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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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“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]
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Baia, E., Amado, L. L., & Venekey, V. (2026) · Invertebrate Reproduction & Development · doi:10.1080/07924259.2026.2625741
Les nanotubes comme nouvelle voie de transfert et de propagation de la protéine Tau pathologique
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Small Animal Models in Alzheimer’s Disease: Insights from Zebrafish and Caenorhabditis elegans
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Ding, X., Wang, P., Zhou, L., & Li, X. (2026) · Biology · doi:10.3390/biology15161351
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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
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