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  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
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We are analyzing https://link.springer.com/article/10.1007/s11481-009-9163-5.

Title:
Life and Death of Microglia | Journal of Neuroimmune Pharmacology
Description:
The importance of microglial cells in the maintenance of a well-functioning central nervous system (CNS) cannot be overstated. As descendants of the myelomonocytic lineage they are industrious housekeepers and watchful sentries that safeguard a homeostatic environment through a number of mechanisms designed to provide protection of fastidious neurons at all times. Microglia become particularly active after homeostasis has been perturbed by physical injury or other insults and they enter into a state of activation which is determined largely by the nature and severity of the lesion. Microglial activation is the main cellular event in acute neuroinflammation and essential for wound healing in the CNS. Recent studies from this laboratory have been focused on microglia in the aging brain and identified structural abnormalities, termed microglial dystrophy, that are consistent with cell senescence and progress to a form of accidental cell death that is marked by cytoplasmic degeneration and has been termed cytorrhexis. Cytorrhexis of microglia is infrequent in the normally aged human brain and non-detectable in aged rodents, but its occurrence increases dramatically during neurodegenerative conditions, including Alzheimer’s disease (AD) in humans and motoneuron disease in transgenic rats. The identification of degenerating microglia has given rise to a novel theory of AD pathogenesis, the microglial dysfunction hypothesis, which views the loss of microglial neuroprotection as a central event in neurodegenerative disease development.
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 7,642,828 visitors per month in the current month.

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

We see no obvious way the site makes money.

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 {🔍}

article, google, scholar, pubmed, microglial, microglia, brain, streit, cells, res, neurosci, glia, disease, aging, neurol, cns, rat, alzheimers, injury, activation, cell, graeber, xue, activated, exp, privacy, cookies, content, journal, neuroinflammation, aged, development, access, kreutzberg, rev, neuropathol, normal, developing, macrophages, function, information, publish, search, death, wolfgang, system, nature, senescence, degeneration, human,

Topics {✒️}

month download article/chapter main cellular event confocal time-lapse analysis aging brain—bad news situ dna fragmentation full article pdf privacy choices/manage cookies excitotoxic cns injury hoyt rf jr adult subventricular zone increased amyloid production thrombin-induced activation cell senescence ed1-expressing cells termed microglial dystrophy resting microglial cells amoeboid microglial cell neuronal network plasticity activated microglial cells peripheral nerve injury traumatic brain injury neuroimmune pharmacology aims occurrence increases dramatically adult visual system adult mouse brain multinucleated giant cells aging-related neurobehavioral microglial senescence article streit amoeboid microglial cells accidental cell death postnatal rat brain european economic area identified structural abnormalities high proliferative potential parkinsonian substantia nigra alpha-synuclein deposition monoclonal antibodies ed1 dicicco-bloom em colony-stimulating factors semple-rowland sl periventricular white matter tumor necrosis factor glutamate transporter glt-1 fetal cerebral cortex cytokine mrna profiles long-term accumulation marshall gp 2nd white matter weeks health grant ag023665

Questions {❓}

  • Jones LL, Banati RB, Graeber MB, Bonfanti L, Raivich G, Kreutzberg GW (1997) Population control of microglia: does apoptosis play a role?
  • Schwartz M, Butovsky O, Bruck W, Hanisch UK (2006) Microglial phenotype: is the commitment reversible?
  • Streit WJ (2006) Microglial senescence: does the brain's immune system have an expiration date?
  • Streit WJ, Miller KR, Lopes KO, Njie E (2008) Microglial degeneration in the aging brain—bad news for neurons?

Schema {🗺️}

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         description:The importance of microglial cells in the maintenance of a well-functioning central nervous system (CNS) cannot be overstated. As descendants of the myelomonocytic lineage they are industrious housekeepers and watchful sentries that safeguard a homeostatic environment through a number of mechanisms designed to provide protection of fastidious neurons at all times. Microglia become particularly active after homeostasis has been perturbed by physical injury or other insults and they enter into a state of activation which is determined largely by the nature and severity of the lesion. Microglial activation is the main cellular event in acute neuroinflammation and essential for wound healing in the CNS. Recent studies from this laboratory have been focused on microglia in the aging brain and identified structural abnormalities, termed microglial dystrophy, that are consistent with cell senescence and progress to a form of accidental cell death that is marked by cytoplasmic degeneration and has been termed cytorrhexis. Cytorrhexis of microglia is infrequent in the normally aged human brain and non-detectable in aged rodents, but its occurrence increases dramatically during neurodegenerative conditions, including Alzheimer’s disease (AD) in humans and motoneuron disease in transgenic rats. The identification of degenerating microglia has given rise to a novel theory of AD pathogenesis, the microglial dysfunction hypothesis, which views the loss of microglial neuroprotection as a central event in neurodegenerative disease development.
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