Cited by 311Alzheimer's disease research and treatmentsGenetics, Aging, and Longevity in Model OrganismsNeurobiology and Insect Physiology Research

Use of Caenorhabditis elegans as a model to study Alzheimer’s disease and other neurodegenerative diseases

Open access
Alexander, Adanna G., Marfil, Vanessa, Li, Chris·2014·Frontiers in Genetics

Abstract

Advances in research and technology has increased our quality of life, allowed us to combat diseases, and achieve increased longevity. Unfortunately, increased longevity is accompanied by a rise in the incidences of age-related diseases such as Alzheimer's disease (AD). AD is the sixth leading cause of death, and one of the leading causes of dementia amongst the aged population in the USA. It is a progressive neurodegenerative disorder, characterized by the prevalence of extracellular Aβ plaques and intracellular neurofibrillary tangles, derived from the proteolysis of the amyloid precursor protein (APP) and the hyperphosphorylation of microtubule-associated protein tau, respectively. Despite years of extensive research, the molecular mechanisms that underlie the pathology of AD remain unclear. Model organisms, such as the nematode, Caenorhabditis elegans, present a complementary approach to addressing these questions. C. elegans has many advantages as a model system to study AD and other neurodegenerative diseases. Like their mammalian counterparts, they have complex biochemical pathways, most of which are conserved. Genes in which mutations are correlated with AD have counterparts in C. elegans, including an APP-related gene, apl-1, a tau homolog, ptl-1, and presenilin homologs, such as sel-12 and hop-1. Since the neuronal connectivity in C. elegans has already been established, C. elegans is also advantageous in modeling learning and memory impairments seen during AD. This article addresses the insights C. elegans provide in studying AD and other neurodegenerative diseases. Additionally, we explore the advantages and drawbacks associated with using this model.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.3389/fgene.2014.00279

Cites

320 of 321 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • The most notable example is the lack of Aβ in Drosophila and C. Elegans.

    “The most notable example is the lack of Aβ in Drosophila and C. Elegans [1, 38].”

    From Alzheimer's disease: experimental models and reality (2017) · cites this paper as [1]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

1 of the 322 references couldn’t be matched to a known paper.

Cited by

Sorted by citations

Authors
Alexander, A. G., Marfil, V., & Li, C.
Affiliations
  • The Graduate Center, CUNY (US)
  • City College of New York (US)
Corresponding author
Li, Chris
Venue
Frontiers in Genetics
Published
2014-09-05
Volume
5
Pages
279-279
ISSN
1664-8021 (ISSN-L)
OpenAlex
W1983814182
Cited by
310
References
322
Citations by year
2026: 13 · 2025: 19 · 2024: 38 · 2023: 42 · 2022: 40 · 2021: 35 · 2020: 39 · 2019: 19 · 2018: 23 · 2017: 14 · 2016: 20 · 2015: 6 · 2014: 1 · 2013: 1
FWCI
9.09
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Frontiers in Genetics (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • CUNY Academic Works (City University of New York) (submittedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Science Foundation
  • National Institutes of Health
  • National Institute on Aging (R01AG032042)
  • National Institute of General Medical Sciences (R25GM056833)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurobiology and Insect Physiology Research
Keywords
Alzheimer's disease, Caenorhabditis elegans, neurodegenerative diseases, amyloid plaques, neurofibrillary tangles, amyloid precursor protein, tau hyperphosphorylation, presenilin, learning and memory impairment

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review