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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
  8. Questions
  9. Schema
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We are analyzing https://link.springer.com/article/10.1007/s00401-015-1526-9.

Title:
Pathological α-synuclein distribution in subjects with coincident Alzheimer’s and Lewy body pathology | Acta Neuropathologica
Description:
We investigated the distribution patterns of Lewy body-related pathology (LRP) and the effect of coincident Alzheimer disease (AD) pathology using a data-driven clustering approach that identified groups with different LRP pathology distributions without any diagnostic or researcher’s input in two cohorts including: Parkinson disease patients without (PD, n = 141) and with AD (PD-AD, n = 80), dementia with Lewy bodies subjects without AD (DLB, n = 13) and demented subjects with AD and LRP pathology (Dem-AD-LB, n = 308). The Dem-AD-LB group presented two LRP patterns, olfactory-amygdala and limbic LRP with negligible brainstem pathology, that were absent in the PD groups, which are not currently included in the DLB staging system and lacked extracranial LRP as opposed to the PD group. The Dem-AD-LB individuals showed relative preservation of substantia nigra cells and dopamine active transporter in putamen. PD cases with AD pathology showed increased LRP. The cluster with occipital LRP was associated with non-AD type dementia clinical diagnosis in the Dem-AD-LB group and a faster progression to dementia in the PD groups. We found that (1) LRP pathology in Dem-AD-LB shows a distribution that differs from PD, without significant brainstem or extracranial LRP in initial phases; (2) coincident AD pathology is associated with increased LRP in PD indicating an interaction; (3) LRP and coincident AD pathology independently predict progression to dementia in PD, and (4) evaluation of LRP needs to acknowledge different LRP spreading patterns and evaluate substantia nigra integrity in the neuropathological assessment and consider the implications of neuropathological heterogeneity for clinical and biomarker characterization.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {šŸ“š}

  • Education
  • Science
  • Health & Fitness

Content Management System {šŸ“}

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 {šŸ“ˆ}

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? {šŸ’ø}

We see no obvious way the site makes money.

Not all websites are made for profit; some exist to inform or educate users. Or any other reason why people make websites. And this might be the case. Link.springer.com might have a hidden revenue stream, but it's not something we can detect.

Keywords {šŸ”}

pubmed, article, google, scholar, disease, pathology, central, parkinsons, cas, alzheimers, dementia, acta, lewy, lrp, neuropathol, braak, research, neurology, brain, institute, diagnosis, dois, body, toledo, neuropathological, beach, bodies, staging, clinical, assessment, neurol, aging, national, usa, subjects, coincident, access, arizona, disord, del, tredici, dickson, alphasynuclein, department, privacy, cookies, content, distribution, december, lee,

Topics {āœ’ļø}

month download article/chapter pathological α-synuclein distribution dem-ad-lb group presented dem-ad-lb shows dem-ad-lb group central cholinergic integrity data-driven clustering approach lewy body-related pathology full article pdf dem-ad-lb body donation program coincident neuropathological diseases privacy choices/manage cookies alpha-synuclein pathology lewy bodies subjects article toledo lewy body pathology lewy body variant lewy-related pathology toledo jb clinico-pathological study disease core center lewy body disorders brain pathology related beach tg cerad neuropathology protocol pallavi gopal pennsylvania medical center coincident ad pathology consensus recommendations transgenic mouse brain author information authors article log nervous system pathology european economic area substantia nigra cells dopamine active transporter jansen steur en cingulate island sign pdd boundary issues dorsal root ganglia dickson dw disease-related pathology invited article conditions privacy policy beta-amyloid morphotypes beta-amyloid fibrils negligible brainstem pathology multimodal biomarker correlates population-based cohort

Questions {ā“}

  • Aarsland D, Ballard CG, Halliday G (2004) Are Parkinson’s disease with dementia and dementia with Lewy bodies the same entity?
  • Berg D, Postuma RB, Bloem B, Chan P, Dubois B, Gasser T et al (2014) Time to redefine PD?
  • Tsuboi Y, Dickson DW (2005) Dementia with Lewy bodies and Parkinson’s disease with dementia: are they different?

Schema {šŸ—ŗļø}

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         headline:Pathological α-synuclein distribution in subjects with coincident Alzheimer’s and Lewy body pathology
         description:We investigated the distribution patterns of Lewy body-related pathology (LRP) and the effect of coincident Alzheimer disease (AD) pathology using a data-driven clustering approach that identified groups with different LRP pathology distributions without any diagnostic or researcher’s input in two cohorts including: Parkinson disease patients without (PD, nĀ =Ā 141) and with AD (PD-AD, nĀ =Ā 80), dementia with Lewy bodies subjects without AD (DLB, nĀ =Ā 13) and demented subjects with AD and LRP pathology (Dem-AD-LB, nĀ =Ā 308). The Dem-AD-LB group presented two LRP patterns, olfactory-amygdala and limbic LRP with negligible brainstem pathology, that were absent in the PD groups, which are not currently included in the DLB staging system and lacked extracranial LRP as opposed to the PD group. The Dem-AD-LB individuals showed relative preservation of substantia nigra cells and dopamine active transporter in putamen. PD cases with AD pathology showed increased LRP. The cluster with occipital LRP was associated with non-AD type dementia clinical diagnosis in the Dem-AD-LB group and a faster progression to dementia in the PD groups. We found that (1) LRP pathology in Dem-AD-LB shows a distribution that differs from PD, without significant brainstem or extracranial LRP in initial phases; (2) coincident AD pathology is associated with increased LRP in PD indicating an interaction; (3) LRP and coincident AD pathology independently predict progression to dementia in PD, and (4) evaluation of LRP needs to acknowledge different LRP spreading patterns and evaluate substantia nigra integrity in the neuropathological assessment and consider the implications of neuropathological heterogeneity for clinical and biomarker characterization.
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      headline:Pathological α-synuclein distribution in subjects with coincident Alzheimer’s and Lewy body pathology
      description:We investigated the distribution patterns of Lewy body-related pathology (LRP) and the effect of coincident Alzheimer disease (AD) pathology using a data-driven clustering approach that identified groups with different LRP pathology distributions without any diagnostic or researcher’s input in two cohorts including: Parkinson disease patients without (PD, nĀ =Ā 141) and with AD (PD-AD, nĀ =Ā 80), dementia with Lewy bodies subjects without AD (DLB, nĀ =Ā 13) and demented subjects with AD and LRP pathology (Dem-AD-LB, nĀ =Ā 308). The Dem-AD-LB group presented two LRP patterns, olfactory-amygdala and limbic LRP with negligible brainstem pathology, that were absent in the PD groups, which are not currently included in the DLB staging system and lacked extracranial LRP as opposed to the PD group. The Dem-AD-LB individuals showed relative preservation of substantia nigra cells and dopamine active transporter in putamen. PD cases with AD pathology showed increased LRP. The cluster with occipital LRP was associated with non-AD type dementia clinical diagnosis in the Dem-AD-LB group and a faster progression to dementia in the PD groups. We found that (1) LRP pathology in Dem-AD-LB shows a distribution that differs from PD, without significant brainstem or extracranial LRP in initial phases; (2) coincident AD pathology is associated with increased LRP in PD indicating an interaction; (3) LRP and coincident AD pathology independently predict progression to dementia in PD, and (4) evaluation of LRP needs to acknowledge different LRP spreading patterns and evaluate substantia nigra integrity in the neuropathological assessment and consider the implications of neuropathological heterogeneity for clinical and biomarker characterization.
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         Alzheimer disease
         Parkinson disease
         Dementia with Lewy bodies
         Neuropathology
         Diagnosis
         Classification
         Pathology
         Neurosciences
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