Overview of Beneficial Effects of (Poly)phenol Metabolites in the Context of Neurodegenerative Diseases on Model Organisms.

Diogo Carregosa,Cláudia Nunes Dos Santos,Cláudia Nunes Dos Santos,Regina Menezes,Regina Menezes,Regina Menezes,Rita Teodoro,Natasa Loncarevic-Vasiljkovic,Natasa Loncarevic-Vasiljkovic,Sofia Ferreira,Sofia Ferreira,Sara Mota,Sara Mota,Carolina Lage Crespo,Beatriz Alves-Dias

doi:10.3390/nu13092940

Abstract

The rise of neurodegenerative diseases in an aging population is an increasing problem of health, social and economic consequences. Epidemiological and intervention studies have demonstrated that diets rich in (poly)phenols can have potent health benefits on cognitive decline and neurodegenerative diseases. Meanwhile, the role of gut microbiota is ever more evident in modulating the catabolism of (poly)phenols to dozens of low molecular weight (poly)phenol metabolites that have been identified in plasma and urine. These metabolites can reach circulation in higher concentrations than parent (poly)phenols and persist for longer periods of time. However, studies addressing their potential brain effects are still lacking. In this review, we will discuss different model organisms that have been used to study how low molecular weight (poly)phenol metabolites affect neuronal related mechanisms gathering critical insight on their potential to tackle the major hallmarks of neurodegeneration.

Highlights

CEDOC, Chronic Diseases Research Centre, NOVA Medical School, Universidade NOVA de Lisboa, iBET, Institute of Experimental and Technological Biology, Apartado 12, 2781-901 Oeiras, Portugal
Researchers have leveraged a host of different in vivo models in order to dissect neurodegenerative diseases that are commonly heterogeneous in their clinical presentations and are multigenic and multifactorial
In this review we have shown the current evidence of low molecular weight (poly)phenol metabolites (LMWPM) on some of the most used gold standard models in science for the study of neurodegenerative diseases: S. cerevisiae, C. elegans, Drosophila, zebrafish, mice and rats

Summary

15 Generations

Associated with Oxidative and Cytoskeleton Stress, ER Stress and Vesicular Trafficking [85]. Aβ42 —Amyloid beta 42; AHP1—Alkyl HydroPeroxide reductase 1 gene (involved in cellular response against oxidative stress); GFP—Green Fluorescent Protein; ADH6—Alcohol Dehydrogenase 6 gene; ADH7—Alcohol Dehydrogenase 7 gene; ER—Endoplasmic. Reticulum; GND1—6—phosphoGlucoNateDehydrogenase 1 gene (involved in cellular response against oxidative stress); GND2—6—. Pleiotropic Drug Resistance 12 gene; PDR5—Pleiotropic Drug Resistance 5 gene; prApe1—precursor amminopeptidase I; VAC8—VACuole related 8 gene; WT—Wilde type; YAL005C—Stress–Seventy subfamily A; YER153C—PETite colonies; YPR125W—Yeast LETM1 Homolog; ZRT1—Zinc–Regulated Transporter 1 gene; ZRT2—Zinc-Regulated Transporter 2 gene; ZWF1—ZwischenFerment 1 gene (Cytoplasmic glucose–6—phosphate dehydrogenase involved in adapting to oxidative stress). (Poly)phenol metabolites are named the recommendations recently published [32] the name cited in the original publications where the effect is described is indicated in brackets. Pleiotropic Drug Resistance 12 gene; PDR5—Pleiotropic Drug Resistance 5 gene; prApe1—precursor amminopeptidase I; VAC8—VACuole related 8 gene; WT—Wilde type; YAL005C—Stress–Seventy subfamily A; YER153C—PETite colonies; YPR125W—Yeast LETM1 Homolog; ZRT1—Zinc–Regulated Transporter 1 gene; ZRT2—Zinc-Regulated Transporter 2 gene; ZWF1—ZwischenFerment 1 gene (Cytoplasmic glucose–6—phosphate dehydrogenase involved in adapting to oxidative stress). (Poly)phenol metabolites are named the recommendations recently published [32] the name cited in the original publications where the effect is described is indicated in brackets. ↑—increased ↓—decreased

O2 for 1 h

Drosophila

Findings

Conclusions