We are analyzing https://link.springer.com/article/10.1007/s00702-010-0438-z.

Title:
Neuroinflammatory processes in Alzheimer’s disease | Journal of Neural Transmission
Description:
Generation of neurotoxic amyloid β peptides and their deposition along with neurofibrillary tangle formation represent key pathological hallmarks in Alzheimer’s disease (AD). Recent evidence suggests that inflammation may be a third important component which, once initiated in response to neurodegeneration or dysfunction, may actively contribute to disease progression and chronicity. Various neuroinflammatory mediators including complement activators and inhibitors, chemokines, cytokines, radical oxygen species and inflammatory enzyme systems are expressed and released by microglia, astrocytes and neurons in the AD brain. Degeneration of aminergic brain stem nuclei including the locus ceruleus and the nucleus basalis of Meynert may facilitate the occurrence of inflammation in their projection areas given the antiinflammatory and neuroprotective action of their key transmitters norepinephrine and acetylcholine. While inflammation has been thought to arise secondary to degeneration, recent experiments demonstrated that inflammatory mediators may stimulate amyloid precursor protein processing by various means and therefore can establish a vicious cycle. Despite the fact that some aspects of inflammation may even be protective for bystander neurons, antiinflammatory treatment strategies should therefore be considered. Non-steroidal anti-inflammatory drugs have been shown to reduce the risk and delay the onset to develop AD. While, the precise molecular mechanism underlying this effect is still unknown, a number of possible mechanisms including cyclooxygenase 2 or γ-secretase inhibition and activation of the peroxisome proliferator activated receptor γ may alone or, more likely, in concert account for the epidemiologically observed protection.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Education
Science
Health & Fitness

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month

Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
However, some sources were not loaded, we suggest to reload the page to get complete results.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Link.springer.com Make Money? {💸}

The income method remains a mystery to us.

Not every website is profit-driven; some are created to spread information or serve as an online presence. Websites can be made for many reasons. This could be one of them. Link.springer.com might be making money, but it's not detectable how they're doing it.

Keywords {🔍}

google, scholar, pubmed, cas, article, disease, alzheimers, brain, neurosci, expression, amyloid, microglia, receptor, alzheimer, mice, neurol, nitric, oxide, heneka, antiinflammatory, transgenic, inflammation, inflammatory, cell, betaamyloid, activation, microglial, neurochem, beta, neurobiol, protein, res, astrocytes, cells, synthase, sci, peroxisome, neuronal, model, receptors, role, neurons, cyclooxygenase, human, aging, obanion, mouse, rat, interleukin, drugs,

Topics {✒️}

peroxisome proliferator-activated receptor-gamma g-protein-coupled receptor mfpr2 tumor-necrosis-factor-alpha stimulate tumor necrosis factor-alpha/lipopolysaccharide peroxisome proliferator-activated receptors beta-catenin/t-cell factor bone-marrow-derived cells contribute month download article/chapter beta-amyloid-induced glial expression beta-amyloid-stimulated proinflammatory responses tumor-necrosis-factor-alpha tumor necrosis factor-alpha tumor necrosis factor-alpha long-term potentiation nonsteroidal anti-inflammatory drug oxidative stress–mediated neuroinflammation steroidal anti-inflammatory drugs nonsteroidal anti-inflammatory drugs oligomeric beta-amyloid peptide widespread peroxynitrite-mediated damage amyloid-beta-induced chemokine production ischemia-induced oxidative damage anti-inflammatory cyclopentenone prostaglandins amyloid-beta peptide-receptor nitric oxide-mediated apoptosis ischaemia-induced hippocampal lesions nmda-induced neuronal injury bind monomeric beta-amyloid flurbiprofen target gamma-secretase lack abeta-activated neurotoxicity beta1 integrin-dependent mechanism prostaglandin e2-mediated neuroprotection neuron-astrocyte cross-talk experimental autoimmune encephalomyelitis a-beta amyloid plaque cxc chemokine-mediated angiogenesis macrophage-colony stimulating factor macrophage colony-stimulating factor cholinergic anti-inflammatory pathway inflammation-mediated neurodegenerative diseases pro-amyloidogenic alpha1-antichymotrypsin app[v717i] transgenic mice tumor necrosis factor {beta}-stimulated microglial activation beta-amyloid-mediated inhibition microglia kill amyloid-beta disease amyloid beta-protein microglial-produced nitric-oxide alzheimer beta-amyloid peptides inflammatory cytokines ifn-gamma

Questions {❓}

Breitner JC, Zandi PP (2001) Do nonsteroidal antiinflammatory drugs reduce the risk of Alzheimer’s disease?
Davis S, Laroche S (2003) What can rodent models tell us about cognitive decline in Alzheimer’s disease?
Feinstein DL, Spagnolo A, Akar C, Weinberg G, Murphy P, Gavrilyuk V, Russo CD (2005) Receptor-independent actions of PPAR thiazolidinedione agonists: is mitochondrial function the key?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Neuroinflammatory processes in Alzheimer’s disease
         description:Generation of neurotoxic amyloid β peptides and their deposition along with neurofibrillary tangle formation represent key pathological hallmarks in Alzheimer’s disease (AD). Recent evidence suggests that inflammation may be a third important component which, once initiated in response to neurodegeneration or dysfunction, may actively contribute to disease progression and chronicity. Various neuroinflammatory mediators including complement activators and inhibitors, chemokines, cytokines, radical oxygen species and inflammatory enzyme systems are expressed and released by microglia, astrocytes and neurons in the AD brain. Degeneration of aminergic brain stem nuclei including the locus ceruleus and the nucleus basalis of Meynert may facilitate the occurrence of inflammation in their projection areas given the antiinflammatory and neuroprotective action of their key transmitters norepinephrine and acetylcholine. While inflammation has been thought to arise secondary to degeneration, recent experiments demonstrated that inflammatory mediators may stimulate amyloid precursor protein processing by various means and therefore can establish a vicious cycle. Despite the fact that some aspects of inflammation may even be protective for bystander neurons, antiinflammatory treatment strategies should therefore be considered. Non-steroidal anti-inflammatory drugs have been shown to reduce the risk and delay the onset to develop AD. While, the precise molecular mechanism underlying this effect is still unknown, a number of possible mechanisms including cyclooxygenase 2 or γ-secretase inhibition and activation of the peroxisome proliferator activated receptor γ may alone or, more likely, in concert account for the epidemiologically observed protection.
         datePublished:2010-07-15T00:00:00Z
         dateModified:2010-07-15T00:00:00Z
         pageStart:919
         pageEnd:947
         sameAs:https://doi.org/10.1007/s00702-010-0438-z
         keywords:
            Alzheimer’s disease
            Neuroinflammation
            Amyloid beta
            Peroxisome proliferator activated receptor gamma
            Cytokines
            Locus ceruleus
            Neurology
            Psychiatry
            Neurosciences
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00702-010-0438-z/MediaObjects/702_2010_438_Fig1_HTML.gif
         isPartOf:
            name:Journal of Neural Transmission
            issn:
               1435-1463
               0300-9564
            volumeNumber:117
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Springer Vienna
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Michael T. Heneka
               affiliation:
                     name:University of Bonn
                     address:
                        name:Department of Neurology, Clinical Neurosciences, University of Bonn, Bonn, Germany
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
               name:M. Kerry O’Banion
               affiliation:
                     name:University of Rochester
                     address:
                        name:Department of Neurobiology and Anatomy, University of Rochester, Rochester, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Dick Terwel
               affiliation:
                     name:University of Bonn
                     address:
                        name:Department of Neurology, Clinical Neurosciences, University of Bonn, Bonn, Germany
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Markus Peter Kummer
               affiliation:
                     name:University of Bonn
                     address:
                        name:Department of Neurology, Clinical Neurosciences, University of Bonn, Bonn, Germany
                        type:PostalAddress
                     type:Organization
               type:Person
         isAccessibleForFree:
         hasPart:
            isAccessibleForFree:
            cssSelector:.main-content
            type:WebPageElement
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Neuroinflammatory processes in Alzheimer’s disease
      description:Generation of neurotoxic amyloid β peptides and their deposition along with neurofibrillary tangle formation represent key pathological hallmarks in Alzheimer’s disease (AD). Recent evidence suggests that inflammation may be a third important component which, once initiated in response to neurodegeneration or dysfunction, may actively contribute to disease progression and chronicity. Various neuroinflammatory mediators including complement activators and inhibitors, chemokines, cytokines, radical oxygen species and inflammatory enzyme systems are expressed and released by microglia, astrocytes and neurons in the AD brain. Degeneration of aminergic brain stem nuclei including the locus ceruleus and the nucleus basalis of Meynert may facilitate the occurrence of inflammation in their projection areas given the antiinflammatory and neuroprotective action of their key transmitters norepinephrine and acetylcholine. While inflammation has been thought to arise secondary to degeneration, recent experiments demonstrated that inflammatory mediators may stimulate amyloid precursor protein processing by various means and therefore can establish a vicious cycle. Despite the fact that some aspects of inflammation may even be protective for bystander neurons, antiinflammatory treatment strategies should therefore be considered. Non-steroidal anti-inflammatory drugs have been shown to reduce the risk and delay the onset to develop AD. While, the precise molecular mechanism underlying this effect is still unknown, a number of possible mechanisms including cyclooxygenase 2 or γ-secretase inhibition and activation of the peroxisome proliferator activated receptor γ may alone or, more likely, in concert account for the epidemiologically observed protection.
      datePublished:2010-07-15T00:00:00Z
      dateModified:2010-07-15T00:00:00Z
      pageStart:919
      pageEnd:947
      sameAs:https://doi.org/10.1007/s00702-010-0438-z
      keywords:
         Alzheimer’s disease
         Neuroinflammation
         Amyloid beta
         Peroxisome proliferator activated receptor gamma
         Cytokines
         Locus ceruleus
         Neurology
         Psychiatry
         Neurosciences
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00702-010-0438-z/MediaObjects/702_2010_438_Fig1_HTML.gif
      isPartOf:
         name:Journal of Neural Transmission
         issn:
            1435-1463
            0300-9564
         volumeNumber:117
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer Vienna
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Michael T. Heneka
            affiliation:
                  name:University of Bonn
                  address:
                     name:Department of Neurology, Clinical Neurosciences, University of Bonn, Bonn, Germany
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
            name:M. Kerry O’Banion
            affiliation:
                  name:University of Rochester
                  address:
                     name:Department of Neurobiology and Anatomy, University of Rochester, Rochester, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Dick Terwel
            affiliation:
                  name:University of Bonn
                  address:
                     name:Department of Neurology, Clinical Neurosciences, University of Bonn, Bonn, Germany
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Markus Peter Kummer
            affiliation:
                  name:University of Bonn
                  address:
                     name:Department of Neurology, Clinical Neurosciences, University of Bonn, Bonn, Germany
                     type:PostalAddress
                  type:Organization
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Journal of Neural Transmission
      issn:
         1435-1463
         0300-9564
      volumeNumber:117
Organization:
      name:Springer Vienna
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:University of Bonn
      address:
         name:Department of Neurology, Clinical Neurosciences, University of Bonn, Bonn, Germany
         type:PostalAddress
      name:University of Rochester
      address:
         name:Department of Neurobiology and Anatomy, University of Rochester, Rochester, USA
         type:PostalAddress
      name:University of Bonn
      address:
         name:Department of Neurology, Clinical Neurosciences, University of Bonn, Bonn, Germany
         type:PostalAddress
      name:University of Bonn
      address:
         name:Department of Neurology, Clinical Neurosciences, University of Bonn, Bonn, Germany
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Michael T. Heneka
      affiliation:
            name:University of Bonn
            address:
               name:Department of Neurology, Clinical Neurosciences, University of Bonn, Bonn, Germany
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:M. Kerry O’Banion
      affiliation:
            name:University of Rochester
            address:
               name:Department of Neurobiology and Anatomy, University of Rochester, Rochester, USA
               type:PostalAddress
            type:Organization
      name:Dick Terwel
      affiliation:
            name:University of Bonn
            address:
               name:Department of Neurology, Clinical Neurosciences, University of Bonn, Bonn, Germany
               type:PostalAddress
            type:Organization
      name:Markus Peter Kummer
      affiliation:
            name:University of Bonn
            address:
               name:Department of Neurology, Clinical Neurosciences, University of Bonn, Bonn, Germany
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Department of Neurology, Clinical Neurosciences, University of Bonn, Bonn, Germany
      name:Department of Neurobiology and Anatomy, University of Rochester, Rochester, USA
      name:Department of Neurology, Clinical Neurosciences, University of Bonn, Bonn, Germany
      name:Department of Neurology, Clinical Neurosciences, University of Bonn, Bonn, Germany
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {🔗}(1004)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref

5.41s.

LINK . SPRINGER . COM {}