Emerging Signal Regulating Potential of Genistein Against Alzheimer’s Disease: A Promising Molecule of Interest

Uddin, Md. Sahab; Kabir, Md. Tanvir

doi:10.3389/fcell.2019.00197

Cited by 92 publications

(40 citation statements)

References 106 publications

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“…Growing evidence confirms that flavonoids display promising neuroprotective potential due to their ability to lessen the progression of age-related neurodegenerative disorders or avert the onset of neurodegeneration [92,93]. Their attitudes to influence learning and cognition in animal models of disease and also in humans have been exhibited by dietary supplementation experiments involving flavonoid-rich food or plant extracts [94][95][96][97][98].…”

Section: Flavonoidsmentioning

confidence: 99%

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

et al. 2020

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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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Section: Flavonoidsmentioning

confidence: 99%

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

et al. 2020

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“…In addition, epidemiological data suggest a correlation between estrogen replacement therapy, amelioration of cognitive functions (e.g 60 mg total isoflavone equivalent/day, 12 weeks), and delayed onset of PD and Alzheimer's disease (AD) [28][29][30][31], suggesting that the consumption of phytoestrogens in isoflavone-rich foods and plant medicines could slow functional decline of the aging brain. In support of this idea, isoflavones and isoflavone-rich extracts have exhibit neuroprotective activity in preclinical models of AD and cognitive impairment [32,33]. Individual isoflavones such as genistein, a major isoflavone found in soy, have also been reported to attenuate Parkinsonian symptoms in rodents exposed to MPTP, 6-OHDA, or LPS by restoring motor functions and preserving dopaminergic neurons [34][35][36][37][38][39].…”

Section: Introductionmentioning

confidence: 94%

Neuroprotective mechanisms of red clover and soy isoflavones in Parkinson’s disease models

Jacquet

Ambaw

Tambe

et al. 2020

Preprint

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Parkinson's disease (PD) is a neurodegenerative disorder characterized by nigrostriatal degeneration and the spreading of aggregated forms of the presynaptic protein alpha-synuclein (aSyn) throughout the brain. PD patients are currently only treated with symptomatic therapies, and strategies to slow or stop the progressive neurodegeneration underlying the disease's motor and cognitive symptoms are greatly needed. The time between the first neurobiochemical alterations and the initial presentation of symptoms is thought to span several years, and early neuroprotective dietary interventions could delay the disease onset or slow PD progression. This study aimed at characterizing the neuroprotective effects of isoflavones, a class of dietary polyphenols found in soy products and in the medicinal plant red clover (Trifolium pratense). We found that isoflavone-rich extracts and individual isoflavones rescued the loss of dopaminergic neurons and the shortening of neurites in primary mesencephalic cultures exposed to two PD-related insults, the environmental toxin rotenone and adenovirus encoding the A53T aSyn mutant. The extracts and individual isoflavones also activated the Nrf2-mediated antioxidant response in astrocytes via a mechanism involving inhibition of the ubiquitin-proteasome system, and they alleviated deficits in mitochondrial respiration. Furthermore, an isoflavone-enriched soy extract reduced motor dysfunction exhibited by rats lesioned with the PD-related neurotoxin 6-OHDA. These findings suggest that plant-derived isoflavones could serve as dietary supplements to delay PD onset in at-risk individuals and mitigate neurodegeneration in the brains of patients.

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“…Alzheimer's Disease APOE is a chylomicron lipoprotein that is necessary for the transport of lipids and the metabolism of lipoproteins, and it is encoded by the APOE gene which is situated in the long arm of chromosome 19q13.2 [59,60] ( Figure 1). The APOE gene has 3 variants, called APOE2, APOE3, and APOE4, which are present at~7%, 79%, and~14%, respectively in the whole populace, and these show dissimilarities in lipid-as well as receptor-binding efficiency.…”

Section: Apoe-polymorphism and Susceptibility Tomentioning

confidence: 99%

Molecular Insight into the Therapeutic Promise of TargetingAPOE4for Alzheimer’s Disease

Mamun

Uddin

Bashar

et al. 2020

Oxidative Medicine and Cellular Longevity

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Alzheimer’s disease (AD) is a progressive neurodegenerative disease that causes chronic cognitive dysfunction. Most of the AD cases are late onset, and the apolipoprotein E (APOE) isoform is a key genetic risk factor. The APOE gene has 3 key alleles in humans including APOE2, APOE3, and APOE4. Among them, APOE4 is the most potent genetic risk factor for late-onset AD (LOAD), while APOE2 has a defensive effect. Research data suggest that APOE4 leads to the pathogenesis of AD through various processes such as accelerated beta-amyloid aggregations that raised neurofibrillary tangle formation, cerebrovascular diseases, aggravated neuroinflammation, and synaptic loss. However, the precise mode of actions regarding in what way APOE4 leads to AD pathology remains unclear. Since APOE contributes to several pathological pathways of AD, targeting APOE4 might serve as a promising strategy for the development of novel drugs to combat AD. In this review, we focus on the recent studies about APOE4-targeted therapeutic strategies that have been advanced in animal models and are being prepared for use in humans for the management of AD.

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Emerging Signal Regulating Potential of Genistein Against Alzheimer’s Disease: A Promising Molecule of Interest

Cited by 92 publications

References 106 publications

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

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

Neuroprotective mechanisms of red clover and soy isoflavones in Parkinson’s disease models

Molecular Insight into the Therapeutic Promise of TargetingAPOE4for Alzheimer’s Disease

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