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DOI . ORG {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Doi.org Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
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We began analyzing https://link.springer.com/article/10.1007/s00401-009-0532-1, but it redirected us to https://link.springer.com/article/10.1007/s00401-009-0532-1. The analysis below is for the second page.

Title[redir]:
Classification and basic pathology of Alzheimer disease | Acta Neuropathologica
Description:
The lesions of Alzheimer disease include accumulation of proteins, losses of neurons and synapses, and alterations related to reactive processes. Extracellular Aβ accumulation occurs in the parenchyma as diffuse, focal or stellate deposits. It may involve the vessel walls of arteries, veins and capillaries. The cases in which the capillary vessel walls are affected have a higher probability of having one or two apoε 4 alleles. Parenchymal as well as vascular Aβ deposition follows a stepwise progression. Tau accumulation, probably the best histopathological correlate of the clinical symptoms, takes three aspects: in the cell body of the neuron as neurofibrillary tangle, in the dendrites as neuropil threads, and in the axons forming the senile plaque neuritic corona. The progression of tau pathology is stepwise and stereotyped from the entorhinal cortex, through the hippocampus, to the isocortex. The neuronal loss is heterogeneous and area-specific. Its mechanism is still discussed. The timing of the synaptic loss, probably linked to Aβ peptide itself, maybe as oligomers, is also controversial. Various clinico-pathological types of Alzheimer disease have been described, according to the type of the lesions (plaque only and tangle predominant), the type of onset (focal onset), the cause (genetic or sporadic) and the associated lesions (Lewy bodies, vascular lesions, hippocampal sclerosis, TDP-43 inclusions and argyrophilic grain disease).

Matching Content Categories {📚}

  • Education
  • Science
  • Health & Fitness

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of doi.org 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.
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How Does Doi.org Make Money? {💸}

We can't figure out the monetization strategy.

Some websites aren't about earning revenue; they're built to connect communities or raise awareness. There are numerous motivations behind creating websites. This might be one of them. Doi.org might be making money, but it's not detectable how they're doing it.

Keywords {🔍}

google, scholar, pubmed, cas, disease, alzheimers, neuropathol, alzheimer, neurol, brain, acta, amyloid, dois, dementia, neurobiol, aging, neurofibrillary, braak, doi, pathology, duyckaerts, tau, abeta, senile, plaques, loss, exp, neurosci, protein, tangles, human, hauw, pathol, neuronal, cerebral, ann, study, dickson, doibf, jellinger, deposits, plaque, doiana, res, neurology, sci, neurons, betaamyloid, cognitive, smith,

Topics {✒️}

benoît delatour & marie-claude potier month download article/chapter n-terminal-truncated abeta deposits n-terminal truncated fragments extensive protein cross-linking abeta oligomer-induced aberrations ldl receptor-related protein-1 beta a4-protein deposition characteristic beta-amyloid pathology de la fourniere de la moëlle exogenous soluble beta-amyloid alpha-synuclein brainstem pathology tangle-bearing nerve cells beta-amyloid protein immunoreactivity diffuse amyloid beta-protein long-term effects beta-protein/a4 deposits amyloid beta-peptide levels amyloid-beta peptide composition neuronal a-beta peptide beta-protein deposition staging peptide-related cerebral amyloidosis intraneuronal beta-amyloid aggregates cell-specific pathology isolates 4r tau-specific immunohistochemistry neurofibrillary tangle-bearing neurons van de steeg van de voorde ter laak hj vascular beta-amyloid disorders acetylated alpha-tubulin immunoreactivity de waal rmw van der kolk early neurodegenerative event presenilin-1 double-transgenic mice age-related plaque morphology aging-mci-ad continuum mutation-specific pathologic phenotype cerebral amyloid angiopathy voxel-based morphometry study spires-jones tl de vos ra beta-amyloid protein amyloid beta-protein alzheimer beta-amyloid plaques human entorhinal cortex amyloid beta plaque privacy choices/manage cookies beta-amyloid burden

Questions {❓}

  • Duyckaerts C, Hauw JJ (1997) Prevalence, incidence and duration of Braak’s stages in the general population: can we know?

Schema {🗺️}

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         headline:Classification and basic pathology of Alzheimer disease
         description:The lesions of Alzheimer disease include accumulation of proteins, losses of neurons and synapses, and alterations related to reactive processes. Extracellular Aβ accumulation occurs in the parenchyma as diffuse, focal or stellate deposits. It may involve the vessel walls of arteries, veins and capillaries. The cases in which the capillary vessel walls are affected have a higher probability of having one or two apoε 4 alleles. Parenchymal as well as vascular Aβ deposition follows a stepwise progression. Tau accumulation, probably the best histopathological correlate of the clinical symptoms, takes three aspects: in the cell body of the neuron as neurofibrillary tangle, in the dendrites as neuropil threads, and in the axons forming the senile plaque neuritic corona. The progression of tau pathology is stepwise and stereotyped from the entorhinal cortex, through the hippocampus, to the isocortex. The neuronal loss is heterogeneous and area-specific. Its mechanism is still discussed. The timing of the synaptic loss, probably linked to Aβ peptide itself, maybe as oligomers, is also controversial. Various clinico-pathological types of Alzheimer disease have been described, according to the type of the lesions (plaque only and tangle predominant), the type of onset (focal onset), the cause (genetic or sporadic) and the associated lesions (Lewy bodies, vascular lesions, hippocampal sclerosis, TDP-43 inclusions and argyrophilic grain disease).
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      headline:Classification and basic pathology of Alzheimer disease
      description:The lesions of Alzheimer disease include accumulation of proteins, losses of neurons and synapses, and alterations related to reactive processes. Extracellular Aβ accumulation occurs in the parenchyma as diffuse, focal or stellate deposits. It may involve the vessel walls of arteries, veins and capillaries. The cases in which the capillary vessel walls are affected have a higher probability of having one or two apoε 4 alleles. Parenchymal as well as vascular Aβ deposition follows a stepwise progression. Tau accumulation, probably the best histopathological correlate of the clinical symptoms, takes three aspects: in the cell body of the neuron as neurofibrillary tangle, in the dendrites as neuropil threads, and in the axons forming the senile plaque neuritic corona. The progression of tau pathology is stepwise and stereotyped from the entorhinal cortex, through the hippocampus, to the isocortex. The neuronal loss is heterogeneous and area-specific. Its mechanism is still discussed. The timing of the synaptic loss, probably linked to Aβ peptide itself, maybe as oligomers, is also controversial. Various clinico-pathological types of Alzheimer disease have been described, according to the type of the lesions (plaque only and tangle predominant), the type of onset (focal onset), the cause (genetic or sporadic) and the associated lesions (Lewy bodies, vascular lesions, hippocampal sclerosis, TDP-43 inclusions and argyrophilic grain disease).
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         Entorhinal Cortex
         Senile Plaque
         Cerebral Amyloid Angiopathy
         Neuritic Plaque
         Pathology
         Neurosciences
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External Links {🔗}(1051)

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Libraries {📚}

  • Clipboard.js
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Mail Servers:

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CDN Services {📦}

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