Evidence map›Paper›PMID 30847986›Full record

ArticleNeuropathology : official journal of the Japanese Society of Neuropathology2019

Variably protease-sensitive prionopathy mimicking frontotemporal dementia.

Miren Aizpurua, Sashika Selvackadunco, Helen Yull, Christopher M Kipps, James W Ironside, Istvan Bodi

Open access · hybridAbstract readCase Reports
In one paragraph

Article in Neuropathology : official journal of the Japanese Society of Neuropathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

6 citing papers in PubMed, 32 citations in OpenAlex.

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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

6 authors at 4 institutions in 1 country.

Miren AizpuruaClinical Neuropathology, King's College Hospital, NHS Foundation Trust, London, UK.
Sashika SelvackaduncoLondon Neurodegenerative Diseases Brain Bank, IOPPN, London, UK.
Helen YullNational Creutzfeldt-Jakob Disease Research & Surveillance Unit, Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK.
Christopher M KippsWessex Neurological Centre, University Hospital Southampton NHS Foundation Trust, Southampton, UK.
James W IronsideNational Creutzfeldt-Jakob Disease Research & Surveillance Unit, Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK.
Istvan BodiClinical Neuropathology, King's College Hospital, NHS Foundation Trust, London, UK.ORCID https://orcid.org/0000-0002-2533-4758
King's College Hospital NHS Foundation Trust · GBUniversity of Edinburgh · GBBank of England · GBUniversity Hospital Southampton NHS Foundation Trust · GB

Funding

Medical Research Council MR/L016397/1
6 · The paper itself

Abstract

Sporadic prion diseases are fatal neurodegenerative disorders characterized clinically by rapidly progressive dementia and myoclonus. Variably protease-sensitive prionopathy (VPSPr) is a recently identified sporadic human prion disorder that may present with a lengthy atypical clinical history. Here, we describe a case of VPSPr in a patient with a long history of suspected frontotemporal dementia (FTD). A 61-year-old man presented with speech difficulties, including naming objects and constructing multipart sentences, while there was no difficulty in comprehension. Movement abnormalities included slightly jerky pursuit, minor dysmetria of saccades and brisk reflexes. There was no family history of dementia. Later he developed swallowing difficulties and the possibility of FTD with motor neuron disease was suspected. He died at the age of 71 and his brain was donated to the London Neurodegenerative Diseases Brain Bank. The brain (1004 g) showed mild to moderate atrophy, predominantly in the frontal lobe. Histology revealed moderate spongiform microvacuolation mostly affecting the frontal and parietal cortices, but also present focally in the basal ganglia and the cerebellum. Only mild Alzheimer pathology was found by extensive immunohistochemistry, in keeping with BrainNet Europe stage II. Trans-activation response DNA-binding protein 43 kDa and α-synuclein immunostains were negative. Immunostaining for prion protein (PrP) showed granular/synaptic positivity in a patchy distribution, mainly within the deeper cortex, and also revealed microplaques in the cerebellum and basal ganglia. Western blotting confirmed a low molecular weight protease-resistant PrP band with a faint ladder-like pattern in the absence of types 1 and 2 isoforms. These features are diagnostic of VPSPr. VPSPr can mimic various neurodegenerative conditions; diagnosis requires both PrP immunohistochemistry and Western blotting. The presence of patchy spongiform change in the absence of other neurodegenerative pathology should raise suspicion of VPSPr, even in elderly patients with a lengthy clinical history.

Indexed as

AgedBrainDiagnosis, DifferentialEndopeptidase KFrontotemporal DementiaHumansMalePrion DiseasesPrion ProteinsEndopeptidase KPrion ProteinsCreutzfeldt-Jakob diseaseprion diseasesprion proteinprionsvariably protease-sensitive prionopathy

Identifiers

PMID30847986
PMCPMC6778052
OpenAlexW2921588440

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.