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Use of Caenorhabditis elegans as a model to study Alzheimer’s disease and other neurodegenerative diseases
Open accessAbstract
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.
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Genetic analysis of age-dependent defects of the Caenorhabditis elegans touch receptor neurons
Pan, C., Peng, C.-Y., Chen, C., & McIntire, S. L. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1011711108 · Cited by 168
αB crystallin and HSP28 are enhanced in the cerebral cortex of patients with Alzheimer's disease
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Flagged first, then by citations
1 of the 322 references couldn’t be matched to a known paper.
Cited by
Sorted by citations
The Amyloid-β Oligomer Hypothesis: Beginning of the Third Decade
Cline, E. N., Bicca, M. A., Viola, K. L., & Klein, W. L. (2018) · Journal of Alzheimer's Disease · doi:10.3233/jad-179941 · Cited by 870
Alzheimer's disease: experimental models and reality
Drummond, E., & Wisniewski, T. (2017) · Acta Neuropathologica · doi:10.1007/s00401-016-1662-x · Cited by 810
The C. elegans model in toxicity testing
Hunt, P. R. (2016) · Journal of Applied Toxicology · doi:10.1002/jat.3357 · Cited by 613
Phase separation and neurodegenerative diseases: a disturbance in the force
Zbinden, A., Pérez-Berlanga, M., De Rossi, P., & Polymenidou, M. (2020) · Developmental Cell · doi:10.1016/j.devcel.2020.09.014 · Cited by 500
Pohl, F., & Lin, P. K. T. (2018) · Molecules · doi:10.3390/molecules23123283 · Cited by 284
Metadata
- 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
- Publisher
- Frontiers Media SA
- Published
- 2014-09-05
- Volume
- 5
- Pages
- 279-279
- ISSN
- 1664-8021 (ISSN-L)
- PMC
- PMC4155875
- 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
- FWCI
- 9.09
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- 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
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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 ›
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