Fucosterol exerts protection against amyloid β-induced neurotoxicity, reduces intracellular levels of amyloid β and enhances the mRNA expression of neuroglobin in amyloid β-induced SH-SY5Y cells

Gan, Sook Yee; Wong, Li Zhe; Wong, Jia Wun; Tan, Eng Lai

doi:10.1016/j.ijbiomac.2018.10.021

Cited by 30 publications

(19 citation statements)

References 88 publications

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“…For instance, it was shown by ATR-FTIR that whey proline-rich peptides suppressed both oligomerization and the formation of antiparallel β-sheet (Bharadwaj et al, 2013), leading to a rescue of yeast and neuronal cells. Such modulation of the folding pathway of Aβ 1-42 has also been shown for Fucosterol, which protected neuronal cells against Aβ 1-42 -induced toxicity (Gan et al, 2019). Using ThT fluorescence, AFM, and molecular dynamics, Castro-Silva and co-workers demonstrated that fucosterol inhibits Aβ 1-42 aggregation by binding to structural regions of the monomers involved in the formation of antiparallel β strand of the Aβ 1-42 oligomer (Castro-Silva et al, 2020).…”

Section: Discussionmentioning

confidence: 75%

High Speed AFM and NanoInfrared Spectroscopy Investigation of Aβ1–42 Peptide Variants and Their Interaction With POPC/SM/Chol/GM1 Model Membranes

Feuillie

Lambert

Ewald

et al. 2020

Front. Mol. Biosci.

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Due to an aging population, neurodegenerative diseases such as Alzheimer's disease (AD) have become a major health issue. In the case of AD, Aβ 1-42 peptides have been identified as one of the markers of the disease with the formation of senile plaques via their aggregation, and could play a role in memory impairment and other tragic syndromes associated with the disease. Many studies have shown that not only the morphology and structure of Aβ 1-42 peptide assembly are playing an important role in the formation of amyloid plaques, but also the interactions between Aβ 1-42 and the cellular membrane are crucial regarding the aggregation processes and toxicity of the amyloid peptides. Despite the increasing amount of information on AD associated amyloids and their toxicity, the molecular mechanisms involved still remain unclear and require in-depth investigation at the local scale to clearly decipher the role of the sequence of the amyloid peptides, of their secondary structures, of their oligomeric states, and of their interactions with lipid membranes. In this original study, through the use of Atomic Force Microscopy (AFM) related-techniques, high-speed AFM and nanoInfrared AFM, we tried to unravel at the nanoscale the link between aggregation state, structure and interaction with membranes in the amyloid/membrane interaction. Using three mutants of Aβ peptides, L34T, oG37C, and WT Aβ 1-42 peptides, with differences in morphology, structure and assembly process, as well as model lipidic membranes whose composition and structure allow interactions with the peptides, our AFM study coupling high spatial and temporal resolution and nanoscale structure information clearly evidences a local correlation between the secondary structure of the peptides, their fibrillization kinetics and their interactions with model membranes. Membrane disruption is associated to small transient oligomeric entities in the early stages of aggregation that strongly interact with the membrane, and present an antiparallel β-sheet secondary structure. The strong effect on membrane integrity that exists when these oligomeric Aβ 1-42 peptides interact with membranes of a particular composition could be a lead for therapeutic studies.

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Section: Discussionmentioning

confidence: 75%

High Speed AFM and NanoInfrared Spectroscopy Investigation of Aβ1–42 Peptide Variants and Their Interaction With POPC/SM/Chol/GM1 Model Membranes

Feuillie

Lambert

Ewald

et al. 2020

Front. Mol. Biosci.

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“…The neuroprotective roles of fucosterol have been reviewed in our recent article [ 81 ]. In brief, fucosterol attenuated Aβ-induced neurotoxicity in hippocampal neurons [ 172 ] and SH-SY5Y cells [ 173 ]. In addition, three isolated compounds including α-tocospirone, (23E)-3β-hydroxy-stigmasta-5,23-dien-28-one and (22E)-3β-hydroxy-cholesta-5,22-dien-24-one from Caulerpa racemose attenuated Aβ25-35-induced toxicity in SHSY5Y cells [ 174 ].…”

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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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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“…In a study carried out by Alghazwi et al [63], some species of Australian brown, green, and red algae attenuated Aβ-induced toxicity in PC12 cells. Fucosterol from Padina australis was evaluated for its neuroprotective effects in SH-SY5Y cells treated with Aβ [64]. The result revealed that fucosterol ameliorated the neurotoxic effect of Aβ and triggered the downregulation of APP expression.…”

Section: Therapeutic Role Of Some Macroalgae In the Management Of Admentioning

confidence: 99%

Macroalgae as a Valuable Source of Naturally Occurring Bioactive Compounds for the Treatment of Alzheimer’s Disease

2019

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Alzheimer’s disease (AD) is a neurological condition that affects mostly aged individuals. Evidence suggests that pathological mechanisms involved in the development of AD are associated with cholinergic deficit, glutamate excitotoxicity, beta-amyloid aggregation, tau phosphorylation, neuro-inflammation, and oxidative damage to neurons. Currently there is no cure for AD; however, synthetic therapies have been developed to effectively manage some of the symptoms at the early stage of the disease. Natural products from plants and marine organisms have been identified as important sources of bioactive compounds with neuroprotective potentials and less adverse effects compared to synthetic agents. Seaweeds contain several kinds of secondary metabolites such as phlorotannins, carotenoids, sterols, fucoidans, and poly unsaturated fatty acids. However, their neuroprotective effects and mechanisms of action have not been fully explored. This review discusses recent investigations and/or updates on interactions of bioactive compounds from seaweeds with biomarkers involved in the pathogenesis of AD using reports in electronic databases such as Web of science, Scopus, PubMed, Science direct, Scifinder, Taylor and Francis, Wiley, Springer, and Google scholar between 2015 and 2019. Phlorotannins, fucoidans, sterols, and carotenoids showed strong neuroprotective potentials in different experimental models. However, there are no data from human studies and/or clinical trials.

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Fucosterol exerts protection against amyloid β-induced neurotoxicity, reduces intracellular levels of amyloid β and enhances the mRNA expression of neuroglobin in amyloid β-induced SH-SY5Y cells

Cited by 30 publications

References 88 publications

High Speed AFM and NanoInfrared Spectroscopy Investigation of Aβ1–42 Peptide Variants and Their Interaction With POPC/SM/Chol/GM1 Model Membranes

High Speed AFM and NanoInfrared Spectroscopy Investigation of Aβ1–42 Peptide Variants and Their Interaction With POPC/SM/Chol/GM1 Model Membranes

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

Macroalgae as a Valuable Source of Naturally Occurring Bioactive Compounds for the Treatment of Alzheimer’s Disease

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