Skip to main content

Home/ Dr. Goodyear/ Group items tagged microglial

Rss Feed Group items tagged

Nathan Goodyear

Antiinflammatory Effects of Estrogen on Microglial Activation - 0 views

  •  
    Estradiol (E2) shown to be neuroprotective in those with microglial excitotoxicity diseases, such as Parkinson's and Alzheimer's disease.  this study looked at a rat model.  The effect was not through inhibition of NF-kappaB, but through MAP kinase.
Nathan Goodyear

Microglial cells in neurodegenerative disorders. [Folia Neuropathol. 2005] - PubMed result - 0 views

  •  
    nice article on microglial cells and how they contribute to Parkinson's, Alzheimer's, and other neurodegenerative diseases
Nathan Goodyear

Access : Neuroimmunology: Estrogen receptor ligands suppress inflammatory responses in ... - 0 views

  •  
    Granted, this study was in an animal model of MS, but signaling through ER-beta was shown to decrease inflammation from astrocytes and microglial cells in the brain.  These immune cells are known to play prominent roles in excitotoxic diseases such as MS.  So, again, it is not just about the message, but also about how the message is interpreted.
Nathan Goodyear

Microglial Activation And Neurodegeneration - 0 views

  •  
    short and brief discussion of how microglial inflammation cause neurodegeneration via excitotoxicity.  Dr. Blaylock is the author of this short article.  
Nathan Goodyear

Inflammatory Mechanisms in Alzheimer's Disease: Inhibition of β-Amyloid-Stimu... - 0 views

  • The activated microglia mount a complex local proinflammatory response
  • PPARγ plays a critical role in regulating the inflammatory responses of microglia and monocytes to β-amyloid
  •  
    microglial and inflammatory response in Alzheimer's disease.  Agonists of PPAR-gamma inhibit this action.  This has important implications in reducing the local inflammatory response found in the brains of those with Alzheimers and other neuordegenerative disease.
Nathan Goodyear

Inflammatory Mechanisms in Alzheimer's Disease: Inhibition of β-Amyloid-Stimu... - 0 views

  • PPARγ agonists were shown to inhibit the β-amyloid-stimulated expression of the cytokine genes interleukin-6 and tumor necrosis factor α. Furthermore, PPARγ agonists inhibited the expression of cyclooxygenase-2.
  •  
    Not that we are recommending NSAIDS to reduce inflammation: but the learned biochemical pathways of inflammation involved with AD, allows a natural approach to reduce microglial associated inflammation through PPAR-gamma activation.
Nathan Goodyear

Omega-3 polyunsaturated fatty acid supplementation attenuates microglial-indu... - 0 views

  •  
    Omega 3 supplementation found to blunt microglial TBI inflammation. 
Nathan Goodyear

Aluminum induced immunoexcitotoxicity in neurodevelopmental and neurodegenerative disor... - 0 views

  •  
    Great review of the scientific evidence of Aluminum in microglial activation and immunoexcitotoxicity and neurodegeneration of the brain.
Nathan Goodyear

Changes in the number of astrocytes and micr... [Neurotoxicology. 1996] - PubMed - NCBI - 0 views

  •  
    low methylmercury shown to accumulate in the brains of monkeys in the form of inorganic mercury.  Specifically, astrocytes and microglial cells accumulated the inorganic mercury.  Long-term low exposure can result in neuro-accumulation of inorganic mercury and neurotoxicity.
Nathan Goodyear

Antidepressants inhibit interferon-gamma-induced ... [Exp Neurol. 2007] - PubMed - NCBI - 0 views

  •  
    anti-depressants inhibit inflammatory IL-6 production from microglial cells in brain, suggesting anti-inflammatory effects of antidepressants as role in improving depression symptoms
Nathan Goodyear

Minimal Penetration of Lipopolysaccharide Across the Murine Blood-brain Barrier - 0 views

  •  
    Study finds very small % of LPS actually is able to penetrate BBB, yet based on other studies, this is enough to trigger microglial activation and damage/death to astrocytes and other brain cells.
Nathan Goodyear

Lipopolysaccharide (LPS) potentiates hydrogen peroxide toxicity in T98G astrocytoma cel... - 0 views

  •  
    good review of proposed mechanism of how LPS aids in cell death of astrocytes in vivo: LPS damages the endothelium of the BBB, leading to increase permeability.  This exposes astrocytes to LPS directly.  LPS suppressed genetic expression of antioxidant genes.  LPS stimulates cytokine production, including the production of H2O2 from microglial cells in the brain.  An up regulation of iNOS occurs and in the presence of weakened ability to protect against NO and its metabolites occurs.  
Nathan Goodyear

The Complex Role of Estrogens in Inflammation - 0 views

  • These studies suggest inflammation-dependent up-regulation of ERβ relative to ERα.
  • up-regulation of ERβ relative to ERα under hypoxic conditions, which might lead to a preponderance of signaling through ERβ pathways
  • it seems that E2 at periovulatory to pregnancy levels inhibited proinflammatory cytokines from PBMCs
  • ...26 more annotations...
  • it is clear that E2 can stimulate antibody production by B cells, probably by inhibiting T cell suppression of B cells
  • In cycling women, the largest quantities of Ig were detected before ovulation
  • In contrast, E2 at high concentrations leads to a suppression of B-lymphocyte lineage precursors
  • E2 at periovulatory to pregnancy serum levels is able to stimulate antibody secretion under healthy conditions but also in autoimmune diseases, whereas similar serum levels of E2 lead to a suppression of bone marrow B cell lineage precursors
  • In chronic inflammatory disorders, where B cells play a decisive role, E2 would promote the disease when autoaggressive B cells are already present, whereas chronically elevated E2 would inhibit initiation of an autoimmune disease when no such B cells are available. This might be a good reason why particularly B cell-dependent diseases such as SLE, mixed connective tissue disease (Sharp syndrome), IgA nephropathy, dermatitis herpetiformis, gluten sensitive enteropathy, myasthenia gravis, and thyroiditis appear in women in the reproductive years, predominantly, in the third or fourth decades of life
  • Th17 cells are thought to be the main responsible cells for chronic inflammatory tissue destruction in autoimmune diseases
  • IFN-γ, IL-12, and TNF were allocated to Th1 reactions
  • IL-4, IL-5, and IL-10 to Th2 responses
  • antiinflammatory T regulatory cells producing TGF-β and proinflammatory T helper type 17 cells (Th17) producing IL-17
  • no direct effects of estrogens on Th17 cells or IL-17 secretion have been described until now.
  • So-called Th17 cells producing IL-17 are the main T cells responsible for chronic inflammation.
  • Because IFN-γ has been allocated a Th17-inhibiting role (Fig. 1⇑), its increase by E2 at pregnancy doses and the E2-mediated inhibition of TNF must be viewed as a favorable effect in chronic inflammation
  • in humans and mice, E2 at periovulatory to pregnancy levels stimulates IL-4, IL-10, and IFN-γ but inhibits TNF from CD4+ T cells
  • In humans and mice, E3 and E2, respectively, at pregnancy levels inhibit T cell-dependent delayed type hypersensitivity
  • increased IL-4, IL-10, and IFN-γ in the presence of low TNF support an antiaggressive immune response
  • secretion of IL-1β is increased at periovulatory/proestrus to early pregnancy levels, whereas IL-1 secretion is inhibited at high pregnancy levels
  • The dichotomous effect of E2 on IL-1β and TNF at high and low concentrations is most probably due to inhibition of NF-κB at high concentrations
  • experiments with mouse and rat macroglial and microglial cells demonstrate that E2 at proestrus to pregnancy levels exerts neuroprotective effects by increasing TGF-β and by inhibiting iNOS and NO release, and reducing expression of proinflammatory cytokines and prostaglandin E2 production.
  • E2 at periovulatory to pregnancy levels inhibits NF-κB activation, which must be viewed as an antiinflammatory signal
  • It was shown that E2 concentrations equal to or above 10−10 m are necessary to inhibit NF-κB activation
  • important proinflammatory cytokines are typically inhibited at periovulatory (proestrus) to pregnancy levels of E2, which is evident for IL-6, IL-8, and TNF
  • low E2 concentrations were demonstrated to have no or even stimulatory effects
  • This renders a woman in the postmenopausal phase to a more proinflammatory situation
  • most in vitro studies demonstrated a stimulatory effect of E2 on secretion of IL-4, IL-10, and TGF-β typically at periovulatory to pregnancy levels
  • E2 at periovulatory to pregnancy levels has an ameliorating effect on chronic inflammatory diseases as long as B cell-dependent immunity or an overshooting fibrotic tissue repair process do not play a crucial pathogenic role. However, when the B cell plays an important role, E2 might even stimulate the disease process as substantiated by flare-ups in SLE during pregnancy
    • Nathan Goodyear
       
      SLE, mixed connective tissue disease (Sharp syndrome), IgA nephropathy, dermatitis herpetiformis, gluten sensitive enteropathy, myasthenia gravis, and thyroiditis
  • Short-term administration of E2 at pregnancy levels was shown to induce an inflammatory response specific to the lateral prostate of the castrated male rat
  •  
    great review of the complex interaction between Estrogens and inflammation.  Reference here is in females.
1 - 13 of 13
Showing 20 items per page