Evidence map›Paper›PMID 28545550›Full record

ReviewHuman genomics2017

Genetic variation in neurodegenerative diseases and its accessibility in the model organism Caenorhabditis elegans.

Yiru Anning Wang, Jan Edward Kammenga, Simon Crawford Harvey

Abstract readReview
In one paragraph

Review in Human genomics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 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

3 authors.

Yiru Anning WangBiomolecular Research Group, School of Human and Life Science, Canterbury Christ Church University, Canterbury, CT1 1QU, UK.
Jan Edward KammengaLaboratory of Nematology, Wageningen University, 6708 PB, Wageningen, The Netherlands.
Simon Crawford HarveyBiomolecular Research Group, School of Human and Life Science, Canterbury Christ Church University, Canterbury, CT1 1QU, UK. simon.harvey@canterbury.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeurodegenerative diseases (NGDs) such as Alzheimer's and Parkinson's are debilitating and largely untreatable conditions strongly linked to age. The clinical, neuropathological, and genetic components of NGDs indicate that neurodegeneration is a complex trait determined by multiple genes and by the environment. MAIN BODY: The symptoms of NGDs differ among individuals due to their genetic background, and this variation affects the onset and progression of NGD and NGD-like states. Such genetic variation affects the molecular and cellular processes underlying NGDs, leading to differential clinical phenotypes. So far, we have a limited understanding of the mechanisms of individual background variation. Here, we consider how variation between genetic backgrounds affects the mechanisms of aging and proteostasis in NGD phenotypes. We discuss how the nematode Caenorhabditis elegans can be used to identify the role of variation between genetic backgrounds. Additionally, we review advances in C. elegans methods that can facilitate the identification of NGD regulators and/or networks.

conclusionGenetic variation both in disease genes and in regulatory factors that modulate onset and progression of NGDs are incompletely understood. The nematode C. elegans represents a valuable system in which to address such questions.

Indexed as

Disease Models, AnimalGenetic VariationAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsHumansNeurodegenerative DiseasesPhenotypeCaenorhabditis elegans ProteinsC. elegansNatural variationNeurodegenerative diseasesQuantitative genetics

Identifiers

PMID28545550
PMCPMC5445269

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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.