Natural Bioactive Products and Alzheimer’s Disease Pathology: Lessons from <i>Caenorhabditis elegans</i> Transgenic Models
María D. Navarro-Hortal,
Jose M. Romero-Márquez,
Safa Osta,
Victoria Jiménez-Trigo,
Pedro Muñoz-Ollero,
Alfonso Varela-López
Affiliations
María D. Navarro-Hortal
Biomedical Research Center, Department of Physiology, Institute of Nutrition and Food Technology “José Mataix Verdú”, University of Granada, Avda del Conocimiento s/n., 18100 Granada, Spain
Jose M. Romero-Márquez
Biomedical Research Center, Department of Physiology, Institute of Nutrition and Food Technology “José Mataix Verdú”, University of Granada, Avda del Conocimiento s/n., 18100 Granada, Spain
Safa Osta
Biomedical Research Center, Department of Physiology, Institute of Nutrition and Food Technology “José Mataix Verdú”, University of Granada, Avda del Conocimiento s/n., 18100 Granada, Spain
Victoria Jiménez-Trigo
Biomedical Research Center, Department of Physiology, Institute of Nutrition and Food Technology “José Mataix Verdú”, University of Granada, Avda del Conocimiento s/n., 18100 Granada, Spain
Pedro Muñoz-Ollero
Biomedical Research Center, Department of Physiology, Institute of Nutrition and Food Technology “José Mataix Verdú”, University of Granada, Avda del Conocimiento s/n., 18100 Granada, Spain
Alfonso Varela-López
Biomedical Research Center, Department of Physiology, Institute of Nutrition and Food Technology “José Mataix Verdú”, University of Granada, Avda del Conocimiento s/n., 18100 Granada, Spain
Alzheimer’s disease (AD) is an age-dependent, progressive disorder affecting millions of people. Currently, the therapeutics for AD only treat the symptoms. Although they have been used to discover new products of interest for this disease, mammalian models used to investigate the molecular determinants of this disease are often prohibitively expensive, time-consuming and very complex. On the other hand, cell cultures lack the organism complexity involved in AD. Given the highly conserved neurological pathways between mammals and invertebrates, Caenorhabditis elegans has emerged as a powerful tool for the investigation of the pathophysiology of human AD. Numerous models of both Tau- and Aβ-induced toxicity, the two prime components observed to correlate with AD pathology and the ease of performing RNA interference for any gene in the C. elegans genome, allow for the identification of multiple therapeutic targets. The effects of many natural products in main AD hallmarks using these models suggest promising health-promoting effects. However, the way in which they exert such effects is not entirely clear. One of the reasons is that various possible therapeutic targets have not been evaluated in many studies. The present review aims to explore shared therapeutical targets and the potential of each of them for AD treatment or prevention.
