Oxidative stress accelerates amyloid deposition and memory impairment in a double-transgenic mouse model of Alzheimer's disease

Kanamaru, Takuya; Kamimura, Naomi; Yokota, Takashi; Iuchi, Katsuya; Nishimaki, Kiyomi; Takami, Shinya; Akashiba, Hiroki; Shitaka, Yoshitsugu; Katsura, Ken‐ichiro; Kimura, Kazumi; Ohta, Shigeo

doi:10.1016/j.neulet.2014.12.033

Cited by 48 publications

(29 citation statements)

References 29 publications

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“…In a double-transgenic mouse model of AD (APP/DAL), over-expression of a mutant form of human amyloid precursor protein (APP) and a dominant-negative mutant of mitochondrial aldehyde dehydrogenase 2 (ALDH2) was shown to increase oxidative stress. Furthermore, these transgenic APP/DAL mice showed impaired performance on Y-maze and object recognition tests at 3 months of age, suggesting that oxidative stress accelerates cognitive dysfunction and pathological insults in the brain (Ohsawa et al, 2008; Kanamaru et al, 2015). Although the underlying causes for cognitive deficits are uncharacterized, it is likely that mitochondrial function of these animals would be significantly suppressed due to increased oxidative stress, compared to those of the corresponding wild-type mice.…”

Section: Mitochondrial Dysfunctions In Selected Neurodegenerative mentioning

confidence: 99%

Mitochondrial dysfunction and cell death in neurodegenerative diseases through nitroxidative stress

et al. 2016

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Mitochondria are important for providing cellular energy ATP through the oxidative phosphorylation pathway. They are also critical in regulating many cellular functions including the fatty acid oxidation, the metabolism of glutamate and urea, the anti-oxidant defense, and the apoptosis pathway. Mitochondria are an important source of reactive oxygen species leaked from the electron transport chain while they are susceptible to oxidative damage, leading to mitochondrial dysfunction and tissue injury. In fact, impaired mitochondrial function is commonly observed in many types of neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, alcoholic dementia, brain ischemia-reperfusion related injury, and others, although many of these neurological disorders have unique etiological factors. Mitochondrial dysfunction under many pathological conditions is likely to be promoted by increased nitroxidative stress, which can stimulate post-translational modifications (PTMs) of mitochondrial proteins and/or oxidative damage to mitochondrial DNA and lipids. Furthermore, recent studies have demonstrated that various antioxidants, including naturally occurring flavonoids and polyphenols as well as synthetic compounds, can block the formation of reactive oxygen and/or nitrogen species, and thus ultimately prevent the PTMs of many proteins with improved disease conditions. Therefore, the present review is aimed to describe the recent research developments in the molecular mechanisms for mitochondrial dysfunction and tissue injury in neurodegenerative diseases and discuss translational research opportunities.

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Section: Mitochondrial Dysfunctions In Selected Neurodegenerative mentioning

confidence: 99%

Mitochondrial dysfunction and cell death in neurodegenerative diseases through nitroxidative stress

et al. 2016

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“…However, in the case of AD, increased oxidative stress is not only a significant component of pathology exacerbating the neurodegenerative process [55][56][57][58][59] , but it is also believed to be one of the earliest events in the disease development that could even precede Aβ deposition [122] . Oxidative stress may stimulate Aβ production [123,124] , as well as tau hyperphosphorylation and polymerization [125,126] .…”

Section: Nrf2 Gene Transfer For Chronic Neurological Disordersmentioning

confidence: 99%

Applications of the Keap1–Nrf2 system for gene and cell therapy

Pomeshchik

Leinonen

Malm

et al. 2015

Free Radical Biology and Medicine

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“…These beneficial effects include anti-microbial, antiinflammatory, antitumour and antineoplastic effects. [11][12][13][14] Recently, the protective effects of honey on chemical oxidative liver injury has been validated by increasing researchers, making honey a potential good hepatoprotective product. 10 And accumulating scientific researches demonstrates that the antioxidant activity of honey empowers its therapeutic effect on acting against several chronic disease caused by oxidative damage including cardiovascular, cancer, diabetes and Alzheimer's disease.…”

Section: Introductionmentioning

confidence: 99%

Antioxidant and hepatoprotective activity of vitex honey against paracetamol induced liver damage in mice

Wang

Cheng

et al. 2015

Food Funct.

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Fourteen vitex honeys from China were investigated to evaluate its antioxidant and hepatoprotective activity against paracetamol-induced liver damage. All honey samples exhibited high total phenolic content (344-520 mg GAE per kg), total flavonoid content (19-31 mg Rutin per kg), and strong antioxidant activity in DPPH radical scavenging, ferric reducing antioxidant power and Ferrous ion-chelating ability. Nine phenolic acids were detected in vitex honey samples, in which caffeic acid was the main compound. Honey from Heibei Zanhuang (S2) ranked the highest antioxidant activity was orally administered to mice (5 g kg(-1), 20 g kg(-1)) for 70 days. In high-dose (20 g kg(-1)), vitex honey pretreatment resulting in significant increase in serum oxygen radical absorbance capacity (15.07%) and decrease in Cu(2+)-mediate lipoprotein oxidation (80.07%), and suppression in alanine aminotransferase (75.79%) and aspartate aminotransferase (74.52%), enhancement in the superoxide dismutase and glutathione peroxidase activities and reduction in malondialdehyde (36.15%) and 8-hydroxy-2'-deoxyguanosine (19.6%) formation compared with paracetamol-intoxicated group. The results demonstrated the hepatoprotection of vitex honey against paracetamol-induced liver damage might attribute to its antioxidant and/or perhaps pro-oxidative property.

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Oxidative stress accelerates amyloid deposition and memory impairment in a double-transgenic mouse model of Alzheimer's disease

Cited by 48 publications

References 29 publications

Mitochondrial dysfunction and cell death in neurodegenerative diseases through nitroxidative stress

Mitochondrial dysfunction and cell death in neurodegenerative diseases through nitroxidative stress

Applications of the Keap1–Nrf2 system for gene and cell therapy

Antioxidant and hepatoprotective activity of vitex honey against paracetamol induced liver damage in mice

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