RT info:eu-repo/semantics/article
T1 Modeling Alzheimer’s Disease in Caenorhabditis elegans
A1 Álvarez Martín, Javier
A1 Álvarez Illera, María Pilar
A1 Santo Domingo Mayoral, Jaime
A1 Fonteriz García, Rosalba Inés
A1 Montero Zoccola, María Teresa
K1 C. elegans;  -amyloid; amyloid precursor protein; tau protein; presenilin; new therapies
AB 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.
PB MDPI
SN 2227-9059
YR 2022
FD 2022
LK https://uvadoc.uva.es/handle/10324/66234
UL https://uvadoc.uva.es/handle/10324/66234
LA eng
NO Biomedicines, Enero 2022, 10, 288
NO Producción Científica
DS UVaDOC
RD 31-oct-2024