Microglia-mediated neurotoxicity: uncovering the molecular mechanisms
Top Cited Papers
- 1 January 2007
- journal article
- review article
- Published by Springer Nature in Nature Reviews Neuroscience
- Vol. 8 (1) , 57-69
- https://doi.org/10.1038/nrn2038
Abstract
Mounting evidence indicates that microglial activation contributes to neuronal damage in neurodegenerative diseases. Recent studies show that in response to certain environmental toxins and endogenous proteins, microglia can enter an overactivated state and release reactive oxygen species (ROS) that cause neurotoxicity. Pattern recognition receptors expressed on the microglial surface seem to be one of the primary, common pathways by which diverse toxin signals are transduced into ROS production. Overactivated microglia can be detected using imaging techniques and therefore this knowledge offers an opportunity not only for early diagnosis but, importantly, for the development of targeted anti-inflammatory therapies that might slow or halt the progression of neurodegenerative disease.Keywords
This publication has 225 references indexed in Scilit:
- Microglia, major player in the brain inflammation: their roles in the pathogenesis of Parkinson's diseaseExperimental & Molecular Medicine, 2006
- Pathogen Recognition and Innate ImmunityCell, 2006
- Cannabinoids in Microglia: A New Trick for Immune Surveillance and NeuroprotectionNeuron, 2006
- Retrograde dopaminergic neuron degeneration following intrastriatal proteasome inhibitionNeuroscience Letters, 2005
- Iron, brain ageing and neurodegenerative disordersNature Reviews Neuroscience, 2004
- Systemic exposure to proteasome inhibitors causes a progressive model of Parkinson's diseaseAnnals of Neurology, 2004
- Inflammatory processes in amyotrophic lateral sclerosisMuscle & Nerve, 2002
- Activation of NADPH Oxidase in Alzheimer's Disease BrainsBiochemical and Biophysical Research Communications, 2000
- RAGE and amyloid-β peptide neurotoxicity in Alzheimer's diseaseNature, 1996
- Neuroglial cells in the cerebral cortex of rats from young adulthood to old age: An electron microscope studyJournal of Neurocytology, 1974