Systemic LPS causes chronic neuroinflammation and progressive neurodegeneration
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Summary
It is demonstrated that through TNFα, peripheral inflammation in adult animals can activate brain microglia to produce chronically elevated pro‐inflammatory factors and induce delayed and progressive loss of DA neurons in the SN, providing valuable insight into the potential pathogenesis and self‐propelling nature of Parkinson's disease.
- Type
- article
- Published
- 2007-04-01
- Cited by
- 2,156
- References
- 48
- Access
- Open access
- OpenAlex
- https://openalex.org/W2055750901
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:40951364
Keywords
Neuroinflammation, Microglia, Tumor necrosis factor alpha, Neurodegeneration, Inflammation
References
- Corticotropin-releasing factor-producing neurons in the rat activated by interleukin-1.
- Exacerbation of Motor Neuron Disease by Chronic Stimulation of Innate Immunity in a Mouse Model of Amyotrophic Lateral Sclerosis
- Prenatal exposure to the bacteriotoxin lipopolysaccharide leads to long-term losses of dopamine neurons in offspring: a potential, new model of Parkinson's disease.
- Microglial activation‐mediated delayed and progressive degeneration of rat nigral dopaminergic neurons: relevance to Parkinson's disease
- Cytokine production by human fetal microglia and astrocytes. Differential induction by lipopolysaccharide and IL-1 beta.
- Effects of circulating tumor necrosis factor on the neuronal activity and expression of the genes encoding the tumor necrosis factor receptors (p55 and p75) in the rat brain: a view from the blood-brain barrier.
- Inflammation, the complement system and the diseases of aging.
- Interactions between tumor necrosis factor-alpha, hypothalamic corticotropin-releasing hormone, and adrenocorticotropin secretion in the rat.
- Neuroprotective properties of the innate immune system and bone marrow stem cells in Alzheimer's disease
- Innate immunity: the missing link in neuroprotection and neurodegeneration?
- Heterogeneity in the distribution and morphology of microglia in the normal adult mouse brain.
- Presence of reactive microglia in monkey substantia nigra years after 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine administration
- Interleukin-1 stimulates the secretion of hypothalamic corticotropin-releasing factor.
- Rotenone potentiates dopamine neuron loss in animals exposed to lipopolysaccharide prenatally.
- Microglia provide neuroprotection after ischemia
- NADPH Oxidase Mediates Lipopolysaccharide-induced Neurotoxicity and Proinflammatory Gene Expression in Activated Microglia*
- Role of Nitric Oxide in Inflammation‐Mediated Neurodegeneration
- Evidence of active nerve cell degeneration in the substantia nigra of humans years after 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine exposure
- Progressive dopamine neuron loss following supra-nigral lipopolysaccharide (LPS) infusion into rats exposed to LPS prenatally.
- Reciprocal Interactions Between Microglia and Neurons: From Survival to Neuropathology
Cited by
- Persistent activation of microglia is associated with neuronal dysfunction of callosal projecting pathways and multiple sclerosis-like lesions in relapsing--remitting experimental autoimmune encephalomyelitis.
- Mesenchymal stem cell transplantation attenuates blood brain barrier damage and neuroinflammation and protects dopaminergic neurons against MPTP toxicity in the substantia nigra in a model of Parkinson's disease.
- Normalization of the increased translocation of endotoxin from gram negative enterobacteria (leaky gut) is accompanied by a remission of chronic fatigue syndrome.
- Running exercise protects the substantia nigra dopaminergic neurons against inflammation-induced degeneration via the activation of BDNF signaling pathway.
- Effects of immune activation on the retrieval of spatial memory
- Peripheral inflammation increases the deleterious effect of CNS inflammation on the nigrostriatal dopaminergic system.
- Neuroprotective Effects of Pretreatment with Propofol in LPS-Induced BV-2 Microglia Cells: Role of TLR4 and GSK-3β
- Inhibitory Effects of Ginsenoside Rb1 on Neuroinflammation Following Systemic Lipopolysaccharide Treatment in Mice
- Anti-inflammatory Effect of Acetylpuerarin on Eicosanoid Signaling Pathway in Primary Rat Astrocytes
- Current hypotheses on the mechanisms of alcoholism
- The role of hepcidin in chronic mild stress-induced depression.
- Discovery of a high affinity and selective pyridine analog as a potential positron emission tomography imaging agent for cannabinoid type 2 receptor.
- The choreography of neuroinflammation in Huntington’s disease
- Ginsenoside Rg1 attenuates motor impairment and neuroinflammation in the MPTP-probenecid-induced parkinsonism mouse model by targeting α-synuclein abnormalities in the substantia nigra.
- The impact of inflammation on respiratory plasticity
- Anthocyanins protect against LPS-induced oxidative stress-mediated neuroinflammation and neurodegeneration in the adult mouse cortex.
- Trans-cinnamaldehyde improves memory impairment by blocking microglial activation through the destabilization of iNOS mRNA in mice challenged with lipopolysaccharide.
- Brain and Peripheral Atypical Inflammatory Mediators Potentiate Neuroinflammation and Neurodegeneration
- Glial and neuroinflammatory targets for treating substance use disorders
- Triggering Receptor Expressed on Myeloid Cells 2 Overexpression Inhibits Proinflammatory Cytokines in Lipopolysaccharide-Stimulated Microglia
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