Evidence map›Paper›PMID 12057909›Full record

ArticleThe American journal of pathology2002

Signature tau neuropathology in gray and white matter of corticobasal degeneration.

Mark S Forman, Victoria Zhukareva, Catherine Bergeron, Steven S-M Chin, Murray Grossman, Chris Clark, Virginia M-Y Lee, John Q Trojanowski

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

70 citing papers in PubMed, 1 synthesis or guideline pooled it, 148 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Differences in the soluble and insoluble proteome between primary tauopathies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  6. Primary retinal tauopathy: A tauopathy with a distinct molecular pattern.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Evaluation of [Brain communications · 2021
    Article
  19. Review
  20. Article

10 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Mark S FormanCenter for Neurodegenerative Disease Research and the Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
Victoria Zhukareva
Catherine Bergeron
Steven S-M Chin
Murray Grossman
Chris Clark
Virginia M-Y Lee
John Q Trojanowski
University of Pennsylvania · USColumbia University · USUniversity of Toronto · CA

Funding

Mechanisms of Tau-Based NeurodegenerationK08AG020073 · NIA · UNIVERSITY OF PENNSYLVANIA · PI FORMAN, MARK S · 2001 to 2005
$624k
NIA NIH HHS AG20073-01NIA NIH HHS K08 AG020073
6 · The paper itself

Abstract

Corticobasal degeneration (CBD) is an adult-onset progressive neurodegenerative disorder characterized by L-dopa-resistant rigidity, focal cortical deficits, and variable dementia. The neuropathological hallmark of CBD is the deposition of filamentous inclusions in neurons and glia composed of hyperphosphorylated tau with only four microtubule-binding repeats (4R-tau). To characterize the regional burden of tau pathology in CBD, we studied 12 brains with the neuropathological diagnosis of CBD using biochemical and histochemical techniques. Eleven brain regions were evaluated including gray and white matter from frontal, parietal, temporal, and occipital lobes and cerebellum as well as basal ganglia. Although the distribution of tau pathology was variable, neuropathological and biochemical data showed a similar burden of tau abnormalities in frontal, temporal, and parietal lobes and basal ganglia of both hemispheres. This included abundant, sarkosyl-insoluble 4R-tau in both gray and white matter of two or more of these cortical regions and basal ganglia, and to a lesser extent, cerebellar white matter. The insoluble tau pathology in gray and white matter showed overlapping but distinct phosphorylated epitopes suggesting cell-type and subcellular localization (ie, cell bodies versus cell processes)-specific differences in tau phosphorylation. In contrast, soluble tau was composed of normal 4R/3R-tau ratios indicating no gross abnormality in tau splicing. Thus, although clinically heterogeneous, CBD is a distinct lobar and basal ganglionic tauopathy with selective aggregation of 4R-tau.

Indexed as

AgedBasal GangliaBlotting, WesternCerebellumCerebral CortexFemaleHumansImmunohistochemistryMaleMiddle AgedPhenotypeTauopathiestau Proteinstau Proteins

Identifiers

PMID12057909
PMCPMC1850831
OpenAlexW2039405182

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.