Neuroprotective effects of resveratrol in Alzheimer disease pathology

Abstract

Alzheimer’s disease is a chronic neurodegenerative disorder characterized by a progressive loss of cognitive and behavioral abilities. Extracellular senile plaques and intracellular neurofibrillary tangles are hallmarks of AD. Researchers aim to analyze the molecular mechanisms underlying AD pathogenesis; however, the therapeutic options available to treat this disease are inadequate. In the past few years, several studies have reported interesting insights about the neuroprotective properties of the polyphenolic compound resveratrol (3, 5, 4′-trihydroxy-trans-stilbene) when used with in vitro and in vivo models of AD. The aim of this review is to focus on the neuroprotective and antioxidant effects of resveratrol on AD and its multiple potential mechanisms of action. In addition, because the naturally occurring forms of resveratrol have a very limited half-life in plasma, a description of potential analogs aimed at increasing the bioavailability in plasma is also discussed.

Systems biology approaches to study the molecular effects of caloric restriction and polyphenols on aging processes

“…In the aging brain, the excessive release of oxidative and inflammatory mediators coupled with impaired autophagy mechanisms result in microvascular dysfunctions, protein oxidation, lipid peroxidation and DNA damage, which eventually lead to ischemic damages, abnormal protein aggregation, neuronal inflammation and cell death common to a number of neurodegenerative disorders (Rubinsztein et al 2011;Rege et al 2014;Salminen and Paul 2014). Moreover, excessive oxidative stress alters synaptic transmission and neuronal excitability, which leads to structural damage of the central nervous system (CNS) and decline of cognitive functions (Rizzo et al 2014;Salminen and Paul 2014).…”

Endogenous Neuroprotective Molecules and Their Mechanisms in the Central Nervous System

“…Therefore, it is believed that protection of neurons from the impairment prior to death is a reasonable strategy for the treatment of nerve disorders and injuries. Although a large number of publications have discussed neuroprotection by pharmaceutical agents and natural products against oxidative stress, inflammation, excitotoxicity in disorders [1][2][3][4] and traumatic injuries 5,6) of the CNS, we would like to mainly discuss endogenous neuroprotective factors in this review.…”

Mitochondrial Function in Alzheimer’s Disease: Focus on Astrocytes

“…For example, conjugated Coenzyme Q with a lipophilic triphenylphosphonium (TPP + ) form MitoQ that protect primary cortical neurons from Aβ toxicity, loss of mitochondrial membrane potential and ROS production [124]; Szeto-Shiller antioxidant peptides allow the localization of antioxidant molecules in the mitochondrial matrix, the major source of ROS, and in particular SS31 shows a neuroprotective effect [125,126]. Furthermore, endogenous compounds such as peroxiredoxine (Prdx) [127] and the natural molecules such as alkaloid caffeine [128], polyphenol resveratrol [129] and gypenoside XVII (GP-17) [130] have been used to modulate the bioenergetic homeostasis at different levels in AD mouse models. The antioxidant approach may have wide applications; however, it could also present some controversial effects on mitochondrial adaptation.…”