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  1. Interleukin 1 (IL-1) is a key mediator of immune responses in health and disease. Although classically the function of IL-1 has been studied in the systemic immune system, research in the past decade has revea...

    Authors: Jeffrey M Craft, D Martin Watterson, Emmet Hirsch and Linda J Van Eldik
    Citation: Journal of Neuroinflammation 2005 2:15
  2. The role of both microglial activation and alpha-synuclein deposition in Parkinson's disease remain unclear. We have tested the hypothesis that if microglia play a primary role in Parkinson's disease pathogene...

    Authors: Emilie Croisier, Linda B Moran, David T Dexter, Ronald KB Pearce and Manuel B Graeber
    Citation: Journal of Neuroinflammation 2005 2:14

    The Research to this article has been published in Journal of Neuroinflammation 2006 3:9

  3. In the nervous system, as in other organs, Cu/Zn superoxide dismutase (Cu/Zn SOD) is a key antioxidant enzyme involved in superoxide detoxification in normal cellular metabolism and after cell injury. Although...

    Authors: Hugo Peluffo, Laia Acarin, Maryam Faiz, Bernardo Castellano and Berta Gonzalez
    Citation: Journal of Neuroinflammation 2005 2:12
  4. Calcium-sensitive fluorescence microscopy and molecular biology analysis have been used to study the effects of platelet-activating factor (PAF) on intracellular calcium [Ca2+]i and IL-6 expression in human micro...

    Authors: Prasongchai Sattayaprasert, Hyun B Choi, Sukumal Chongthammakun and James G McLarnon
    Citation: Journal of Neuroinflammation 2005 2:11
  5. Twitcher mouse (twi/twi) is an authentic murine model of Krabbe's disease. Accumulation of psychosine, resulting in apoptosis of oligodendrocytes and subsequent demyelination, is a cardinal event to the pathogene...

    Authors: Kuriko Kagitani-Shimono, Ikuko Mohri, Yasushi Fujitani, Kinuko Suzuki, Keiichi Ozono, Yoshihiro Urade and Masako Taniike
    Citation: Journal of Neuroinflammation 2005 2:10
  6. Inflammation is believed to play an important role in the pathology of Alzheimer's disease (AD) and cytokine production is a key pathologic event in the progression of inflammatory cascades. The current study ...

    Authors: Nikunj S Patel, Daniel Paris, Venkatarajan Mathura, Amita N Quadros, Fiona C Crawford and Michael J Mullan
    Citation: Journal of Neuroinflammation 2005 2:9
  7. In neuropathological processes associated with neutrophilic infiltrates, such as experimental allergic encephalitis and traumatic injury of the brain, the CXC chemokine, macrophage inflammatory protein-2 (MIP-...

    Authors: Michiyo Tomita, Brita J Holman, Christopher P Santoro and Thomas J Santoro
    Citation: Journal of Neuroinflammation 2005 2:8
  8. Raised activity of the renin-angiotensin system (RAS) may both amplify inflammatory and free radical responses and decrease tissue metabolic efficiency and thus enhance cerebral injury in the preterm infant. T...

    Authors: David R Harding, Sukhbir Dhamrait, David Devadason, Steve E Humphries, Andrew Whitelaw, Neil Marlow and Hugh E Montgomery
    Citation: Journal of Neuroinflammation 2005 2:6
  9. Subventricular microglia (SVMs) are positioned at the interface of the cerebrospinal fluid and brain parenchyma and may play a role in periventricular inflammatory reactions. However, SVMs have not been previo...

    Authors: W Shawn Carbonell, Shin-Ichi Murase, Alan F Horwitz and James W Mandell
    Citation: Journal of Neuroinflammation 2005 2:5
  10. Nicotinic acetylcholine (Ach) receptors are ligand-gated pentameric ion channels whose main function is to transmit signals for the neurotransmitter Ach in peripheral and central nervous system. However, the α...

    Authors: Roberta De Simone, Maria Antonietta Ajmone-Cat, Daniela Carnevale and Luisa Minghetti
    Citation: Journal of Neuroinflammation 2005 2:4
  11. Previous studies suggest that the cyclooxygenase-2 (COX-2) inhibitor nimesulide has a remarkable protective effect against different types of brain injury including ischemia. Since there are no reports on the ...

    Authors: Eduardo Candelario-Jalil, Noël H Mhadu, Armando González-Falcón, Michel García-Cabrera, Eduardo Muñoz, Olga Sonia León and Bernd L Fiebich
    Citation: Journal of Neuroinflammation 2005 2:3
  12. Anti-Aβ immunotherapy in transgenic mice reduces both diffuse and compact amyloid deposits, improves memory function and clears early-stage phospho-tau aggregates. As most Alzheimer disease cases occur well pa...

    Authors: Donna M Wilcock, Amyn Rojiani, Arnon Rosenthal, Sangeetha Subbarao, Melissa J Freeman, Marcia N Gordon and Dave Morgan
    Citation: Journal of Neuroinflammation 2004 1:24
  13. Recent studies suggest that hypercholesterolemia, an established risk factor for atherosclerosis, is also a risk factor for Alzheimer's disease. The myeloid scavenger receptor CD36 binds oxidized lipoproteins ...

    Authors: Vidya V Kunjathoor, Anita A Tseng, Lea A Medeiros, Tayeba Khan and Kathryn J Moore
    Citation: Journal of Neuroinflammation 2004 1:23
  14. Mental fatigue, with decreased concentration capacity, is common in neuroinflammatory and neurodegenerative diseases, often appearing prior to other major mental or physical neurological symptoms. Mental fatig...

    Authors: Lars Rönnbäck and Elisabeth Hansson
    Citation: Journal of Neuroinflammation 2004 1:22
  15. An increasing body of evidence implicates both brain inflammation and oxidative stress in the pathogenesis of Alzheimer's disease (AD). The relevance of their interaction in vivo, however, is unknown. Previous...

    Authors: Yuemang Yao, Cinzia Chinnici, Hanguan Tang, John Q Trojanowski, Virginia MY Lee and Domenico Praticò
    Citation: Journal of Neuroinflammation 2004 1:21
  16. 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
  17. 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
  18. 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
  19. 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
  20. 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
  21. 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
  22. 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
  23. 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
  24. 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
  25. 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
  26. 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
  27. 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
  28. 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
  29. 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
  30. 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
  31. 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

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