Phenolics in Aging and Neurodegenerative Disorders

Calabrese, Vittorio; Perluigi, Marzia; Cornelius, Carolin; Coccia, Raffaella; Domenico, Fabio Di; Pennisi, Giovanni; Cini, Chiara; Dinkova‐Kostova, Albena T.

doi:10.1002/9780470531792.ch18

Cited by 10 publications

(7 citation statements)

References 123 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Among the activators of the vitagene system are several nutrients, including carnosic acid, resveratrol, sulforaphane, dimethyl fumarate, and acetyl- l -carnitine. 31 , 37 , 42–47 This supports the hypothesis that the beneficial effects of some nutrients are mediated through a hormetic stress response.…”

Section: Nuclear Factor Erythroid 2–related Vitagene Network and Hormsupporting

confidence: 77%

Mediterranean diet and inflammaging within the hormesis paradigm

et al. 2017

View full text Add to dashboard Cite

A coherent set of epidemiological data shows that the Mediterranean diet has beneficial effects capable of preventing a variety of age-related diseases in which low-grade, chronic inflammation/inflammaging plays a major role, but the underpinning mechanism(s) is/are still unclear. It is suggested here that the Mediterranean diet can be conceptualized as a form of chronic hormetic stress, similar to what has been proposed regarding calorie restriction, the most thoroughly studied nutritional intervention. Data on the presence in key Mediterranean foods of a variety of compounds capable of exerting hormetic effects are summarized, and the mechanistic role of the nuclear factor erythroid 2 pathway is highlighted. Within this conceptual framework, particular attention has been devoted to the neurohormetic and neuroprotective properties of the Mediterranean diet, as well as to its ability to maintain an optimal balance between pro- and anti-inflammaging. Finally, the European Commission–funded project NU-AGE is discussed because it addresses a number of variables not commonly taken into consideration, such as age, sex, and ethnicity/genetics, that can modulate the hormetic effect of the Mediterranean diet.

show abstract

Section: Nuclear Factor Erythroid 2–related Vitagene Network and Hormsupporting

confidence: 77%

Mediterranean diet and inflammaging within the hormesis paradigm

et al. 2017

View full text Add to dashboard Cite

show abstract

“…Early studies have shown that curcumin has strong antioxidant activity. In fact, the beta-diketone moiety, especially the phenolic hydroxyl group, is critical for the antioxidant activity of curcumin and its analogs (109,151,206). Very recently, many articles have appeared in the literature demonstrating that curcumin and its metabolites interact with several intracellular systems such as transcription factor NFkB, iNOS, and HIF-1 and members of the vitagene family (see below).…”

Section: F Curcuminmentioning

confidence: 99%

“…However, curcumin undergoes a marked firstpass metabolism that limits its systemic bioavailability (*60%) as demonstrated in humans and rodents (102,109). Interestingly, to increase its bioavailability, the coadministration of curcumin with piperine or its complexation with phospholipids to form a curcumin-phospholipids complex has been proposed (12).…”

Section: F Curcuminmentioning

confidence: 99%

“…The protective role played by HO-1 and its products in AD raised new possibilities regarding the possible use of natural substances, which are able to increase HO-1 levels, as potential drugs for the prevention and treatment of AD. In this light very promising are the polyphenolic compounds contained in some herbs and spices, for example, curcumin (102,106,109). Curcumin is the active antioxidant principle in Curcuma longa, a coloring agent and food additive commonly used in Indian culinary preparations.…”

Section: Heme Oxygenasesmentioning

confidence: 99%

“…Curcumin is the active antioxidant principle in Curcuma longa, a coloring agent and food additive commonly used in Indian culinary preparations. This polyphenolic substance has the potential to inhibit lipid peroxidation and to effectively intercept and neutralize ROS and RNS (102,105,109,390). In addition, curcumin has been shown to significantly increase HO-1 in astrocytes and vascular endothelial cells (316,317).…”

Section: Heme Oxygenasesmentioning

confidence: 99%

See 2 more Smart Citations

Cellular Stress Responses, The Hormesis Paradigm, and Vitagenes: Novel Targets for Therapeutic Intervention in Neurodegenerative Disorders

Calabrese

Cornelius

Dinkova‐Kostova

et al. 2010

Antioxidants & Redox Signaling

Self Cite

694

573

View full text Add to dashboard Cite

Despite the capacity of chaperones and other homeostatic components to restore folding equilibrium, cells appear poorly adapted for chronic oxidative stress that increases in cancer and in metabolic and neurodegenerative diseases. Modulation of endogenous cellular defense mechanisms represents an innovative approach to therapeutic intervention in diseases causing chronic tissue damage, such as in neurodegeneration. This article introduces the concept of hormesis and its applications to the field of neuroprotection. It is argued that the hormetic dose response provides the central underpinning of neuroprotective responses, providing a framework for explaining the common quantitative features of their dose-response relationships, their mechanistic foundations, and their relationship to the concept of biological plasticity, as well as providing a key insight for improving the accuracy of the therapeutic dose of pharmaceutical agents within the highly heterogeneous human population. This article describes in mechanistic detail how hormetic dose responses are mediated for endogenous cellular defense pathways, including sirtuin and Nrf2 and related pathways that integrate adaptive stress responses in the prevention of neurodegenerative diseases. Particular attention is given to the emerging role of nitric oxide, carbon monoxide, and hydrogen sulfide gases in hormetic-based neuroprotection and their relationship to membrane radical dynamics and mitochondrial redox signaling.

show abstract