We are analyzing https://link.springer.com/article/10.1186/s13195-015-0125-2.

Title:
The dynamics of monocytes and microglia in Alzheimer’s disease | Alzheimer's Research & Therapy
Description:
Alzheimer’s disease (AD) is the most common neurodegenerative disorder affecting older people worldwide. It is a progressive disorder mainly characterized by the presence of amyloid-beta (Aβ) plaques and neurofibrillary tangles within the brain parenchyma. It is now well accepted that neuroinflammation constitutes an important feature in AD, wherein the exact role of innate immunity remains unclear. Although innate immune cells are at the forefront to protect the brain in the presence of toxic molecules including Aβ, this natural defense mechanism seems insufficient in AD patients. Monocytes are a key component of the innate immune system and they play multiple roles, such as the removal of debris and dead cells via phagocytosis. These cells respond quickly and mobilize toward the inflamed site, where they proliferate and differentiate into macrophages in response to inflammatory signals. Many studies have underlined the ability of circulating and infiltrating monocytes to clear vascular Aβ microaggregates and parenchymal Aβ deposits respectively, which are very important features of AD. On the other hand, microglia are the resident immune cells of the brain and they play multiple physiological roles, including maintenance of the brain’s microenvironment homeostasis. In the injured brain, activated microglia migrate to the inflamed site, where they remove neurotoxic elements by phagocytosis. However, aged resident microglia are less efficient than their circulating sister immune cells in eliminating Aβ deposits from the brain parenchyma, thus underlining the importance to further investigate the functions of these innate immune cells in AD. The present review summarizes current knowledge on the role of monocytes and microglia in AD and how these cells can be mobilized to prevent and treat the disease.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Science
Health & Fitness
Education

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? {💸}

We're unsure if the website is profiting.

The purpose of some websites isn't monetary gain; they're meant to inform, educate, or foster collaboration. Everyone has unique reasons for building websites. This could be an example. Link.springer.com might be earning cash quietly, but we haven't detected the monetization method.

Keywords {🔍}

pubmed, cells, brain, article, microglia, google, scholar, monocytes, microglial, cas, disease, alzheimers, central, cell, macrophages, bbb, involved, role, mice, clearance, receptor, parenchyma, immune, phagocytosis, cerebral, proinflammatory, amyloid, shown, mouse, monocyte, innate, molecules, resident, plaques, inflammatory, activated, deposition, activation, microenvironment, blood, expression, perivascular, model, soluble, early, inflammation, receptors, figure, nat, neurosci,

Topics {✒️}

reduces beta-amyloid deposition bone-marrow-derived cells contribute ayman elali & serge rivest macrophage colony-stimulating factor stem/progenitor cell transplantation low-density lipoprotein receptors microglial β-amyloid binding bm-derived progenitor cells bone marrow-derived macrophages produce beta-amyloid fibrils beta/a4 amyloid fibrils nonsteroidal anti-inflammatory drugs amyloid-β25-35-induced learning article download pdf monocyte-derived microglial cells app + ps1 transgenic mice m-csf treatment increased older people worldwide vascular beta-amyloid deposits brain-derived neurotrophic factor app/ps1 mice irradiation app/ps1 mice showed app/ps1 mouse model intact blood–brain barrier blood–brain barrier disorder central nervous system aβ-induced inflammatory processes cerebral amyloid angiopathy brain-derived inflammatory cues microglial-derived enzymes involved anti-inflammatory monocytes behave aβ-induced inflammatory microenvironment hickman se m-csf receptor overexpression anti-inflammatory monocyte subset ccr2 + ly-6chi monocytes β-amyloid deposition amyloid precursor protein anti-inflammatory ly6clow monocytes microvascular blood–brain barrier beta-amyloid deposition stem cells dev deliver aβ/c3b complex blood-borne molecules constitute amyloid beta-protein cerebral aβ load cx3cl1/cx3cr1 axis plays monocyte chemoattractant protein astrocyte-mediated inflammation interleukin-1β overexpression

Schema {🗺️}

WebPage:
      mainEntity:
         headline:The dynamics of monocytes and microglia in Alzheimer’s disease
         description:Alzheimer’s disease (AD) is the most common neurodegenerative disorder affecting older people worldwide. It is a progressive disorder mainly characterized by the presence of amyloid-beta (Aβ) plaques and neurofibrillary tangles within the brain parenchyma. It is now well accepted that neuroinflammation constitutes an important feature in AD, wherein the exact role of innate immunity remains unclear. Although innate immune cells are at the forefront to protect the brain in the presence of toxic molecules including Aβ, this natural defense mechanism seems insufficient in AD patients. Monocytes are a key component of the innate immune system and they play multiple roles, such as the removal of debris and dead cells via phagocytosis. These cells respond quickly and mobilize toward the inflamed site, where they proliferate and differentiate into macrophages in response to inflammatory signals. Many studies have underlined the ability of circulating and infiltrating monocytes to clear vascular Aβ microaggregates and parenchymal Aβ deposits respectively, which are very important features of AD. On the other hand, microglia are the resident immune cells of the brain and they play multiple physiological roles, including maintenance of the brain’s microenvironment homeostasis. In the injured brain, activated microglia migrate to the inflamed site, where they remove neurotoxic elements by phagocytosis. However, aged resident microglia are less efficient than their circulating sister immune cells in eliminating Aβ deposits from the brain parenchyma, thus underlining the importance to further investigate the functions of these innate immune cells in AD. The present review summarizes current knowledge on the role of monocytes and microglia in AD and how these cells can be mobilized to prevent and treat the disease.
         datePublished:2015-04-15T00:00:00Z
         dateModified:2015-04-15T00:00:00Z
         pageStart:1
         pageEnd:10
         license:http://creativecommons.org/publicdomain/zero/1.0/
         sameAs:https://doi.org/10.1186/s13195-015-0125-2
         keywords:
            Microglial Cell
            Cerebral Amyloid Angiopathy
            Perivascular Macrophage
            Human Umbilical Cord Blood Cell
            Resident Microglial Cell
            Neurosciences
            Neurology
            Geriatrics/Gerontology
            Geriatric Psychiatry
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13195-015-0125-2/MediaObjects/13195_2015_125_Fig1_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13195-015-0125-2/MediaObjects/13195_2015_125_Fig2_HTML.gif
         isPartOf:
            name:Alzheimer's Research & Therapy
            issn:
               1758-9193
            volumeNumber:7
            type:
               Periodical
               PublicationVolume
         publisher:
            name:BioMed Central
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Peter Thériault
               affiliation:
                     name:Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University
                     address:
                        name:Department of Molecular Medicine, Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University, Quebec City, Canada
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Ayman ElAli
               affiliation:
                     name:Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University
                     address:
                        name:Department of Molecular Medicine, Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University, Quebec City, Canada
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Serge Rivest
               affiliation:
                     name:Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University
                     address:
                        name:Department of Molecular Medicine, Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University, Quebec City, Canada
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:The dynamics of monocytes and microglia in Alzheimer’s disease
      description:Alzheimer’s disease (AD) is the most common neurodegenerative disorder affecting older people worldwide. It is a progressive disorder mainly characterized by the presence of amyloid-beta (Aβ) plaques and neurofibrillary tangles within the brain parenchyma. It is now well accepted that neuroinflammation constitutes an important feature in AD, wherein the exact role of innate immunity remains unclear. Although innate immune cells are at the forefront to protect the brain in the presence of toxic molecules including Aβ, this natural defense mechanism seems insufficient in AD patients. Monocytes are a key component of the innate immune system and they play multiple roles, such as the removal of debris and dead cells via phagocytosis. These cells respond quickly and mobilize toward the inflamed site, where they proliferate and differentiate into macrophages in response to inflammatory signals. Many studies have underlined the ability of circulating and infiltrating monocytes to clear vascular Aβ microaggregates and parenchymal Aβ deposits respectively, which are very important features of AD. On the other hand, microglia are the resident immune cells of the brain and they play multiple physiological roles, including maintenance of the brain’s microenvironment homeostasis. In the injured brain, activated microglia migrate to the inflamed site, where they remove neurotoxic elements by phagocytosis. However, aged resident microglia are less efficient than their circulating sister immune cells in eliminating Aβ deposits from the brain parenchyma, thus underlining the importance to further investigate the functions of these innate immune cells in AD. The present review summarizes current knowledge on the role of monocytes and microglia in AD and how these cells can be mobilized to prevent and treat the disease.
      datePublished:2015-04-15T00:00:00Z
      dateModified:2015-04-15T00:00:00Z
      pageStart:1
      pageEnd:10
      license:http://creativecommons.org/publicdomain/zero/1.0/
      sameAs:https://doi.org/10.1186/s13195-015-0125-2
      keywords:
         Microglial Cell
         Cerebral Amyloid Angiopathy
         Perivascular Macrophage
         Human Umbilical Cord Blood Cell
         Resident Microglial Cell
         Neurosciences
         Neurology
         Geriatrics/Gerontology
         Geriatric Psychiatry
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13195-015-0125-2/MediaObjects/13195_2015_125_Fig1_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13195-015-0125-2/MediaObjects/13195_2015_125_Fig2_HTML.gif
      isPartOf:
         name:Alzheimer's Research & Therapy
         issn:
            1758-9193
         volumeNumber:7
         type:
            Periodical
            PublicationVolume
      publisher:
         name:BioMed Central
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Peter Thériault
            affiliation:
                  name:Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University
                  address:
                     name:Department of Molecular Medicine, Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University, Quebec City, Canada
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Ayman ElAli
            affiliation:
                  name:Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University
                  address:
                     name:Department of Molecular Medicine, Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University, Quebec City, Canada
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Serge Rivest
            affiliation:
                  name:Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University
                  address:
                     name:Department of Molecular Medicine, Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University, Quebec City, Canada
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:Alzheimer's Research & Therapy
      issn:
         1758-9193
      volumeNumber:7
Organization:
      name:BioMed Central
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University
      address:
         name:Department of Molecular Medicine, Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University, Quebec City, Canada
         type:PostalAddress
      name:Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University
      address:
         name:Department of Molecular Medicine, Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University, Quebec City, Canada
         type:PostalAddress
      name:Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University
      address:
         name:Department of Molecular Medicine, Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University, Quebec City, Canada
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Peter Thériault
      affiliation:
            name:Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University
            address:
               name:Department of Molecular Medicine, Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University, Quebec City, Canada
               type:PostalAddress
            type:Organization
      name:Ayman ElAli
      affiliation:
            name:Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University
            address:
               name:Department of Molecular Medicine, Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University, Quebec City, Canada
               type:PostalAddress
            type:Organization
      name:Serge Rivest
      affiliation:
            name:Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University
            address:
               name:Department of Molecular Medicine, Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University, Quebec City, Canada
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Molecular Medicine, Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University, Quebec City, Canada
      name:Department of Molecular Medicine, Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University, Quebec City, Canada
      name:Department of Molecular Medicine, Neuroscience Laboratory, CHU de Québec Research Center (CHUL), Faculty of Medicine, Laval University, Quebec City, Canada

External Links {🔗}(284)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref

5.09s.

LINK . SPRINGER . COM {}