In vitro studies of the neuroprotective activities of astaxanthin and fucoxanthin against amyloid beta (Aβ1-42) toxicity and aggregation

Alghazwi, Mousa; Smid, Scott D.; Musgrave, Ian; Zhang, Wei

doi:10.1016/j.neuint.2019.01.010

Cited by 97 publications

(63 citation statements)

References 55 publications

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“…Several metabolites of marine algae have shown anti-amyloidogenic potentials ( Table 1 ). For example, fucoxanthin at variant concentrations reduced the formation of Aβ 1–42 fibril and Aβ1–42 oligomers, when co-incubated with Aβ 1–42 monomers [ 135 , 136 ]. Both studies also demonstrated that fucoxanthin has been shown to inhibit Aβ aggregation [ 135 , 136 ].…”

Section: Neuropharmacological Potentials Of Marine Algae and Theirmentioning

confidence: 99%

“…For example, fucoxanthin at variant concentrations reduced the formation of Aβ 1–42 fibril and Aβ1–42 oligomers, when co-incubated with Aβ 1–42 monomers [ 135 , 136 ]. Both studies also demonstrated that fucoxanthin has been shown to inhibit Aβ aggregation [ 135 , 136 ]. Inhibition of β-site amyloid precursor protein cleaving enzyme 1 (BACE1) with fucoxanthin was of a mixed-type [ 134 ].…”

Section: Neuropharmacological Potentials Of Marine Algae and Theirmentioning

confidence: 99%

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Neuroprotective Potentials of Marine Algae and Their Bioactive Metabolites: Pharmacological Insights and Therapeutic Advances

et al. 2020

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Beyond their significant contribution to the dietary and industrial supplies, marine algae are considered to be a potential source of some unique metabolites with diverse health benefits. The pharmacological properties, such as antioxidant, anti-inflammatory, cholesterol homeostasis, protein clearance and anti-amyloidogenic potentials of algal metabolites endorse their protective efficacy against oxidative stress, neuroinflammation, mitochondrial dysfunction, and impaired proteostasis which are known to be implicated in the pathophysiology of neurodegenerative disorders and the associated complications after cerebral ischemia and brain injuries. As was evident in various preclinical studies, algal compounds conferred neuroprotection against a wide range of neurotoxic stressors, such as oxygen/glucose deprivation, hydrogen peroxide, glutamate, amyloid β, or 1-methyl-4-phenylpyridinium (MPP+) and, therefore, hold therapeutic promise for brain disorders. While a significant number of algal compounds with promising neuroprotective capacity have been identified over the last decades, a few of them have had access to clinical trials. However, the recent approval of an algal oligosaccharide, sodium oligomannate, for the treatment of Alzheimer’s disease enlightened the future of marine algae-based drug discovery. In this review, we briefly outline the pathophysiology of neurodegenerative diseases and brain injuries for identifying the targets of pharmacological intervention, and then review the literature on the neuroprotective potentials of algal compounds along with the underlying pharmacological mechanism, and present an appraisal on the recent therapeutic advances. We also propose a rational strategy to facilitate algal metabolites-based drug development.

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Section: Neuropharmacological Potentials Of Marine Algae and Theirmentioning

confidence: 99%

Section: Neuropharmacological Potentials Of Marine Algae and Theirmentioning

confidence: 99%

Neuroprotective Potentials of Marine Algae and Their Bioactive Metabolites: Pharmacological Insights and Therapeutic Advances

et al. 2020

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“…These findings are of particular interest, as beneficial effects of LXR agonists on cognition are not necessarily accompanied by a reduced Aβ plaque load 14,41 . Recently, it has been reported that other constituents of Sargassum fusiforme, such as fucosterol, fucoidan, and fucoxantin improve learning and memory deficiencies in pharmacological models for cognitive impairment [61][62][63] . Although synergism among constituents of Sargassum fusiforme is likely, future studies should determine whether 24(S)-Saringosterol is sufficient to improve cognitive performance and AD pathology.…”

Section: Discussionmentioning

confidence: 99%

Dietary Sargassum Fusiforme Improves Memory And Reduces Amyloid Plaque Load In An Alzheimer’s Disease Mouse Model

et al. 2019

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Activation of liver X receptors (LXRs) by synthetic agonists was found to improve cognition in Alzheimer's disease (AD) mice. However, these LXR agonists induce hypertriglyceridemia and hepatic steatosis, hampering their use in the clinic. We hypothesized that phytosterols as LXR agonists enhance cognition in AD without affecting plasma and hepatic triglycerides. Phytosterols previously reported to activate LXRs were tested in a luciferase-based LXR reporter assay. Using this assay, we found that phytosterols commonly present in a Western type diet in physiological concentrations do not activate LXRs. However, a lipid extract of the 24(S)-Saringosterol-containing seaweed Sargassum fusiforme did potently activate LXRβ. Dietary supplementation of crude Sargassum fusiforme or a Sargassum fusiforme-derived lipid extract to AD mice significantly improved short-term memory and reduced hippocampal Aβ plaque load by 81%. Notably, none of the side effects typically induced by full synthetic LXR agonists were observed. In contrast, administration of the synthetic LXRα activator, AZ876, did not improve cognition and resulted in the accumulation of lipid droplets in the liver. Administration of Sargassum fusiforme-derived 24(S)-Saringosterol to cultured neurons reduced the secretion of Aβ 42. Moreover, conditioned medium from 24(S)-Saringosterol-treated astrocytes added to microglia increased phagocytosis of Aβ. our data show that Sargassum fusiforme improves cognition and alleviates AD pathology. This may be explained at least partly by 24(S)-Saringosterol-mediated LXRβ activation.

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“…Therefore, the protection of neural cells against oxidative damage may be a potential strategy to treat AD. Several in vitro or in vivo studies have explored the function of antioxidant and antiapoptotic drugs in ameliorating AD [4][5][6] but the approach is time-consuming and costly, plus the safety concern, which limits the use of these drugs in AD treatment. Moreover, the blood-brain barrier (BBB) dampens the efficacy of these drugs, since over 98% of small molecule drugs and *100% of large molecule drugs can not pass the BBB [7].…”

Section: Introductionmentioning

confidence: 99%

Thermal cycling protects SH-SY5Y cells against hydrogen peroxide and β-amyloid-induced cell injury through stress response mechanisms involving Akt pathway

et al. 2020

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Neurodegenerative diseases (NDDs) are becoming a major threat to public health, according to the World Health Organization (WHO). The most common form of NDDs is Alzheimer's disease (AD), boasting 60-70% share. Although some debates still exist, excessive aggregation of β-amyloid protein (Aβ) and neurofibrillary tangles has been deemed one of the major causes for the pathogenesis of AD. A growing number of evidences from studies, however, have suggested that reactive oxygen species (ROS) also play a key role in the onset and progression of AD. Although scientists have had some understanding of the pathogenesis of AD, the disease still cannot be cured, with existing treatment only capable of providing a temporary relief at best, partly due to the obstacle of blood-brain barrier (BBB). The study was aimed to ascertain the neuroprotective effect of thermal cycle hyperthermia (TC-HT) against hydrogen peroxide (H 2 O 2) and Aβ-induced cytotoxicity in SH-SY5Y cells. Treating cells with this physical stimulation beforehand significantly improved the cell viability and decreased the ROS content. The underlying mechanisms may be due to the activation of Akt pathway and the downstream antioxidant and prosurvival proteins. The findings manifest significant potential of TC-HT in neuroprotection, via inhibition of oxidative stress and cell apoptosis. It is believed that coupled with the use of drugs or natural compounds, this methodology can be even more effective in treating NDDs.

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In vitro studies of the neuroprotective activities of astaxanthin and fucoxanthin against amyloid beta (Aβ1-42) toxicity and aggregation

Cited by 97 publications

References 55 publications

Neuroprotective Potentials of Marine Algae and Their Bioactive Metabolites: Pharmacological Insights and Therapeutic Advances

Neuroprotective Potentials of Marine Algae and Their Bioactive Metabolites: Pharmacological Insights and Therapeutic Advances

Dietary Sargassum Fusiforme Improves Memory And Reduces Amyloid Plaque Load In An Alzheimer’s Disease Mouse Model

Thermal cycling protects SH-SY5Y cells against hydrogen peroxide and β-amyloid-induced cell injury through stress response mechanisms involving Akt pathway

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