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Título
Modeling Alzheimer’s Disease in Caenorhabditis elegans
Autor
Año del Documento
2022
Editorial
MDPI
Descripción
Producción Científica
Documento Fuente
Biomedicines, Enero 2022, 10, 288.
Abstract
Alzheimer’s disease (AD) is the most frequent cause of dementia. After decades of research,
we know the importance of the accumulation of protein aggregates such as -amyloid peptide
and phosphorylated tau. We also know that mutations in certain proteins generate early-onset
Alzheimer’s disease (EOAD), and many other genes modulate the disease in its sporadic form.
However, the precise molecular mechanisms underlying AD pathology are still unclear. Because
of ethical limitations, we need to use animal models to investigate these processes. The nematode
Caenorhabditis elegans has received considerable attention in the last 25 years, since the first AD models
overexpressing A peptide were described. We review here the main results obtained using this
model to study AD. We include works studying the basic molecular mechanisms of the disease,
as well as those searching for new therapeutic targets. Although this model also has important
limitations, the ability of this nematode to generate knock-out or overexpression models of any gene,
single or combined, and to carry out toxicity, recovery or survival studies in short timeframes with
many individuals and at low cost is difficult to overcome. We can predict that its use as a model for
various diseases will certainly continue to increase.
Palabras Clave
Alzheimer’s; C. elegans; -amyloid; amyloid precursor protein; tau protein; presenilin; new therapies
ISSN
2227-9059
Revisión por pares
SI
Patrocinador
MICINN project BFU2017-83509-R
IBGM Escalera de Excelencia, Junta de Castilla y León (Ref. CLU-2019-02)
IBGM Escalera de Excelencia, Junta de Castilla y León (Ref. CLU-2019-02)
Version del Editor
Idioma
eng
Tipo de versión
info:eu-repo/semantics/publishedVersion
Derechos
openAccess
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