Non-steroidal anti-inflammatory drugs have anti-amyloidogenic effects for Alzheimer's β-amyloid fibrils in vitro

Hirohata, Mie; Ono, Kenjiro; Naiki, Hironobu; Yamada, Masahito

doi:10.1016/j.neuropharm.2005.07.004

Cited by 131 publications

(135 citation statements)

References 39 publications

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“…Ab [25][26][27][28][29][30][31][32][33][34][35] (Sigma-Aldrich Co., CA, U.S.A.) was dissolved in phosphate-buffered saline (PBS) and injected into animals at the beginning of each behavioral test trial by i.c.v. (10 mg/10 ml/mouse) according to the procedure established by Lauren and Belknap.…”

Section: Intracerebroventricular (Icv) Injection Of Ab B 25-35mentioning

confidence: 99%

“…Passive Avoidance Test The day before Ab [25][26][27][28][29][30][31][32][33][34][35] injection (at beginning of 5 weeks), mice were trained on a passive avoidance task. Passive avoidance was tested using a two-compartment shuttle chamber (256000 series, TSE Systems, Germany), one illuminated and one dark, equipped with a grid floor and shock generator.…”

Section: Intracerebroventricular (Icv) Injection Of Ab B 25-35mentioning

confidence: 99%

“…During the training trial, each mouse was placed in the lit compartment, and as soon as it entered the dark compartment, the door was closed and it received an inescapable shock (0.3 mA, 3 s). The day after Ab [25][26][27][28][29][30][31][32][33][34][35] injection, the mouse was again placed in the lit compartment, and the time until it returned to the dark compartment was measured as the step-through latency (with a maximum of 300 s). If the mouse did not enter the dark compartment within 300 s, the mouse was assumed to have memorized the passive avoidance training after one training trial.…”

Section: Intracerebroventricular (Icv) Injection Of Ab B 25-35mentioning

confidence: 99%

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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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Section: Intracerebroventricular (Icv) Injection Of Ab B 25-35mentioning

confidence: 99%

Section: Intracerebroventricular (Icv) Injection Of Ab B 25-35mentioning

confidence: 99%

Section: Intracerebroventricular (Icv) Injection Of Ab B 25-35mentioning

confidence: 99%

See 1 more Smart Citation

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

Ahn

Kim

et al. 2009

Biological & Pharmaceutical Bulletin

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“…Aspirin is widely utilized for the treatment of vascular dementia and possesses potential as a therapeutic agent in neurodegenerative disorders (12,13). Aspirin has been revealed to target pathological pathways in neurodegenerative disorders (14,15), however, the exact mechanisms of action of aspirin have yet to be elucidated. Furthermore, there is limited data concerning the therapeutic efficacy of aspirin on the opioid system in AD.…”

Section: Introductionmentioning

confidence: 99%

Memory-enhancing effect of aspirin is mediated through opioid system modulation in an AlCl3-induced neurotoxicity mouse model

Rizwan

Idrees

Ashraf

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. Neurodegenerative disorders such as Alzheimer's disease (AD) are multifaceted and there are currently a limited number of therapeutic strategies available to treat them. Aspirin is known to act on multiple therapeutic targets and is a successful anti-inflammatory agent in various tissues. The present study aimed to ascertain the performance of aspirin when employed as a therapeutic agent to treat neurodegeneration on novel targets, including opioid system genes, in an AlCl 3 -induced neurotoxicity mouse model. The effects of two doses of aspirin (5 and 20 mg/kg aspirin for 12 days) were investigated in an AlCl 3 -induced neurotoxicity mouse model (150 mg/kg AlCl 3 for 12 days). Neurological improvements were assessed through different behavioral tests and the effects of aspirin on opioid system gene expression levels were assessed by reverse transcription-polymerase chain reaction. Both doses resulted in improvements in cognitive behavior. A 5 mg/kg dose of aspirin was revealed to be effective for spatial memory improvement (7.14±0.84 sec), whilst a 20 mg/kg dose was superior for improving extinction learning (7.63±4.04%). Aspirin (5 mg/kg) also significantly improved contextual memory (48.05±10.6%) when compared with the AlCl 3 -treated group (1.49±0.62%; P<0.001). Aspirin was also observed to significantly decrease δ-opioid receptor expression in the cortex (1.09±0.08 and 1.27±0.08, respectively) at both doses (5 and 20 mg/kg) when compared with the AlCl 3 -treated group (3.69±1.43; P<0.05). Furthermore, aspirin at 5 mg/kg significantly reduced expression of prodynorphin in the cortex (0.57±0.20) when compared with the AlCl 3 -treated group (1.95±0.84; P<0.05). Notably, the effect of aspirin was significant in the cortex but not in the hippocampus. In summary, aspirin was effective in ameliorating the AD-like symptoms via the modulation of opioid systems. However, additional studies are required to determine the long term effects of aspirin on such conditions.

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“…NSAIDs, in particular ibuprofen and flurbiprofen, could act in a COX-independent manner shifting the βAPP metabolism toward shorter, more soluble and less fibrillogenic form of Aβ peptides, interfering with the γ [27] and β-secretases activities. Electron microscopy and fluorescence spectroscopy used to examine the effects of NSAIDs on β-amyloid fibrils demonstrated an inhibition of Aβ fibrils formation in a dosedepend manner as follows (ibuprofen > sulindac > meclofenamic acid > aspirin ~ ketoprofen > flurbiprofen ~ diclofenac > naproxen ~ indomethacin) [28]. In AD mice ibuprofen was able to reduce the number and the total area of β-amyloid deposits.…”

mentioning

confidence: 98%

Rheumatoid Arthritis and Alzheimer Disease: Possible Cellular and Molecular Links

Bahat

Tufan²,

Akın³

et al. 2012

J Gerontol Geriatric Res

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Alzheimer disease (AD) is the most common form of dementia of the old population over 85 years. AD pathogenesis is multifactorial and several findings support the neuroinflammatory pathogenetic hypothesis. There is an inverse relationship between AD and Rheumatoid arthritis (RA) due to different factors. Among them, NSAIDs use acting both on amyloid formation and COX enzymes has been supposed to play a protective role on AD risk. Moreover, new insights on colony stimulating factors (GM-CSF, M-CSF and G-CSF) pathways in immune cells differentiation suggested a possible cellular link between AR and the AD onset. Alzheimer disease (AD) is the most common form of dementia, accounts for 50-60% of all dementia cases. It interests about 20-40% of the old population over 85 years and is characterized by cognitive dysfunction as memory loss, language difficulties, visuospatial deficits, impairment in judgment and decision-making, deficit in higher and subsequently in basic daily activities, behavioral disturbances and psychiatric alterations. The classical AD pathologic hallmarks are senile plaques made by extracellular amyloid beta (Aβ) deposition and neurofibrillary tangles made of hyperphosphorylated Tau proteins [1].

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Non-steroidal anti-inflammatory drugs have anti-amyloidogenic effects for Alzheimer's β-amyloid fibrils in vitro

Cited by 131 publications

References 39 publications

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

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

Memory-enhancing effect of aspirin is mediated through opioid system modulation in an AlCl3-induced neurotoxicity mouse model

Rheumatoid Arthritis and Alzheimer Disease: Possible Cellular and Molecular Links

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