β-Amyloid (1–42)-induced learning and memory deficits in mice: involvement of oxidative burdens in the hippocampus and cerebral cortex

Jhoo, Jin Hyeong; Kim, Hyoung Chun; Nabeshima, Toshitaka; Yamada, Kiyofumi; Shin, Eun Joo; Jhoo, Wang Kee; Kim, Woo-Kyung; Kang, Kee Seok; Jo, Sangmee Ahn; Woo, Jong Inn

doi:10.1016/j.bbr.2004.04.012

Cited by 170 publications

(121 citation statements)

References 50 publications

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“…AICD has been shown to be involved in the transcriptional regulation of various genes (23,24), including patched1 (Ptch1) (25). Recently, we demonstrated that neuronal precursors from the Ts65Dn mouse exhibit derangement of the Sonic Hedgehog (Shh) pathway due to an overexpression of Ptch1, its inhibitory regulator (26).…”

Section: Down Syndrome (Ds)mentioning

confidence: 99%

The Amyloid Precursor Protein (APP) Triplicated Gene Impairs Neuronal Precursor Differentiation and Neurite Development through Two Different Domains in the Ts65Dn Mouse Model for Down Syndrome

Trazzi¹,

Fuchs²,

Valli

et al. 2013

Journal of Biological Chemistry

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Background: Individuals with Down syndrome suffer from mental retardation due to severe neurogenesis impairment. Results: Normalization of the triplicated gene APP expression restores neuronal maturation and differentiation in trisomic neuronal precursors. Conclusion: APP overproduction contributes to neurogenesis impairment in DS.Significance: APP signaling may be a target for therapeutic approaches aiming to improve brain development in DS.

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Section: Down Syndrome (Ds)mentioning

confidence: 99%

The Amyloid Precursor Protein (APP) Triplicated Gene Impairs Neuronal Precursor Differentiation and Neurite Development through Two Different Domains in the Ts65Dn Mouse Model for Down Syndrome

Trazzi¹,

Fuchs²,

Valli

et al. 2013

Journal of Biological Chemistry

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“…Consistent with these findings, infusion of Ab 1-42 in rat brain has been shown to increase levels of 4-hydroxy-2-nonenal (a product of lipid peroxidation) and 8-OHdG. 37) Injection of Ab 25-35 also significantly decreased GPx activity. In accordance with this finding, Prediger et al 38) reported that spatial learning and memory impairments induced by Ab in mice are associated with decreased activity of glutathione (GSH)-dependent antioxidant defense systems.…”

Section: Discussionsupporting

confidence: 58%

“…Number of studies has demonstrated that the capacity to induced impairments of cognitive function is characteristic not only of Ab , but also several fragments such as Ab [25][26][27][28][29][30][31][32][33][34][35] and Ab [35][36][37][38][39][40][41][42] . 6,7,28,29) Ab [25][26][27][28][29][30][31][32][33][34][35] is the functional domain of Ab, responsible for its neurotoxic properties and oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Sesaminol Glucosides Protect .BETA.-Amyloid Peptide-Induced Cognitive Deficits in Mice

Ahn

Kim

et al. 2009

Biological & Pharmaceutical Bulletin

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Alzheimer's disease (AD) is characterized by progressive cognitive function deficits due to the presence of numerous senile plaques and neurofibrillary tangles in certain brain regions.1) The main component of senile plaques is b-amyloid peptide (Ab), which is derived from a large amyloid precursor protein (APP).2) Ab 25-35 contains the residues important for aggregation and toxicity including methionine 35.3) This amyloid fragment has been shown to induce neurotoxicity in vitro as well as in vivo. 4,5) In addition, the intracerebroventricular (i.c.v.) administration of Ab 25-35 into rodent brain induced histological change and cognitive deficit.6,7) The deposition of Ab may cause neuronal death via a number of possible mechanisms including oxidative stress and inflammatory response, which has been suggested to play a key role in AD pathogenesis. 2)Oxidative stress has been hypothesized to play a pivotal role in excitotoxicity, inflammation, and apoptosis in the AD brain. Marker of oxidative stress such as lipid peroxides, protein carbonyl groups, and 8-hydroxyl-2Ј-deoxyguanosine (8-OHdG) are increased in the brains of AD patients than in aged-matched control brains. 8,9) Moreover, it has been reported that Ab induces neurotoxicity via oxidative stress, and some antioxidants, such as vitamin E and ferulic acid, protect neurons from Ab-induced apoptosis. 4,10,11) Therefore, the attenuation of oxidative stress through antioxidant therapies may be useful in the treatment/prevention of AD. 12)Sesame (Sesamum indicum LINN.) is widely known as a natural healthy food, and contains sesame lignan and lignan glycosides.13) Sesame lignan compounds, including sesamin gludosides (SG), have been shown to inhibit endogenous lipid peroxidation as well as oxidative DNA damage in rat liver and kidney.14) These compounds also scavenge peroxyradicals in in vitro experimental systems. [15][16][17] Kang et al. 18) have reported that defatted sesame flour containing SG inhibits lipid peroxidation in hypercholesterolemic rabbits. We also observed that SG had a protective effect against Ab induced neuronal cell death 19) and showed an inhibitory effect on lipopolysaccharide (LPS)-induced inflammatory response in astrocytes. 20) Taking those facts into account, we hypothesized that SG exerts a neuroprotective effect in AD.Since the effect of SG on cognitive function has not been reported, we investigated whether SG can exhibit the protective effect on the Ab 25-35 -induced cognitive impairments. MATERIALS AND METHODSSample Preparation SG isolated form sesame seed was prepared according to the method described by Katsuzaki et al.13) Deffated sesame flour was extracted with distilled water at 95°C for 1 h to obtain a crude extract containing sesaminol glucosides. Crude SG was further purified by Diaion HP 20 (Mitsubishi Chemicals, Co., Tokyo, Japan) column using 60% ethanol. The extracts were concentrated under reduced pressure and freeze-dried for storage until use. Total SG content of the extract was determined by UV spectroscopy, and th...

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“…A passive avoidance (PA) task was performed as described (Jhoo et al, 2004). The PA apparatus consisted of two chambers separated with a gray plastic guillotine door; one (11 cm long Â 5 cm wide, with 13 cm walls) was illuminated and the other (25 cm long Â 25 cm wide, with 20 cm walls) was darkened with a constant current shock generator.…”

Section: Behavioral Testsmentioning

confidence: 99%

Nasal Colivelin Treatment Ameliorates Memory Impairment Related to Alzheimer's Disease

Yamada

Chiba

Sasabe

et al. 2007

Neuropsychopharmacol

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Humanin (HN) and its derivatives, such as Colivelin (CLN), suppress neuronal death induced by insults related to Alzheimer's disease (AD) by activating STAT3 in vitro. They also ameliorate functional memory impairment of mice induced by anticholinergic drugs or soluble toxic amyloid-b (Ab) in vivo when either is directly administered into the cerebral ventricle or intraperitoneally injected. However, the mechanism underlying the in vivo effect remains uncharacterized. In addition, from the standpoint of clinical application, drug delivery methods that are less invasive and specific to the central nervous system (CNS) should be developed. In this study, we show that intranasally (i.n.) administered CLN can be successfully transferred to CNS via the olfactory bulb. Using several behavioral tests, we have demonstrated that i.n. administered CLN ameliorates memory impairment of AD models in a dose-responsive manner. Attenuation of AD-related memory impairment by HN derivatives such as CLN appears to be correlated with an increase in STAT3 phosphorylation levels in the septohippocampal region, suggesting that anti-AD activities of HN derivatives may be mediated by activation of STAT3 in vivo as they are in vitro. We further demonstrate that CLN treatment inhibits an Ab induced decrease in the number of choline acetyltransferase (ChAT)-positive neurons in the medial septum. Combined with the finding that HN derivatives upregulate mRNA expression of neuronal ChAT and vesicular acetylcholine transporter (VAChT) in vitro, it is assumed that CLN may ameliorate memory impairment of AD models by supporting cholinergic neurotransmission, which is at least partly mediated by STAT3-mediated transcriptional upregulation of ChAT and VAChT.

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β-Amyloid (1–42)-induced learning and memory deficits in mice: involvement of oxidative burdens in the hippocampus and cerebral cortex

Cited by 170 publications

References 50 publications

The Amyloid Precursor Protein (APP) Triplicated Gene Impairs Neuronal Precursor Differentiation and Neurite Development through Two Different Domains in the Ts65Dn Mouse Model for Down Syndrome

The Amyloid Precursor Protein (APP) Triplicated Gene Impairs Neuronal Precursor Differentiation and Neurite Development through Two Different Domains in the Ts65Dn Mouse Model for Down Syndrome

Sesaminol Glucosides Protect .BETA.-Amyloid Peptide-Induced Cognitive Deficits in Mice

Nasal Colivelin Treatment Ameliorates Memory Impairment Related to Alzheimer's Disease

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