We are analyzing https://link.springer.com/article/10.1186/1742-2094-5-7.

Title:
The role of interleukin-1 in neuroinflammation and Alzheimer disease: an evolving perspective | Journal of Neuroinflammation
Description:
Elevation of the proinflammatory cytokine Interleukin-1 (IL-1) is an integral part of the local tissue reaction to central nervous system (CNS) insult. The discovery of increased IL-1 levels in patients following acute injury and in chronic neurodegenerative disease laid the foundation for two decades of research that has provided important details regarding IL-1
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Keywords {🔍}

pubmed, google, scholar, cas, brain, disease, interleukin, ilβ, central, injury, expression, role, neuroinflammation, cns, receptor, activation, alzheimers, mice, microglia, microglial, mouse, plaque, amyloid, griffin, recruitment, cells, neurosci, alzheimer, chronic, protein, response, evidence, human, studies, cytokine, acute, transgenic, mrak, system, increased, leukocyte, pathogenesis, neuroinflammatory, neuronal, model, experimental, inflammatory, rothwell, neurobiol, damage,

Topics {✒️}

corticotropin-releasing factor-producing neurons bone-marrow-derived cells contribute bone marrow-derived cells app/ps1/tau triple transgenic nonsteroidal anti-inflammatory drug central nervous system tumor necrosis factor-alpha interleukin-1beta converting enzyme/caspase-1 transforming growth factor-ß1 nonsteroidal anti-inflammatory drugs blood-brain barrier permeability neuritic beta-amyloid plaques antibody-mediated plaque clearance jnk-dependent mapk pathway traditional anti-inflammatory agents neutrophil-mediated host defense include pro-inflammatory cytokines app/ps1 double transgenic polymorphonuclear neutrophil-dependent increases app/ps1 transgenic animals map3k-related kinase involved app+ps1 transgenic mice effective anti-inflammatory therapies tnf-alpha impart neuroprotection interleukin-1beta promotes repair il-1β converting enzyme blood-brain barrier breakdown intact nervous system chronic interleukin-1beta expression mapk-p38-mediated hyperphosphorylation receiving anti-inflammatory therapy tumor necrosis factor article download pdf il-1β genetic loci amyloid precursor protein brain-wide glial activation il-1r1 knockout animals il-1β induced neurotoxicity chronic il-1β expression il-1β elicits rapid il-1r1 knockout mice exogenously administered il-1ra kerry o'banion human beta-amyloid il-1β mediated activation chemokine-dependent neutrophil recruitment drives il-1β synthesis experimental creutzfeldt-jakob disease recent anti-inflammatory trials histocompatibility glycoprotein hla-dr

Questions {❓}

A new view of IL-1's role in AD?
Emerich DF, Dean RL, Bartus RT: The role of leukocytes following cerebral ischemia: pathogenic variable or bystander reaction to emerging infarct?
Wyss-Coray T: Inflammation in Alzheimer disease: driving force, bystander or beneficial response?

Schema {🗺️}

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         headline:The role of interleukin-1 in neuroinflammation and Alzheimer disease: an evolving perspective
         description:Elevation of the proinflammatory cytokine Interleukin-1 (IL-1) is an integral part of the local tissue reaction to central nervous system (CNS) insult. The discovery of increased IL-1 levels in patients following acute injury and in chronic neurodegenerative disease laid the foundation for two decades of research that has provided important details regarding IL-1's biology and function in the CNS. IL-1 elevation is now recognized as a critical component of the brain's patterned response to insults, termed neuroinflammation, and of leukocyte recruitment to the CNS. These processes are believed to underlie IL-1's function in the setting of acute brain injury, where it has been ascribed potential roles in repair as well as in exacerbation of damage. Explorations of IL-1's role in chronic neurodegenerative disease have mainly focused on Alzheimer disease (AD), where indirect evidence has implicated it in disease pathogenesis. However, recent observations in animal models challenge earlier assumptions that IL-1 elevation and resulting neuroinflammatory processes play a purely detrimental role in AD, and prompt a need for new characterizations of IL-1 function. Potentially adaptive functions of IL-1 elevation in AD warrant further mechanistic studies, and provide evidence that enhancement of these effects may help to alleviate the pathologic burden of disease.
         datePublished:2008-02-26T00:00:00Z
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      headline:The role of interleukin-1 in neuroinflammation and Alzheimer disease: an evolving perspective
      description:Elevation of the proinflammatory cytokine Interleukin-1 (IL-1) is an integral part of the local tissue reaction to central nervous system (CNS) insult. The discovery of increased IL-1 levels in patients following acute injury and in chronic neurodegenerative disease laid the foundation for two decades of research that has provided important details regarding IL-1's biology and function in the CNS. IL-1 elevation is now recognized as a critical component of the brain's patterned response to insults, termed neuroinflammation, and of leukocyte recruitment to the CNS. These processes are believed to underlie IL-1's function in the setting of acute brain injury, where it has been ascribed potential roles in repair as well as in exacerbation of damage. Explorations of IL-1's role in chronic neurodegenerative disease have mainly focused on Alzheimer disease (AD), where indirect evidence has implicated it in disease pathogenesis. However, recent observations in animal models challenge earlier assumptions that IL-1 elevation and resulting neuroinflammatory processes play a purely detrimental role in AD, and prompt a need for new characterizations of IL-1 function. Potentially adaptive functions of IL-1 elevation in AD warrant further mechanistic studies, and provide evidence that enhancement of these effects may help to alleviate the pathologic burden of disease.
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         Chronic Neurodegenerative Disease
         Follow Central Nervous System Injury
         Neuroinflammatory Change
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         Neurobiology
         Immunology
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