Is antioxidant therapy effective to treat alzheimer's disease?

Lloret, Ana; Giraldo, Esther; Viña, José

doi:10.5530/ax.2011.4.3

Cited by 4 publications

(3 citation statements)

References 64 publications

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“…The study demonstrated cognitive losses in animals receiving only the Aβ1-42 peptide dilution vehicle compared to the control group receiving only anesthesia, similar to the results obtained in our study. Similar cognitive losses were observed in all groups induced by Aβ1-42, and reported as a model causing greater damage in the induction of AD animals [34]. In our study, reversal of cognitive impairment in the LDN-treated group through behavioral testing may occur due to the hypothesis that modulation of the immune system responds to treatment with Naltrexone by means of a compensation mechanism, where endogenous opioid receptors and opioids themselves such as enkephalin and opioid growth factors (OGF) increase their expression when used at low doses, such as 3-4.5mg / day [15,16].…”

Section: Learning and Memory Spatialsupporting

confidence: 83%

Behavioral, Neurochemical and Histological Changes in the Use of Low Doses of Naltrexone and Donepezil in the Treatment in Experimental Model of Alzheimer’s Disease by Induction of β-Amyloid1-42 in Rats

Moura¹,

Xavier²,

Rodrigues³

et al. 2019

WSR

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Alzheimer's disease (AD) is a progressive neurodegenerative disorder that promotes the involvement of memory-related functions, characterized by the presence of amyloid plaques formed by the β-amyloid peptide (Aβ), and hyperphosphorylated Tau protein neurofibrillary tangles. Evidence suggests that the use of low doses of Naltrexone, an opioid antagonist, possibly promotes a modulation of the immune system and consequent neuroprotective effect. The present study uses the animal model of induction with β-amyloid1-42 (Aβ1-42) to verify the behavioral, neurochemical and histological effects of the use of low doses of Naltrexone. Male wistar rats (250-300g) divided into five groups (N = 8) were used: Control, Sham, Aβ1-42 subdivided into three groups: treated with water, 05 mg Donepezil and 4.5 mg Naltrexone, orally during the 30-day period. Behavioral tests demonstrated the efficacy of induction to the experimental model with reduced memory of Aβ1-42-treated animals as well as reversal of damage in animals treated with Naltrexone. In the structural analysis, observed that the animals induced by Aβ1-42 treated with water alone presented alterations in the pyramidal forms of the hippocampal cells and that the animals treated with Naltrexone presented possibly a reversal of the neuronal damages. In conclusion, treatment with Naltrexone promoted a reversal in the memory impairment of rodents induced to the Alzheimer's model with Aβ1-42 in the behavioral and histological response.

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Section: Learning and Memory Spatialsupporting

confidence: 83%

Behavioral, Neurochemical and Histological Changes in the Use of Low Doses of Naltrexone and Donepezil in the Treatment in Experimental Model of Alzheimer’s Disease by Induction of β-Amyloid1-42 in Rats

Moura¹,

Xavier²,

Rodrigues³

et al. 2019

WSR

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“…Although we provide a rationale for the use of ESC as an antioxidant in AD, several limits to effective antioxidant treatment must also be considered. In particular, several studies that used compounds with the ability to directly scavenge the ROS recorded poor antioxidant effects as well as conflicting data in human clinical trials probably because they act on complex oxidative events ongoing with other neurodegenerative events [ 51 , 52 ]. However, more research is necessary to evaluate the therapeutic impact of bifunctional antioxidants, including the coumarins, on neurodegenerative processes in human.…”

Section: Discussionmentioning

confidence: 99%

Esculetin as a Bifunctional Antioxidant Prevents and Counteracts the Oxidative Stress and Neuronal Death Induced by Amyloid Protein in SH-SY5Y Cells

et al. 2020

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Oxidative stress (OS) appears to be an important determinant during the different stages of progression of Alzheimer’s Disease (AD). In particular, impaired antioxidant defense mechanisms, such as the decrease of glutathione (GSH) and nuclear factor erythroid 2 (NF-E2)-related factor 2 (Nrf2), a master regulator of antioxidant genes, including those for GSH, are associated with OS in the human AD brain. Among the neuropathological hallmarks of AD, the soluble oligomers of amyloid beta (A) peptides seem to promote neuronal death through mitochondrial dysfunction and OS. In this regard, bifunctional antioxidants can exert a dual neuroprotective role by scavenging reactive oxygen species (ROS) directly and concomitant induction of antioxidant genes. In this study, among natural coumarins (esculetin, scopoletin, fraxetin and daphnetin), we demonstrated the ability of esculetin (ESC) to prevent and counteract ROS formation in neuronal SH-SY5Y cells, suggesting its profile as a bifunctional antioxidant. In particular, ESC increased the resistance of the SH-SY5Y cells against OS through the activation of Nrf2 and increase of GSH. In similar experimental conditions, ESC could also protect the SH-SY5Y cells from the OS and neuronal death evoked by oligomers of A1–42 peptides. Further, the use of the inhibitors PD98059 and LY294002 also showed that Erk1/2 and Akt signaling pathways were involved in the neuroprotection mediated by ESC. These results encourage further research in AD models to explore the efficacy and safety profile of ESC as a novel neuroprotective agent.

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“…In fact, abnormal accumulation of Aβ and Tau proteins promote redox imbalance leading to oxidative stress. However, existing antioxidants have been shown to be relatively ineffective in combating AD ( Lloret et al, 2011 ; Lloret et al, 2019 ). There may be several reasons for this.…”

Section: Discussionmentioning

confidence: 99%

Mitoprotective Effects of a Synergistic Nutraceutical Combination: Basis for a Prevention Strategy Against Alzheimer’s Disease

Jayatunga

Hone

Fernando

et al. 2022

Front. Aging Neurosci.

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Evidence to date suggests the consumption of food rich in bioactive compounds, such as polyphenols, flavonoids, omega-3 fatty acids may potentially minimize age-related cognitive decline. For neurodegenerative diseases, such as Alzheimer’s disease (AD), which do not yet have definitive treatments, the focus has shifted toward using alternative approaches, including prevention strategies rather than disease reversal. In this aspect, certain nutraceuticals have become promising compounds due to their neuroprotective properties. Moreover, the multifaceted AD pathophysiology encourages the use of multiple bioactive components that may be synergistic in their protective roles when combined. The objective of the present study was to determine mechanisms of action underlying the inhibition of Aβ1–42-induced toxicity by a previously determined, three-compound nutraceutical combination D5L5U5 for AD. In vitro experiments were carried out in human neuroblastoma BE(2)-M17 cells for levels of ROS, ATP mitophagy, and mitobiogenesis. The component compounds luteolin (LUT), DHA, and urolithin A (UA) were independently protective of mitochondria; however, the D5L5U5 preceded its single constituents in all assays used. Overall, it indicated that D5L5U5 had potent inhibitory effects against Aβ1–42-induced toxicity through protecting mitochondria. These mitoprotective activities included minimizing oxidative stress, increasing ATP and inducing mitophagy and mitobiogenesis. However, this synergistic nutraceutical combination warrants further investigations in other in vitro and in vivo AD models to confirm its potential to be used as a preventative therapy for AD.

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Is antioxidant therapy effective to treat alzheimer's disease?

Cited by 4 publications

References 64 publications

Behavioral, Neurochemical and Histological Changes in the Use of Low Doses of Naltrexone and Donepezil in the Treatment in Experimental Model of Alzheimer’s Disease by Induction of β-Amyloid1-42 in Rats

Behavioral, Neurochemical and Histological Changes in the Use of Low Doses of Naltrexone and Donepezil in the Treatment in Experimental Model of Alzheimer’s Disease by Induction of β-Amyloid1-42 in Rats

Esculetin as a Bifunctional Antioxidant Prevents and Counteracts the Oxidative Stress and Neuronal Death Induced by Amyloid Protein in SH-SY5Y Cells

Mitoprotective Effects of a Synergistic Nutraceutical Combination: Basis for a Prevention Strategy Against Alzheimer’s Disease

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