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  1. The cause-and-effect relationship between innate immune activation and neurodegeneration has been difficult to prove in complex animal models and patients. Here we review findings from a model of direct innate...

    Authors: Dejan Milatovic, Snjezana Zaja-Milatovic, Kathleen S Montine, Feng-Shiun Shie and Thomas J Montine
    Citation: Journal of Neuroinflammation 2004 1:20
  2. Oligodendrocytes, neurons, astrocytes, microglia, and endothelial cells are capable of synthesizing complement inhibitor proteins. Oligodendrocytes are vulnerable to complement attack, which is particularly ob...

    Authors: Masato Hosokawa, Andis Klegeris and Patrick L McGeer
    Citation: Journal of Neuroinflammation 2004 1:17
  3. Brain abscess represents a significant medical problem despite recent advances made in detection and therapy. Due to the emergence of multi-drug resistant strains and the ubiquitous nature of bacteria, the occ...

    Authors: Tammy Kielian
    Citation: Journal of Neuroinflammation 2004 1:16
  4. The apolipoprotein E ε4 allele contributes to the genetic susceptibility underlying a large proportion (~40–60%) of typical, sporadic Alzheimer disease. Apolipoprotein E deficient mice made transgenic for huma...

    Authors: David Sweeney, Ralph Martins, Harry LeVine III, Jonathan D Smith and Sam Gandy
    Citation: Journal of Neuroinflammation 2004 1:15
  5. Microglia make up the innate immune system of the central nervous system and are key cellular mediators of neuroinflammatory processes. Their role in central nervous system diseases, including infections, is d...

    Authors: Wolfgang J Streit, Robert E Mrak and W Sue T Griffin
    Citation: Journal of Neuroinflammation 2004 1:14
  6. Tumor necrosis factor (TNF) and interleukin-(IL)-18 are important mediators of neuroinflammation after closed head injury (CHI). Both mediators have been previously found to be significantly elevated in the in...

    Authors: Oliver I Schmidt, Maria Cristina Morganti-Kossmann, Christoph E Heyde, Daniel Perez, Ido Yatsiv, Esther Shohami, Wolfgang Ertel and Philip F Stahel
    Citation: Journal of Neuroinflammation 2004 1:13
  7. Neuroinflammation plays a prominent role in the progression of Alzheimer's disease and may be responsible for degeneration in vulnerable regions such as the hippocampus. Neuroinflammation is associated with el...

    Authors: Susanna Rosi, Victor Ramirez-Amaya, Beatrice Hauss-Wegrzyniak and Gary L Wenk
    Citation: Journal of Neuroinflammation 2004 1:12
  8. The over-expression of transforming growth factor β-1(TGF-β1) has been reported to cause hydrocephalus, glia activation, and vascular amyloidβ (Aβ) deposition in mouse brains. Since these phenomena partially m...

    Authors: Pierre Lacombe, Paul M Mathews, Stephen D Schmidt, Tilo Breidert, Michael T Heneka, Gary E Landreth, Douglas L Feinstein and Elena Galea
    Citation: Journal of Neuroinflammation 2004 1:11
  9. Inflammation of the central nervous system is an important but poorly understood part of neurological disease. After acute brain injury or infection there is a complex inflammatory response that involves activ...

    Authors: Marion S Buckwalter and Tony Wyss-Coray
    Citation: Journal of Neuroinflammation 2004 1:10
  10. Under pathological conditions, microglia produce proinflammatory mediators which contribute to neurologic damage, and whose levels can be modulated by endogenous factors including neurotransmitters such as nor...

    Authors: Cinzia Dello Russo, Anne I Boullerne, Vitaliy Gavrilyuk and Douglas L Feinstein
    Citation: Journal of Neuroinflammation 2004 1:9
  11. The pathogenesis of HIV-1 glycoprotein 120 (gp120) associated neuroglial toxicity remains unresolved, but oxidative injury has been widely implicated as a contributing factor. In previous studies, exposure of ...

    Authors: Kimberley A Walsh, Joseph F Megyesi, John X Wilson, Jeff Crukley, Victor E Laubach and Robert R Hammond
    Citation: Journal of Neuroinflammation 2004 1:8
  12. Several lines of evidence point to a significant role of neuroinflammation in Parkinson's disease (PD) and other neurodegenerative disorders. In the present study we examined the protective effect of celecoxib...

    Authors: Rosario Sánchez-Pernaute, Andrew Ferree, Oliver Cooper, Meixiang Yu, Anna-Liisa Brownell and Ole Isacson
    Citation: Journal of Neuroinflammation 2004 1:6
  13. Peroxisome proliferator-activated receptors (PPARs) are a class of nuclear transcription factors that are activated by fatty acids and their derivatives. One of these, PPARγ, regulates responsiveness to insuli...

    Authors: Robert E Mrak and Gary E Landreth
    Citation: Journal of Neuroinflammation 2004 1:5
  14. Ligands of the peroxisome proliferator-activated receptor-gamma (PPARγ) induce apoptosis in activated T-lymphocytes and exert anti-inflammatory effects in glial cells. Preclinical studies have shown that the t...

    Authors: Harrihar A Pershadsingh, Michael T Heneka, Rashmi Saini, Navin M Amin, Daniel J Broeske and Douglas L Feinstein
    Citation: Journal of Neuroinflammation 2004 1:3
  15. Roles for excitotoxicity and inflammation in Alzheimer's disease have been hypothesized. Proinflammatory stimuli, including amyloid β-peptide (Aβ), elicit a release of glutamate from microglia. We tested the p...

    Authors: Sheng-Zhou Wu, Angela M Bodles, Mandy M Porter, W Sue T Griffin, Anthony S Basile and Steven W Barger
    Citation: Journal of Neuroinflammation 2004 1:2
  16. Welcome to the Journal of Neuroinflammation, an open-access, peer-reviewed, online journal that focuses on innate immunological responses of the central nervous system, involving microglia, astrocytes, cytokin...

    Authors: Robert E Mrak and W Sue T Griffin
    Citation: Journal of Neuroinflammation 2004 1:1

Annual Journal Metrics

  • Citation Impact 2023
    Journal Impact Factor: 9.3
    5-year Journal Impact Factor: 9.8
    Source Normalized Impact per Paper (SNIP): 1.787
    SCImago Journal Rank (SJR): 2.831

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