Amelioration of Alzheimer's disease by neuroprotective effect of sulforaphane in animal model
Kim HV, Kim HY, Ehrlich HY, Choi SY, Kim DJ, Kim Y
Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis · 124 citations
Review labels
Neutral facts our review recorded about how this study was done. They describe method, never whether we like the result.
How it was studied
- Design
- Animal study (classified by our AI screen)
- Studied in
- Animals
- Main outcome
- Health markers and function
Who paid for it
- Funding
- Funding not disclosed
Publication
- Published
- 2012-12-19 · Amyloid · vol. 20 · issue 1 · pp. 7–12
- Publisher
- Taylor & Francis
- Cited
- 153 citations · more than 94% of similar papers · 3.5× the field average
- Impact
- Top 10% most cited in its field
- References
- 38 works
- Access
- Paywalled
- Research areas
- Genomics, phytochemicals, and oxidative stress · Cholinesterase and Neurodegenerative Diseases · Tryptophan and brain disorders
- Keywords
- Sulforaphane, Chemistry, Neuroprotection, Antioxidant, Oxidative stress, Reactive oxygen species, Pharmacology, Dimethyl sulfoxide, Glutathione, Biochemistry, Medicine, Enzyme
- MeSH
- hippocampus, neurons, cell line, animals, mice, inbred icr, humans, mice, alzheimer disease, disease models, animal, reactive oxygen species, thiocyanates, isothiocyanates, sulfoxides, neuroprotective agents, antioxidants, cognition, avoidance learning, maze learning, oxidative stress, male, amyloid beta-peptides
6 authors
From KR, US
- Hyunjin Vincent KimKorea Institute of Brain Science; Korea Institute of Science and Technology
- Hye Yun KimKorea Institute of Brain Science; Korea Institute of Science and Technology
- Hanna Y. EhrlichTufts University; Korea Institute of Brain Science; Korea Institute of Science and Technology
- Seon Young ChoiKorea Institute of Brain Science; Korea Institute of Science and Technology
- Dong Jin KimKorea Institute of Brain Science; Korea Institute of Science and Technology
- Young Soo Kim · correspondingKorea Institute of Brain Science; Korea Institute of Science and Technology
Abstract
Pathophysiological evidences of AD have indicated that aggregation of Aβ is one of the principal causes of neuronal dysfunction, largely by way of inducing oxidative stresses such as free radical formation. We hypothesized that the known antioxidative attribute of SFN could be harnessed in Alzheimer's treatment. SFN is an indirect, potent antioxidant derived from broccoli that has previously been found to stimulate the Nrf2-ARE pathway and facilitate several other cytoprotective mechanisms. In this study, administration of SFN ameliorated cognitive function of Aβ-induced AD acute mouse models in Y-maze and passive avoidance behavior tests. Interestingly, we found that the therapeutic effect of SFN did not involve inhibition of Aβ aggregation. While the exact mechanism of interaction of SFN in AD has not yet been ascertained, our results suggest that SFN can aid in cognitive impairment and may protect the brain from amyloidogenic damages.
Abstract via Europe PMC. Copyright remains with the authors or publisher.
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