Sulforaphane Inhibits the Generation of Amyloid-β Oligomer and Promotes Spatial Learning and Memory in Alzheimer’s Disease (PS1V97L) Transgenic Mice

Hou, Tingting; Yang, Heyun; Wang, Wei; Wu, Qiaoqi; Tian, Yaru; Jia, Jianping

doi:10.3233/jad-171110

Cited by 55 publications

(55 citation statements)

References 40 publications

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“…In the transgenic PS1V97L mice model of AD, 6month-old animals treated with SFN for 4 months improved their cognitive function in comparison to aged match non-treated animals (Hou et al 2018). In another AD model, the double transgenic amyloid APP/PS1 (precursor protein/presenilin 1) mice, SFN treatment improved the ability of independent exploration in the open field, the environmental adaptability, and ameliorated the Morris maze test (Zhang et al 2017).…”

Section: Sulforaphane In the Treatment Of Different Neuropathologiesmentioning

confidence: 99%

Sulforaphane - role in aging and neurodegeneration

et al. 2019

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In the last several years, numerous molecules derived from plants and vegetables have been tested for their antioxidant, anti-inflammatory, and anti-aging properties. One of them is sulforaphane (SFN), an isothiocyanate present in cruciferous vegetables. SFN activates the antioxidant and anti-inflammatory responses by inducing Nrf2 pathway and inhibiting NF-κB. It also has an epigenetic effect by inhibiting HDAC and DNA methyltransferases and modifies mitochondrial dynamics. Moreover, SFN preserves proteome homeostasis (proteostasis) by activating the proteasome, which has been shown to lead to increased cellular lifespan and prevent neurodegeneration. In this review, we describe some of the molecular and physical characteristics of SFN, its mechanisms of action, and the effects that SFN treatment induces in order to discuss its relevance as a Bmiraculous^drug to prevent aging and neurodegeneration.

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Section: Sulforaphane In the Treatment Of Different Neuropathologiesmentioning

confidence: 99%

Sulforaphane - role in aging and neurodegeneration

et al. 2019

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“…Given the wide range of oxidative stress biomarkers altered by AAS (Table 1), broad spectrum antioxidants such as Nrf2 activators may be especially beneficial in supraphysiologic-dose AAS users and in other groups at risk for developing AD/ADRD. This hypothesis is supported by the observations that genetic knockout of Nrf2 exacerbates Aβ and tau-P burdens and spatial cognition impairments in AD mice (Branca et al, 2017;Rojo et al, 2017) and by the finding that the nutriceutical Nrf2 activator sulforaphane decreases β-secretase and PS-1 expression, Aβ and tau-P burdens, and improves cognition in AD mice (Hou et al, 2018;Lee et al, 2018). In non-AD models, sulforaphane inhibits GSK3β activity (Wang et al, 2016) and increases AQP4 expression (Zhao et al, 2005).…”

Section: Summary and Future Directionsmentioning

confidence: 87%

Supraphysiologic-dose anabolic–androgenic steroid use: A risk factor for dementia?

Kaufman

Kanayama

Hudson

et al. 2019

Neuroscience & Biobehavioral Reviews

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Supraphysiologic-dose anabolic-androgenic steroid (AAS) use is associated with physiologic, cognitive, and brain abnormalities similar to those found in people at risk for developing Alzheimer's Disease and its related dementias (AD/ADRD), which are associated with high brain β-amyloid (Aβ) and hyperphosphorylated tau (tau-P) protein levels. Supraphysiologic-dose AAS induces androgen abnormalities and excess oxidative stress, which have been linked to increased and decreased expression or activity of proteins that synthesize and eliminate, respectively, Aβ and tau-P. Aβ and tau-P accumulation may begin soon after initiating supraphysiologic-dose AAS use, which typically occurs in the early 20s, and their accumulation may be accelerated by other psychoactive substance use, which is common among non-medical AAS users. Accordingly, the widespread use of supraphysiologic-dose AAS may increase the numbers of people who develop dementia. Early diagnosis and correction of sex-steroid level abnormalities and excess oxidative stress could attenuate risk for developing AD/ADRD in supraphysiologic-dose AAS users, in people with other substance use disorders, and in people with low sex-steroid levels or excess oxidative stress associated with aging.

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“…Again, curcumin, myricetin, rosmarinic acid, ferulic acid, quercetin, scutellarin, berberine, resveratrol, and sulforaphane inhibit tau hyperphosphorylation and Aβ formation and destabilize Aβ preformed fibrils, meanwhile decreasing the levels of extracellular and intracellular Aβ in models of AD [ 76 , 210 , 211 , 212 , 213 , 214 , 215 ]. Recent studies aimed at elucidating the mechanisms by which polyphenols affect aggregation showed that the flavonoids gallocatechin gallate and theaflavin could completely inhibit Aβ aggregation, while the two stilbenes resveratrol and its glucoside derivative piceid could also suppress Aβ aggregation, though to a much lesser extent [ 216 ].…”

Section: Phytochemicals and Proteostasismentioning

confidence: 99%

Merging the Multi-Target Effects of Phytochemicals in Neurodegeneration: From Oxidative Stress to Protein Aggregation and Inflammation

et al. 2020

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Wide experimental evidence has been provided in the last decade concerning the neuroprotective effects of phytochemicals in a variety of neurodegenerative disorders. Generally, the neuroprotective effects of bioactive compounds belonging to different phytochemical classes are attributed to antioxidant, anti-aggregation, and anti-inflammatory activity along with the restoration of mitochondrial homeostasis and targeting alterations of cell-clearing systems. Far from being independent, these multi-target effects represent interconnected events that are commonly implicated in the pathogenesis of most neurodegenerative diseases, independently of etiology, nosography, and the specific misfolded proteins being involved. Nonetheless, the increasing amount of data applying to a variety of neurodegenerative disorders joined with the multiple effects exerted by the wide variety of plant-derived neuroprotective agents may rather confound the reader. The present review is an attempt to provide a general guideline about the most relevant mechanisms through which naturally occurring agents may counteract neurodegeneration. With such an aim, we focus on some popular phytochemical classes and bioactive compounds as representative examples to design a sort of main highway aimed at deciphering the most relevant protective mechanisms which make phytochemicals potentially useful in counteracting neurodegeneration. In this frame, we emphasize the potential role of the cell-clearing machinery as a kernel in the antioxidant, anti-aggregation, anti-inflammatory, and mitochondrial protecting effects of phytochemicals.

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Sulforaphane Inhibits the Generation of Amyloid-β Oligomer and Promotes Spatial Learning and Memory in Alzheimer’s Disease (PS1V97L) Transgenic Mice

Cited by 55 publications

References 40 publications

Sulforaphane - role in aging and neurodegeneration

Sulforaphane - role in aging and neurodegeneration

Supraphysiologic-dose anabolic–androgenic steroid use: A risk factor for dementia?

Merging the Multi-Target Effects of Phytochemicals in Neurodegeneration: From Oxidative Stress to Protein Aggregation and Inflammation

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