were able to decrease microglial extracellular trap formation and neovascularisation, shedding light on potential therapeutic targets for this condition. [Extracted from the article]

The article discusses the impact of excessive alcohol use on the brain, particularly in corticolimbic regions like the hippocampus and rhinal cortices, leading to cognitive issues. It explores the role of microglia, brain-resident immune cells, in alcohol-induced neurodegeneration in male rats. By depleting microglia using a CSF1R inhibitor, researchers found a reduction in alcohol-induced neuronal death, highlighting the potential for therapeutic interventions to mitigate alcohol-related damage. This study emphasizes the importance of understanding alcohol-microglia interactions for developing treatments that can protect against neurotoxic effects. [Extracted from the article]

A recent study from Southwest University in China explored the therapeutic effects of a combination of four herbal components - catalpol, puerarin, gastrodin, and borneol - on Alzheimer's disease. The study found that this combination modulated the Tlr4/Myd88/NF-kB signaling pathway, leading to reduced inflammation in microglia and improved cognitive function in AD models. These findings suggest that traditional Chinese medicines may offer new insights for treating Alzheimer's disease. [Extracted from the article]

Researchers from the University of Alabama at Birmingham have conducted a study on Parkinson's disease, focusing on the role of disease-associated microglia (DAM) in neurodegenerative diseases. The study highlights the unique characteristics of DAM in Alzheimer's Disease and raises questions about their role in other neurodegenerative conditions like Parkinson's disease. The researchers suggest using a multi-omics model to further investigate the triggers and functions of DAM in Parkinson's disease. This study provides valuable insights into the potential heterogeneity of DAM across different neurodegenerative pathologies. [Extracted from the article]

Researchers at Rutgers - State University of New Jersey have investigated the role of microglial exosomes in ethanol-induced neuronal death of stress-regulatory proopiomelanocortin neurons in the developing hypothalamus. The study found that ethanol exposure during development increases levels of MCP1 in microglial exosomes, leading to apoptosis of b-endorphin neurons and subsequent hormonal and behavioral stress responses. The research suggests that targeting MCP1/CCR2 signaling may help mitigate the effects of alcohol exposure on neuronal health and stress regulation. [Extracted from the article]

Researchers at the Achucarro Basque Center for Neuroscience in Spain conducted a study on the effects of Extreme Low Frequency Electromagnetic Stimulation (ELF-EMS) on neuronal and microglial cells under oxygen-glucose deprivation conditions, simulating ischemic stroke. The study found that ELF-EMS reduced neuronal cell death and ischemic-induced calcium overload, as well as modulated microglia activation and cell death. The researchers suggest that ELF-EMS may have potential therapeutic benefits in limiting irreversible damage in ischemic stroke, calling for further preclinical validations. The study was published in Frontiers in Cellular Neuroscience and can be accessed for free online. [Extracted from the article]

Researchers at McGill University conducted a study on experimental autoimmune encephalomyelitis (EAE) and its relation to senescence in microglia. The research found that senolytic treatment, specifically using a BCL2-family inhibitor called Navitoclax (ABT-263), reduced the presence of microglia and macrophages in the EAE spinal cord, leading to improvements in disease severity. This study suggests that targeting senescent microglia and macrophages could be a novel strategy to address disease progression in multiple sclerosis. The findings were published in the Journal of Neuroinflammation. [Extracted from the article]

A study by scientists at Gladstone Institutes found that in the presence of the APOE4 protein, the most important genetic risk factor for Alzheimer's disease, immune cells called microglia cause harmful inflammation and clumps of misfolded proteins in the brain. The researchers created a new research model involving transplanting human neurons producing APOE4 into the brains of mice, which led to increased deposits of amyloid and tau proteins. The study suggests that drugs reducing microglia may be useful in treating Alzheimer's disease, especially in individuals with the APOE4 gene. [Extracted from the article]

The article discusses the effects of constitutive expression of CX3CR1-BAC-Cre on microglia in mice, comparing it to the inducible model. The study found subtle region- and sex-specific changes in microglial density, volume, and morphology during development, which normalized by adulthood in most brain regions except the hippocampus. No behavioral effects were observed, suggesting that the constitutive-Cre model may be less detrimental than the inducible model, emphasizing the importance of proper controls in research. [Extracted from the article]

A recent study conducted at University Hospital explored the role of microglia in chronic kidney disease (CKD) and its impact on cognitive impairment. The researchers found that IL-1b maturation in microglia is independent of the NLRP3-caspase-1 interaction in CKD, instead involving a noncanonical pathway mediated by cathepsin C and caspase-8. This discovery suggests a potential therapeutic target to address microglia-induced neuronal dysfunction in CKD and potentially other peripheral diseases. The study was published in Nephrology Dialysis Transplantation by researchers including Silke Zimmermann and Berend Isermann. [Extracted from the article]

Researchers at Duke University have conducted a study on polio virotherapy targeting malignant gliomas, a type of brain tumor. The study found that treatment with the poliovirus chimera PVSRIPO led to long-term survival and tumor regression in patients with recurrent glioblastoma. The research suggests that glioma-associated macrophages and microglia play a significant role in the antitumor effects of PVSRIPO. This study has been peer-reviewed and published in Neuro-Oncology. [Extracted from the article]