Evidence map›Paper›PMID 35994032›Full record

ArticleHuman molecular genetics2022

From bugs to bedside: functional annotation of human genetic variation for neurological disorders using invertebrate models.

Melanie Mew, Kim A Caldwell, Guy A Caldwell

Open access · greenAbstract read
In one paragraph

Article in Human molecular genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. UtilizingJournal of developmental biology · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Attenuation of Dopaminergic Neurodegeneration in aJournal of developmental biology · 2023
    Article
  7. Article
  8. Integrated regulation of dopaminergic and epigenetic effectors of neuroprotection in Parkinson's disease models.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  9. Human Molecular Genetics Review Issue 2022.Human molecular genetics · 2022
    Article
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 at 1 institution in 2 countries.

Melanie MewDepartment of Biological Sciences, The University of Alabama, Tuscaloosa, AL 35487, USA.ORCID 0000-0001-5371-4064
Kim A CaldwellDepartment of Biological Sciences, The University of Alabama, Tuscaloosa, AL 35487, USA.ORCID 0000-0003-1580-6122
Guy A CaldwellDepartment of Biological Sciences, The University of Alabama, Tuscaloosa, AL 35487, USA.ORCID 0000-0002-8283-9090
University of Alabama · US

Funding

Functional Analysis Of The Intersection of Mitochondrial Stress and NeurodegenerationR15NS106460 · NINDS · UNIVERSITY OF ALABAMA IN TUSCALOOSA · PI CALDWELL, KIM A · 2018 to 2020
$556k
MECHANISMS AND MODULATORS OF RESILIENCE TO DOPAMINERGIC NEURODEGENERATIONR15NS104857 · NINDS · UNIVERSITY OF ALABAMA IN TUSCALOOSA · PI CALDWELL, GUY A · 2018 to 2018
$422k
NIH HHS R15NS104857NINDS NIH HHS R15 NS104857NINDS NIH HHS R15 NS106460
6 · The paper itself

Abstract

The exponential accumulation of DNA sequencing data has opened new avenues for discovering the causative roles of single-nucleotide polymorphisms (SNPs) in neurological diseases. The opportunities emerging from this are staggering, yet only as good as our abilities to glean insights from this surplus of information. Whereas computational biology continues to improve with respect to predictions and molecular modeling, the differences between in silico and in vivo analysis remain substantial. Invertebrate in vivo model systems represent technically advanced, experimentally mature, high-throughput, efficient and cost-effective resources for investigating a disease. With a decades-long track record of enabling investigators to discern function from DNA, fly (Drosophila) and worm (Caenorhabditis elegans) models have never been better poised to serve as living engines of discovery. Both of these animals have already proven useful in the classification of genetic variants as either pathogenic or benign across a range of neurodevelopmental and neurodegenerative disorders-including autism spectrum disorders, ciliopathies, amyotrophic lateral sclerosis, Alzheimer's and Parkinson's disease. Pathogenic SNPs typically display distinctive phenotypes in functional assays when compared with null alleles and frequently lead to protein products with gain-of-function or partial loss-of-function properties that contribute to neurological disease pathogenesis. The utility of invertebrates is logically limited by overt differences in anatomical and physiological characteristics, and also the evolutionary distance in genome structure. Nevertheless, functional annotation of disease-SNPs using invertebrate models can expedite the process of assigning cellular and organismal consequences to mutations, ascertain insights into mechanisms of action, and accelerate therapeutic target discovery and drug development for neurological conditions.

Indexed as

Neurodegenerative DiseasesParkinson DiseaseAnimalsCaenorhabditis elegansDisease Models, AnimalDrosophilaHumansMutationPolymorphism, Single Nucleotide

Identifiers

PMID35994032
PMCPMC9585664
OpenAlexW4292648751

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.