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Molecular Insight into the Therapeutic Promise of Flavonoids against Alzheimer’s Disease

Alzheimer’s disease (AD) is one of the utmost chronic neurodegenerative disorders, which is characterized from a neuropathological point of view by the aggregates of amyloid beta (Aβ) peptides that are deposited as senile plaques and tau proteins which form neurofibrillary tangles (NFTs). Even thoug...

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Autores principales: Uddin, Md. Sahab, Kabir, Md. Tanvir, Niaz, Kamal, Jeandet, Philippe, Clément, Christophe, Mathew, Bijo, Rauf, Abdur, Rengasamy, Kannan R.R., Sobarzo-Sánchez, Eduardo, Ashraf, Ghulam Md, Aleya, Lotfi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7143946/
https://www.ncbi.nlm.nih.gov/pubmed/32168835
http://dx.doi.org/10.3390/molecules25061267
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author Uddin, Md. Sahab
Kabir, Md. Tanvir
Niaz, Kamal
Jeandet, Philippe
Clément, Christophe
Mathew, Bijo
Rauf, Abdur
Rengasamy, Kannan R.R.
Sobarzo-Sánchez, Eduardo
Ashraf, Ghulam Md
Aleya, Lotfi
author_facet Uddin, Md. Sahab
Kabir, Md. Tanvir
Niaz, Kamal
Jeandet, Philippe
Clément, Christophe
Mathew, Bijo
Rauf, Abdur
Rengasamy, Kannan R.R.
Sobarzo-Sánchez, Eduardo
Ashraf, Ghulam Md
Aleya, Lotfi
author_sort Uddin, Md. Sahab
collection PubMed
description Alzheimer’s disease (AD) is one of the utmost chronic neurodegenerative disorders, which is characterized from a neuropathological point of view by the aggregates of amyloid beta (Aβ) peptides that are deposited as senile plaques and tau proteins which form neurofibrillary tangles (NFTs). Even though advancement has been observed in order to understand AD pathogenesis, currently available therapeutic methods can only deliver modest symptomatic relief. Interestingly, naturally occurring dietary flavonoids have gained substantial attention due to their antioxidative, anti-inflammatory, and anti-amyloidogenic properties as alternative candidates for AD therapy. Experimental proof provides support to the idea that some flavonoids might protect AD by interfering with the production and aggregation of Aβ peptides and/or decreasing the aggregation of tau. Flavonoids have the ability to promote clearance of Aβ peptides and inhibit tau phosphorylation by the mTOR/autophagy signaling pathway. Moreover, due to their cholinesterase inhibitory potential, flavonoids can represent promising symptomatic anti-Alzheimer agents. Several processes have been suggested for the aptitude of flavonoids to slow down the advancement or to avert the onset of Alzheimer’s pathogenesis. To enhance cognitive performance and to prevent the onset and progress of AD, the interaction of flavonoids with various signaling pathways is proposed to exert their therapeutic potential. Therefore, this review elaborates on the probable therapeutic approaches of flavonoids aimed at averting or slowing the progression of the AD pathogenesis.
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spelling pubmed-71439462020-04-13 Molecular Insight into the Therapeutic Promise of Flavonoids against Alzheimer’s Disease Uddin, Md. Sahab Kabir, Md. Tanvir Niaz, Kamal Jeandet, Philippe Clément, Christophe Mathew, Bijo Rauf, Abdur Rengasamy, Kannan R.R. Sobarzo-Sánchez, Eduardo Ashraf, Ghulam Md Aleya, Lotfi Molecules Review Alzheimer’s disease (AD) is one of the utmost chronic neurodegenerative disorders, which is characterized from a neuropathological point of view by the aggregates of amyloid beta (Aβ) peptides that are deposited as senile plaques and tau proteins which form neurofibrillary tangles (NFTs). Even though advancement has been observed in order to understand AD pathogenesis, currently available therapeutic methods can only deliver modest symptomatic relief. Interestingly, naturally occurring dietary flavonoids have gained substantial attention due to their antioxidative, anti-inflammatory, and anti-amyloidogenic properties as alternative candidates for AD therapy. Experimental proof provides support to the idea that some flavonoids might protect AD by interfering with the production and aggregation of Aβ peptides and/or decreasing the aggregation of tau. Flavonoids have the ability to promote clearance of Aβ peptides and inhibit tau phosphorylation by the mTOR/autophagy signaling pathway. Moreover, due to their cholinesterase inhibitory potential, flavonoids can represent promising symptomatic anti-Alzheimer agents. Several processes have been suggested for the aptitude of flavonoids to slow down the advancement or to avert the onset of Alzheimer’s pathogenesis. To enhance cognitive performance and to prevent the onset and progress of AD, the interaction of flavonoids with various signaling pathways is proposed to exert their therapeutic potential. Therefore, this review elaborates on the probable therapeutic approaches of flavonoids aimed at averting or slowing the progression of the AD pathogenesis. MDPI 2020-03-11 /pmc/articles/PMC7143946/ /pubmed/32168835 http://dx.doi.org/10.3390/molecules25061267 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Uddin, Md. Sahab
Kabir, Md. Tanvir
Niaz, Kamal
Jeandet, Philippe
Clément, Christophe
Mathew, Bijo
Rauf, Abdur
Rengasamy, Kannan R.R.
Sobarzo-Sánchez, Eduardo
Ashraf, Ghulam Md
Aleya, Lotfi
Molecular Insight into the Therapeutic Promise of Flavonoids against Alzheimer’s Disease
title Molecular Insight into the Therapeutic Promise of Flavonoids against Alzheimer’s Disease
title_full Molecular Insight into the Therapeutic Promise of Flavonoids against Alzheimer’s Disease
title_fullStr Molecular Insight into the Therapeutic Promise of Flavonoids against Alzheimer’s Disease
title_full_unstemmed Molecular Insight into the Therapeutic Promise of Flavonoids against Alzheimer’s Disease
title_short Molecular Insight into the Therapeutic Promise of Flavonoids against Alzheimer’s Disease
title_sort molecular insight into the therapeutic promise of flavonoids against alzheimer’s disease
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7143946/
https://www.ncbi.nlm.nih.gov/pubmed/32168835
http://dx.doi.org/10.3390/molecules25061267
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