Emerging signal regulating potential of small molecule biflavonoids to combat neuropathological insults of Alzheimer's disease
Author(s)
Uddin, Md Sahab
Kabir, Md Tanvir
Tewari, Devesh
Mathew, Bijo
Aleya, Lotfi
Griffith University Author(s)
Year published
2020
Metadata
Show full item recordAbstract
Alzheimer's disease (AD) is a progressive, chronic and severe neurodegenerative disorder linked with cognitive and memory impairment that eventually lead to death. There are several processes which can cause AD, including mitochondrial dysfunction-mediated oxidative stress (OS), intracellular buildup of hyper-phosphorylated tau as neurofibrillary tangles (NFTs) and excessive buildup of extracellular amyloid beta (Aβ) plaques, and/or genetic as well as the environmental factors. Existing treatments can only provide symptomatic relief via providing temporary palliative therapy which can weaken the rate of AD-associated cognitive ...
View more >Alzheimer's disease (AD) is a progressive, chronic and severe neurodegenerative disorder linked with cognitive and memory impairment that eventually lead to death. There are several processes which can cause AD, including mitochondrial dysfunction-mediated oxidative stress (OS), intracellular buildup of hyper-phosphorylated tau as neurofibrillary tangles (NFTs) and excessive buildup of extracellular amyloid beta (Aβ) plaques, and/or genetic as well as the environmental factors. Existing treatments can only provide symptomatic relief via providing temporary palliative therapy which can weaken the rate of AD-associated cognitive decline. Plants are the fundamental building blocks for the environment and produce various secondary metabolites. Biflavonoids are one among such secondary metabolite that possesses the potential to mediate noticeable change in the aggregation of tau, Aβ and also efficiently can decrease the toxic effects of Aβ oligomers in comparison with the monoflavonoid moieties. Nevertheless, the molecular processes remain to be exposed, flavonoids are found to cause a change in the Aβ and tau aggregation pathway to generate non-toxic aggregates. In this review, we discuss the neuroprotective action of small molecule biflavonoid to reduce the neurodegenerative events of AD. Furthermore, this appraisal advances our knowledge to develop potential new targets for the treatment of AD.
View less >
View more >Alzheimer's disease (AD) is a progressive, chronic and severe neurodegenerative disorder linked with cognitive and memory impairment that eventually lead to death. There are several processes which can cause AD, including mitochondrial dysfunction-mediated oxidative stress (OS), intracellular buildup of hyper-phosphorylated tau as neurofibrillary tangles (NFTs) and excessive buildup of extracellular amyloid beta (Aβ) plaques, and/or genetic as well as the environmental factors. Existing treatments can only provide symptomatic relief via providing temporary palliative therapy which can weaken the rate of AD-associated cognitive decline. Plants are the fundamental building blocks for the environment and produce various secondary metabolites. Biflavonoids are one among such secondary metabolite that possesses the potential to mediate noticeable change in the aggregation of tau, Aβ and also efficiently can decrease the toxic effects of Aβ oligomers in comparison with the monoflavonoid moieties. Nevertheless, the molecular processes remain to be exposed, flavonoids are found to cause a change in the Aβ and tau aggregation pathway to generate non-toxic aggregates. In this review, we discuss the neuroprotective action of small molecule biflavonoid to reduce the neurodegenerative events of AD. Furthermore, this appraisal advances our knowledge to develop potential new targets for the treatment of AD.
View less >
Journal Title
Science of the Total Environment
Volume
700
Subject
Science & Technology
Life Sciences & Biomedicine
Environmental Sciences
Environmental Sciences & Ecology
Bioflavonoids
Alzheimer’s disease
Amyloid plaque
Neurofibrillary tangles