TY - JOUR
T1 - Dietary Flavonoids in the Management of Huntington’s Disease
T2 - Mechanism and Clinical Perspective
AU - Khan, Haroon
AU - Ullah, Hammad
AU - Tundis, Rosa
AU - Belwal, Tarun
AU - Devkota, Hari Prasad
AU - Daglia, Maria
AU - Cetin, Zafer
AU - Saygili, Eyup Ilker
AU - Campos, Maria da Graça
AU - Capanoglu, Esra
AU - Du, Ming
AU - Dar, Parsa
AU - Xiao, Jianbo
N1 - Publisher Copyright:
© 2020 The Authors. eFood published by John Wiley & Sons Australia, Ltd on behalf of International Association of Dietetic Nutrition and Safety.
PY - 2020/2
Y1 - 2020/2
N2 - Huntington’s disease (HD) is a neurodegenerative disorder characterized by progressive loss of neurons, which leads to behavioral systems and mental decline. HD is linked to repeat expansions of cytosine, adenine, and guanine in the Huntingtin (HTT) gene that give rise to mutation, leading to the formation of the HTT protein product. Oxidative stress also provokes the initiation and progression of HD as it leads to protein misfolding that results in the formation of inclusion which clumps together and alters neurotransmission. Despite the advancement in the field of pharmaceutical sciences, current therapeutic approaches suppress only the severity of symptoms and no therapy exists that can cure HD from its root cause. Flavonoids are the most abundant polyphenols widely present in daily dietary sources. Dietary flavonoids have a wide range of pharmacological bioactivities and many therapeutic applications. Dietary flavonoids including hesperidin, naringin, quercetin, rutin, fisetin, myricetin, luteolin, and epigallocatechin 3-O-gallate can prevent and manage HD through exerting antioxidant and anti-inflammatory activities, altering intracellular pathways, genetic alterations, and metal ion chelation. This review highlights flavonoids as therapeutic options for HD and will open new dimensions for flavonoids as safe and effective therapeutic agents in diminishing HD.
AB - Huntington’s disease (HD) is a neurodegenerative disorder characterized by progressive loss of neurons, which leads to behavioral systems and mental decline. HD is linked to repeat expansions of cytosine, adenine, and guanine in the Huntingtin (HTT) gene that give rise to mutation, leading to the formation of the HTT protein product. Oxidative stress also provokes the initiation and progression of HD as it leads to protein misfolding that results in the formation of inclusion which clumps together and alters neurotransmission. Despite the advancement in the field of pharmaceutical sciences, current therapeutic approaches suppress only the severity of symptoms and no therapy exists that can cure HD from its root cause. Flavonoids are the most abundant polyphenols widely present in daily dietary sources. Dietary flavonoids have a wide range of pharmacological bioactivities and many therapeutic applications. Dietary flavonoids including hesperidin, naringin, quercetin, rutin, fisetin, myricetin, luteolin, and epigallocatechin 3-O-gallate can prevent and manage HD through exerting antioxidant and anti-inflammatory activities, altering intracellular pathways, genetic alterations, and metal ion chelation. This review highlights flavonoids as therapeutic options for HD and will open new dimensions for flavonoids as safe and effective therapeutic agents in diminishing HD.
KW - Anti-inflammatory
KW - Huntington’s disease
KW - antioxidant
KW - clinical perspective
KW - flavonoids
KW - intracellular pathways
UR - http://www.scopus.com/inward/record.url?scp=85085901272&partnerID=8YFLogxK
U2 - 10.2991/efood.k.200203.001
DO - 10.2991/efood.k.200203.001
M3 - Review article
AN - SCOPUS:85085901272
SN - 2666-3066
VL - 1
SP - 38
EP - 52
JO - eFood
JF - eFood
IS - 1
ER -