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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
  12. Libraries
  13. CDN Services

We are analyzing https://link.springer.com/article/10.1007/s12035-012-8262-0.

Title:
Cell Cycle Activation and Aneuploid Neurons in Alzheimer's Disease | Molecular Neurobiology
Description:
Molecular Neurobiology - Alzheimer
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Science
  • Telecommunications

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 8,280,528 visitors per month in the current month.

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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 has a secret sauce for making money, but we can't detect it yet.

Keywords {🔍}

google, scholar, cas, article, pubmed, disease, brain, alzheimers, cell, dna, human, neurons, chromosome, aneuploidy, neuronal, arendt, content, genet, cells, res, neurosci, cortex, med, cycle, expression, development, purkinje, alzheimer, neurol, rat, death, chromosomal, acta, yang, analysis, increased, neuropathol, biol, chun, yurov, iourov, vorsanova, cerebral, cerebellum, molecular, normal, pnas, science, mol, histochem,

Topics {✒️}

cytophotometrische dns-messungen month download article/chapter van der ploeg cell cycle-related proteins biulleten’ eksperimental’noĭ biologii fast-green histone estimations alpha-synuclein locus triplication linking cell-cycle dysfunction wave-length-scanning method childhood-onset psychotic disorders post-natal dna synthesis genome-wide phylogenetic analysis cell cycle activation chromosome segregation defects neuronal cell death selective neuronal vulnerability age-related neurodegenerative disorders full article pdf cell cycle regulation cell cycle regulators selective cell death privacy choices/manage cookies de la hera amyloid-ß peptide progenitor cell division cell cycle markers cell-cycle mechanisms low-level chromosomal aneuploidy neuronal differentiation control mammalian neuronal cells inversely recapitulates ontogenetic central nervous system measure chromosome instability european economic area mountcastle vb article arendt separate progenitor cells cell division markers oval cell proliferation individual cell nuclei kolichestvo kletok purkin iadrakh kletok purkin cell-cycle kinetics genome sequencing reveals neuronal nuclei polyploid chronic neurodegenerative disorder purkinje cell nuclei] induced gene expression critical molecular events premature centromere division

Questions {❓}

  • Bernocchi G, Redi CA, Scherini E (1979) Feulgen-DNA content of the Purkinje neuron: “diploid” or “tetraploid”?
  • Bregnard A, Knüsel A, Kuenzle CC (1975) Are all the neuronal nuclei polyploid?
  • Herrup K, Yang Y (2007) Cell cycle regulation in the postmitotic neuron: oxymoron or new biology?
  • Swartz FJ, Bhatnagar KP (1981) Are CNS neurons polyploid?
  • Vincent I, Rosado M, Davies P (1996) Mitotic mechanisms in Alzheimer's disease?

Schema {🗺️}

WebPage:
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         headline:Cell Cycle Activation and Aneuploid Neurons in Alzheimer's Disease
         description:Alzheimer's disease (AD) is a chronic neurodegenerative disorder, characterized by synaptic degeneration associated with fibrillar aggregates of the amyloid-ß peptide and the microtubule-associated protein tau. The progression of neurofibrillary degeneration throughout the brain during AD follows a predictive pattern which provides the basis for the neuropathological staging of the disease. This pattern of selective neuronal vulnerability against neurofibrillary degeneration matches the regional degree of neuronal plasticity and inversely recapitulates ontogenetic and phylogenetic brain development which links neurodegenerative cell death to neuroplasticity and brain development. Here, we summarize recent evidence for a loss of neuronal differentiation control as a critical pathogenetic event in AD, associated with a reactivation of the cell cycle and a partial or full replication of DNA giving rise to neurons with a content of DNA above the diploid level. Neurons with an aneuploid set of chromosomes are also present at a low frequency in the normal brain where they appear to be well tolerated. In AD, however, where the number of aneuploid neurons is highly increased, a rather selective cell death of neurons with this chromosomal aberrancy occurs. This finding add aneuploidy to the list of critical molecular events that are shared between neurodegeneration and oncogenesis. It defines a molecular signature for neuronal vulnerability and directs our attention to a failure of neuronal differentiation control as a critical pathogenetic event and potential therapeutic target in AD.
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            Cell Biology
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      headline:Cell Cycle Activation and Aneuploid Neurons in Alzheimer's Disease
      description:Alzheimer's disease (AD) is a chronic neurodegenerative disorder, characterized by synaptic degeneration associated with fibrillar aggregates of the amyloid-ß peptide and the microtubule-associated protein tau. The progression of neurofibrillary degeneration throughout the brain during AD follows a predictive pattern which provides the basis for the neuropathological staging of the disease. This pattern of selective neuronal vulnerability against neurofibrillary degeneration matches the regional degree of neuronal plasticity and inversely recapitulates ontogenetic and phylogenetic brain development which links neurodegenerative cell death to neuroplasticity and brain development. Here, we summarize recent evidence for a loss of neuronal differentiation control as a critical pathogenetic event in AD, associated with a reactivation of the cell cycle and a partial or full replication of DNA giving rise to neurons with a content of DNA above the diploid level. Neurons with an aneuploid set of chromosomes are also present at a low frequency in the normal brain where they appear to be well tolerated. In AD, however, where the number of aneuploid neurons is highly increased, a rather selective cell death of neurons with this chromosomal aberrancy occurs. This finding add aneuploidy to the list of critical molecular events that are shared between neurodegeneration and oncogenesis. It defines a molecular signature for neuronal vulnerability and directs our attention to a failure of neuronal differentiation control as a critical pathogenetic event and potential therapeutic target in AD.
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         Chromosome segregation
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         Neurobiology
         Cell Biology
         Neurology
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External Links {🔗}(478)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
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CDN Services {📦}

  • Crossref

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