Evidence map›Paper›PMID 10525997›Full record

ReviewJournal of neurology1999

Neuropathologic differentiation of progressive supranuclear palsy and corticobasal degeneration.

D W Dickson

Registry-linked trialOpen access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Journal of neurology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01056965 (A 12 Week Randomized, Double Blind, Placebo-Controlled Pilot Study of Davunetide), which is not on this map. Cited by 165 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
165citing papers in PubMed, 4 pooled it
5.3field-weighted citation impact, top 4% 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.

NCT01056965 phase1completednot on this mapstarted 2010, after this paper: background citation

A 12 Week Randomized, Double Blind, Placebo-Controlled Pilot Study of Davunetide (NAP, AL-108) in Predicted Tauopathies

TypeinterventionalSponsorUniversity of California, San FranciscoRan2010 to 2012Enrolled12ConditionsPredicted Tauopathies, Including, Progressive Supranuclear Palsy, Frontotemporal Dementia With Parkinsonism Linked to Chromosome 17, Corticobasal Degeneration SyndromeArmsdavunetide (AL-108, NAP), Placebo nasal spray
3 · Its place in the literature

Who cites it

165 citing papers in PubMed, 4 syntheses or guidelines pooled it, 412 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Genotype-Phenotype Relations for the Atypical Parkinsonism Genes: MDSGene Systematic Review.Movement disorders : official journal of the Movement Disorder Society · 2021
    Pooled it
  4. Which ante mortem clinical features predict progressive supranuclear palsy pathology?Movement disorders : official journal of the Movement Disorder Society · 2017
    Pooled it
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  17. Subtracting First Principal Component May Improve 4R Tau Detectability on [Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2026
    Article
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105 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

1 author at 1 institution in 1 country.

D W DicksonDepartment of Pathology, Mayo Clinic Jacksonville, 4500 San Pablo Road, Jacksonville, FL 32224, USA, Email: dickson.dennis@mayo.edu.
Jacksonville College · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) are usually sporadic multi-system degenerations associated with filamentous tau inclusions in neurons and glia. As such they can be considered sporadic tauopathies in contrast to familial tauopathies linked to mutations in the tau gene. Mutations have not been found in the tau gene in either PSP or CBD. The clinical syndromes and neuroimaging of typical cases of PSP and CBD are distinct; however, atypical cases are described that have overlapping clinical and pathologic features. Both PSP and CBD have similar biochemical alterations in the tau protein, with the abnormal tau protein containing predominantly four-repeat tau. While there is overlap in the pathology in PSP and CBD, there are sufficient differences to continue the present day trend to consider these separate disorders. Several important pathologic features differentiate PSP from CBD. Ballooned neurons are frequent and nearly a sine qua non for CBD, but they are found in PSP at a frequency similar to that of other neurodegenerative diseases, such as Alzheimer's disease. Astrocytic lesions are different, with tufted astrocytes found in motor cortex and striatum in PSP and astrocytic plaques in focal atrophic cortices in CBD. The most characteristic neuronal tau pathology in CBD is wispy, fine filamentous inclusions within neuronal cell bodies, while affected neurons in PSP have compact, dense filamentous aggregates characteristic of globose neurofibrillary tangles. Thread-like processes in gray and white matter are much more numerous and widespread in CBD than in PSP. The brunt of the pathology in CBD is in the cerebrum, while the basal ganglia, diencephalon and brainstem are the targets of PSP. Further clinicopathologic studies will refine our understanding of these disorders and open the possibility that common etiologic factors may be identified for these unusual sporadic tauopathies.

Indexed as

Basal GangliaCerebral CortexHumansNerve DegenerationSupranuclear Palsy, Progressive

Identifiers

PMID10525997
OpenAlexW2075964404

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.