68 research outputs found
Microglial activation and chronic neurodegeneration
Microglia, the resident innate immune cells in the brain, have long been implicated in the pathology of neurode-generative diseases. Accumulating evidence points to activated microglia as a chronic source of multiple neurotoxic factors, including tumor necrosis factor-α, nitric oxide, interleukin-1β, and reactive oxygen species (ROS), driving progressive neuron damage. Microglia can become chronically activated by either a single stimulus (e.g., lipopolysaccharide or neuron damage) or multiple stimuli exposures to result in cumulative neuronal loss with time. Although the mechanisms driving these phenomena are just beginning to be understood, reactive microgliosis (the microglial response to neuron damage) and ROS have been implicated as key mechanisms of chronic and neurotoxic microglial activation, particularly in the case of Parkinson’s disease. We review the mechanisms of neurotoxicity associated with chronic microglial activation and discuss the role of neuronal death and microglial ROS driving the chronic and toxic microglial phenotype
Dark cisternal fields: Specialized formations of the endoplasmic reticulum in striatal neurons of a rat
Microhelices in the endoplasmic reticulum of murine neurons infected with a group B arbovirus
Ultrastructural transformations in the idiopathic hemorrhagic-serous otitis (otitis nigra)
Bone Morphogenetic Protein-2,4,6 and Transforming Growth Factor-.BETA.1 Are Induced in Rat Facial Nuclei Following Motoneuron Axotomy.
A further type of intraventricular bulb-like axon endings in the 4th ventricle of the brain (rabbit)
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