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| http://dx.doi.org/10.1016/j.psyneuen.2021.105359 | DOI Listing |
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Modulating intestinal neuroimmune VIPergic signaling attenuates the reduction in ILC3-derived IL-22 and hepatic steatosis in MASLD.
Hepatol Commun
November 2024
Department of Cell Biology, New York University School of Medicine, New York, New York, USA.
Article Synopsis
- MASLD (formerly NAFLD) is a significant cause of liver disease and there are limited treatment options available to prevent liver fat accumulation.
- Research indicates that vasoactive intestinal peptide-producing neurons (VIP-neurons) impact fat absorption and IL-22 production, which may help protect the liver.
- In experiments on mice, decreased communication between VIP-neurons and type 3 innate lymphoid cells (ILC3) led to increased IL-22 production and reduced liver fat, suggesting this neuroimmune pathway could be a promising target for new therapies.
Preferential clustering of microglia and astrocytes around neuritic plaques during progression of Alzheimer's disease neuropathological changes.
J Neurochem
January 2025
Center for Translational Research in Neurodegenerative Disease, College of Medicine, University of Florida, Gainesville, Florida, USA.
Neuroinflammation plays an important role in the pathological cascade of Alzheimer's disease (AD) along with aggregation of extracellular amyloid-β (Aβ) plaques and intracellular aggregates of tau protein. In animal models of amyloidosis, local immune activation is centered around Aβ plaques, which are usually of uniform morphology, dependent on the transgenic model used. In postmortem human brains a diversity of Aβ plaque morphologies is seen including diffuse plaques (non-neuritic plaques, non-NP), dense-core plaques, cotton-wool plaques, and NP.
View Article and Find Full Text PDFPharmacological depletion of microglia protects against alcohol-induced corticolimbic neurodegeneration during intoxication in male rats.
bioRxiv
November 2024
The University of Texas at Austin, College of Pharmacy, Division of Pharmacology & Toxicology, Austin, TX USA.
Excessive alcohol use damages the brain, especially corticolimbic regions such as the hippocampus and rhinal cortices, leading to learning and memory problems. While neuroimmune reactivity is hypothesized to underly alcohol-induced damage, direct evidence of the causative role of microglia, brain-resident immune cells, in this process is lacking. Here, we depleted microglia using PLX5622 (PLX), a CSF1R inhibitor commonly used in mice, but rarely in rats, and assessed cell death following binge-like alcohol exposure in male rats.
View Article and Find Full Text PDFNeuroinflammation in Post COVID-19 Sequelae: Neuroinvasion and Neuroimmune Crosstalk.
Rev Med Virol
November 2024
Department of Infectious Diseases and Microbiology, School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in December 2019 triggered a swift global spread, leading to a devastating pandemic. Alarmingly, approximately one in four individuals diagnosed with coronavirus disease 2019 (COVID-19) experience varying degrees of cognitive impairment, raising concerns about a potential increase in neurological sequelae cases. Neuroinflammation seems to be the key pathophysiological hallmark linking mild respiratory COVID-19 to cognitive impairment, fatigue, and neurological sequelae in COVID-19 patients, highlighting the interaction between the nervous and immune systems following SARS-CoV-2 infection.
View Article and Find Full Text PDFPsilocin, the Psychoactive Metabolite of Psilocybin, Modulates Select Neuroimmune Functions of Microglial Cells in a 5-HT Receptor-Dependent Manner.
Molecules
October 2024
Laboratory of Cellular and Molecular Pharmacology, Department of Biology, University of British Columbia Okanagan Campus, Kelowna, BC V1V 1V7, Canada.
Neuroinflammation that is caused by microglia, the main immune cells of the brain, contributes to neurodegenerative diseases. Psychedelics, including psilocybin and lysergic acid diethylamide (LSD), possess certain anti-inflammatory properties and, therefore, should be considered as drug candidates for treating neuroinflammatory pathologies. When ingested, psilocybin is rapidly dephosphorylated to yield psilocin, which crosses the blood-brain barrier and exerts psychotropic activity by interacting with the 5-hydroxytryptamine 2A receptors (5-HTRs) on neurons.
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