Innate immunity: the missing link in neuroprotection and neurodegeneration?

By Minh N. H. Nguyen, J. Julien, S. Rivest. Nature Reviews Neuroscience, 2002

737 citations recorded by the source corpus.

Subfields: Biological Psychiatry, Immunology, Neurology

View Paper: https://www.semanticscholar.org/paper/84d17e14a468a4c35eb857215ea05f34eead35ae

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Biological Psychiatry

1. T. Wyss‐Coray
2. S. Rivest
3. B. Barres
4. Jonathan P. Godbout
5. A. Vezzani
6. David J. Loane
7. Alok Kumar

In Immunology

1. T. Wyss‐Coray
2. M. Block
3. S. Rivest
4. A. Vezzani
5. Jau-Shyong Hong
6. J. Rogers
7. Beth Stevens
8. E. Milligan

In Neurology

1. M. Block
2. Jau-Shyong Hong
3. T. Wyss‐Coray
4. B. Barres
5. Beth Stevens
6. S. Rivest
7. Linda R. Watkins
8. A. Vezzani

Citations in the corpus

• Role of Microglia in Central Nervous System Infections (2004, background): “However, activated microglia have been the focus of many studies, and in this functional phase they have been shown to express a number of such receptors, e.g., members of the immunoglobulin superfamily, complement receptors , cytokine/chemokine receptors, and Toll-like receptors (TLRs) (Table 1).”
• The complement system: an unexpected role in synaptic pruning during development and disease. (2012, background): “Neuroinflammation, including microglial activation, reactive gliosis, and massive and early activation of the classical complement cascade, is a cardinal feature of AD and many or most other neurodegenerative diseases (Nguyen et al. 2002, Wyss-Coray & Mucke 2002).”
• Long-term Air Pollution Exposure Is Associated with Neuroinflammation, an Altered Innate Immune Response, Disruption of the Blood-Brain Barrier, Ultrafine Particulate Deposition, and Accumulation of Amyloid β-42 and α-Synuclein in Children and Young Adults (2008, background): “Both Aβ42 and α-synuclein are proteins capable of aggregation and misfolding, leading to progressive neurodegeneration that develops insidiously over the lifetime of the individual (Jellinger 2003; McGeer et al. 2006; Nguyen et al. 2002; Selkoe 2001, 2002).”
• Bone marrow-derived microglia play a critical role in restricting senile plaque formation in Alzheimer's disease. (2006, background): “Indeed, activated microglia are known to favor the release of many neurotrophic molecules that have clear beneficial properties for CNS elements, including neurons and oligodendrocytes (Nguyen et al., 2002).”
• Neuroglial activation and neuroinflammation in the brain of patients with autism (2005, background): “The microglial and astroglial responses in the CNS may then have a dichotomous role in the inflammatory responses of the brain: as a direct effector of injury and on the other hand as neuroprotectant.(46) An issue that remains unclear is how and when microglia and astroglia become activated in the b”
• Innate and adaptive immunity during epileptogenesis and spontaneous seizures: evidence from experimental models and human temporal lobe epilepsy. (2008, background): “The increase in interleukin (IL)-1β, IL-6 and TNF-α in microglia and astrocytes is followed by a cascade of downstream inflammatory events which may recruit cells of the adaptive immune system (Nguyen et al., 2002; Vezzani and Granata, 2005).”
• Pathological and protective roles of glia in chronic pain (2009, background): “Both cell types are key mediators of the CNS innate immune response, which resembles many aspects of the classical immune respons”
• Brain Inflammation in Epilepsy: Experimental and Clinical Evidence (2005, background): “Notable examples exist of the dual role of immunity and inflammation in the CNS: in particular, immunologic/inflammatory challenges may contribute to the etiopathogenesis of some CNS disorders such as Rasmussen encephalitis (RE), stiff-man syndrome, and paraneoplastic neurologic diseases (2).”
• Minocycline attenuates lipopolysaccharide (LPS)-induced neuroinflammation, sickness behavior, and anhedonia (2008, background): “These data are consistent with other studies showing that central or peripheral LPS challenge increases TLR2 mRNA in the brain [6,14].”
• Proinflammatory cytokine synthesis in the injured mouse spinal cord: Multiphasic expression pattern and identification of the cell types involved (2007, background): “Although the receptors for IL-1 and TNF are structurally different, both cytokines share signaling molecules, like NF-kB and AP-1 transcription factors (Nguyen et al., 2002).”
• Regulation of innate immune responses in the brain (2009, background): “Rapid innate immune responses to systemic infection are initiated at these regions, which are followed by the progressive activation of resident microglial cells in the brain parenchym”
• The role of inflammation in epilepsy (2010, neutral): “31,34 These molecules include interleukins (ILs), interferons (IFNs), tumor necrosis factors (TNFs) and growth factors (for example, transforming growth factor [TGF]- β ).”
• Inflammation in Alzheimer disease-a brief review of the basic science and clinical literature. (2012, background): “Stimulation of TLRs, of which there are at least 13 distinct members to date (Iwasaki and Medzhitov 2004), induces activation of NF-kB and subsequent transcriptional activation of numerous proinflammatory genes (Nguyen et al. 2002).”
• Immune activation in brain aging and neurodegeneration: too much or too little? (2009, background): “…of nuclear factor kB and subsequent transcriptional activation of numerous proinflammatory genes, encoding cytokines, chemokines, complement proteins, enzymes (such as cyclooxygenase 2 and the inducible form of nitric oxide synthase ), adhesion molecules, and immune receptors (Nguyen et al., 2002).”
• Selective Ablation of Proliferating Microglial Cells Exacerbates Ischemic Injury in the Brain (2007, background): “However, whether microglial activation has beneficial or detrimental effects on adjacent ischemic neurons remains controversial (Nguyen et al., 2002; Wyss-Coray and Mucke, 2002; Nedergaard and Dirnagl, 2005).”