The proper removal of superfluous neurons through apoptosis and subsequent phagocytosis is essential for normal development of the central nervous system (CNS). During Drosophila embryogenesis, a large number of apoptotic neurons are efficiently engulfed and degraded by phagocytic glia. Here we demonstrate that glial proficiency to phagocytose relies on expression of phagocytic receptors for apoptotic cells, SIMU and DRPR. Moreover, we reveal that the phagocytic ability of embryonic glia is established as part of a developmental program responsible for glial cell fate determination and is not triggered by apoptosis per se. Explicitly, we provide evidence for a critical role of the major regulators of glial identity, gcm and repo, in controlling glial phagocytic function through regulation of SIMU and DRPR specific expression. Taken together, our study uncovers molecular mechanisms essential for establishment of embryonic glia as primary phagocytes during CNS development.
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http://dx.doi.org/10.1016/j.ydbio.2014.07.005 | DOI Listing |
J Neurosci
December 2024
Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis IN, USA
Anti-Aβ immunotherapy use to treat Alzheimer's disease is on the rise. While anti-Aβ antibodies provide hope in targeting Aβ plaques in the brain there still remains a lack of understanding regarding the cellular responses to these antibodies in the brain. In this study we sought to identify acute effects of anti-Aβ antibody on immune responses.
View Article and Find Full Text PDFBrain Behav
January 2025
INEUROPA, Instituto de Neurociencias del Principado de Asturias, Oviedo, Spain.
Purpose: Metabolic dysfunction-associated steatohepatitis (MASH) is a prevalent disease caused by high fat and high cholesterol intake, which leads to systemic deterioration. The aim of this research is to conduct a psychobiological exploration of MASH in adult male rats.
Methods: Subjects who were administered a high-fat and high-cholesterol diet for 14 weeks.
Chemosphere
December 2024
Systems Toxicology Group, Food, Drug & Chemical, Environment and Systems Toxicology Division, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), Vishvigyan Bhawan, 31, Mahatma Gandhi Marg, Lucknow-226001, Uttar Pradesh, India; Academy of Scientific and Innovative Research (AcSIR), Ghaziabad, 201002, India. Electronic address:
The review aims to examine the neurotoxic effects of arsenic, particularly exploring the roles of glial cells-astrocytes, microglia, and oligodendrocytes, amid its widespread environmental contamination and impact on cognitive impairments. It highlights the role of altered neurotrophin and growth factor signaling in disrupting neuronal health and cognitive performance. It elucidates the intricate interactions between oxidative stress, DNA damage, neurotransmitter disruption, and cellular signaling alterations, underscoring the vital importance of the glial cells.
View Article and Find Full Text PDFPLoS One
December 2024
Department of Environmental and Radiological Health Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado, United States of America.
Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb) infection, is a chronic inflammatory disease. Although typically associated with inflammation of the lungs and other peripheral tissues, increasing evidence has uncovered neurological consequences attributable to Mtb infection. These include deficits in memory and cognition, increased risk for neurodegenerative disease, and progressive neuropathology.
View Article and Find Full Text PDFJ Mol Histol
December 2024
Department of Neurosurgery, Quzhou People's Hospital, No. 100, Minjiang Avenue, High-speed Rail, New City, Quzhou, Zhejiang, China.
Traumatic brain injury (TBI) is a common neurosurgical emergency. As a macrophage in brain, microglia involves in secondary TBI injury. UCF-101, an Omi/HtrA2 inhibitor, protects against neurological disorders.
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