Evidence map›Paper›PMID 32604774›Full record

ReviewCells2020

Amyloid Proteins and Peripheral Neuropathy.

Mohammed M H Asiri, Sjoukje Engelsman, Niels Eijkelkamp, Jo W M Höppener

Abstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

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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

4 authors.

Mohammed M H AsiriCenter for Translational Immunology, University Medical Center Utrecht, Utrecht University, 3584 EA Utrecht, The Netherlands.
Sjoukje EngelsmanCenter for Translational Immunology, University Medical Center Utrecht, Utrecht University, 3584 EA Utrecht, The Netherlands.
Niels EijkelkampCenter for Translational Immunology, University Medical Center Utrecht, Utrecht University, 3584 EA Utrecht, The Netherlands.ORCID 0000-0003-0039-7063
Jo W M HöppenerCenter for Translational Immunology, University Medical Center Utrecht, Utrecht University, 3584 EA Utrecht, The Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Painful peripheral neuropathy affects millions of people worldwide. Peripheral neuropathy develops in patients with various diseases, including rare familial or acquired amyloid polyneuropathies, as well as some common diseases, including type 2 diabetes mellitus and several chronic inflammatory diseases. Intriguingly, these diseases share a histopathological feature-deposits of amyloid-forming proteins in tissues. Amyloid-forming proteins may cause tissue dysregulation and damage, including damage to nerves, and may be a common cause of neuropathy in these, and potentially other, diseases. Here, we will discuss how amyloid proteins contribute to peripheral neuropathy by reviewing the current understanding of pathogenic mechanisms in known inherited and acquired (usually rare) amyloid neuropathies. In addition, we will discuss the potential role of amyloid proteins in peripheral neuropathy in some common diseases, which are not (yet) considered as amyloid neuropathies. We conclude that there are many similarities in the molecular and cell biological defects caused by aggregation of the various amyloid proteins in these different diseases and propose a common pathogenic pathway for "peripheral amyloid neuropathies".

Indexed as

Amyloidogenic ProteinsHumansPeripheral Nervous System DiseasesAmyloidogenic Proteinsamyloid neuropathiesamyloidosisamyloid proteinschronic painperipheral neuropathytype 2 diabetes mellitus

Identifiers

PMID32604774
PMCPMC7349787

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.