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oai:uvadoc.uva.es:10324/660802024-12-17T10:56:59Zcom_10324_1134com_10324_931com_10324_894com_10324_32522com_10324_952col_10324_1213col_10324_32523

Álvarez Martín, Javier Álvarez Illera, María Pilar Santo Domingo Mayoral, Jaime Fonteriz García, Rosalba Inés Montero Zoccola, María Teresa 2024-02-09T11:54:57Z 2024-02-09T11:54:57Z 2022 Biomedicines, 2022, vol. 10, n. 2, 288. 2227-9059 https://uvadoc.uva.es/handle/10324/66080 10.3390/biomedicines10020288 288 2 Biomedicines 10 2227-9059 Producción Científica 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. MICINN project BFU2017-83509-R IBGM Escalera de Excelencia, Junta de Castilla y León (Ref. CLU-2019-02) application/pdf eng MDPI info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by/4.0/ © 2022 The authors Attribution 4.0 Internacional Alzheimer’s C. elegans β-amyloid amyloid precursor protein tau protein presenilin new therapies 2415 Biología Molecular Modeling Alzheimer’s disease in Caenorhabditis elegans info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion https://www.mdpi.com/2227-9059/10/2/288 SI