Nicotine breaks down preformed Alzheimer’s β-amyloid fibrils in vitro

Ono, Kenjiro; Hara, Kazuhiro; Yamada, Masahito; Naiki, Hironobu

doi:10.1016/s0006-3223(02)01417-8

Cited by 110 publications

(110 citation statements)

References 29 publications

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“…This negative association is in agreement with postmortem studies showing diminutions of amyloid plaque deposits in former smokers with AD (Hellstrom-Lindahl et al, 2004b). Nicotine treatment appears to interfere with the formation of the amyloid plaques in vitro and in vivo (Hellstrom-Lindahl et al, 2004a;Ono et al, 2002;Utsuki et al, 2002) and to reduce the accumulation of insoluble Aβ42 peptides (Nordberg et al, 2002) through a mechanism mediated by alpha7nAChRs as shown with mecamylamine that blocks the increase of sAPP produced by treating SH-SY5Y neuroblastoma cells with nicotine (Hellstrom-Lindahl et al, 2004a). Several clinical trials indicate that chronic administration of nicotine in individuals with age-associated memory impairments and AD improves cognition in attention but not in memory (Snaedal et al, 1996;Levin, 1999, 2004;Wilson et al, 1995).…”

Section: Epidemiological Implications Of Nicotine In Neurodegenerativsupporting

confidence: 80%

Alpha7 nicotinic acetylcholine receptor: A link between inflammation and neurodegeneration

Conejero-Goldberg

Davies

Ulloa

2008

Neuroscience & Biobehavioral Reviews

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Alzheimer's disease (AD) is the leading cause of dementia affecting over 25 million people worldwide. Classical studies focused on the description and characterization of the pathological hallmarks found in AD patients including the neurofibrillary tangles and the amyloid plaques. Current strategies focus on the etiology of these hallmarks and the different mechanisms contributing to neurodegeneration. Among them, recent studies reveal the close interplay between the immunological and the neurodegenerative processes. This article examines the implications of the alpha7 nicotinic acetylcholine receptor (alpha7nAChR) as a critical link between inflammation and neurodegeneration in AD. Alpha7nAChRs are not only expressed in neurons but also in Glia cells where they can modulate the immunological responses contributing to AD. Successful therapeutic strategies against AD should consider the connections between inflammation and neurodegeneration. Among them, alpha7nAChR may represent a pharmacological target to control these two mechanisms during the pathogenesis of neurodegenerative and behavioral disorders.

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Section: Epidemiological Implications Of Nicotine In Neurodegenerativsupporting

confidence: 80%

Alpha7 nicotinic acetylcholine receptor: A link between inflammation and neurodegeneration

Conejero-Goldberg

Davies

Ulloa

2008

Neuroscience & Biobehavioral Reviews

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“…Taking into consideration the findings we obtained previously by systematic in vitro studies, we judged the overall activity of the anti-amyloidogenic molecules to be in the order of: tannic acid >> NDGA = wine-related polyphenols (myricetin, morin, quercetin) >> Rif = Tc > poly(vinylsulfonic acid, sodium salt) = 1,3-propanedisulfonic acid, disodium salt > iAß5 > nicotine (Ono et al, 2002a;2002b;2004a). In this study, we observed that the activity of SSide and Ibu is similar to that of Rif (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…Fresh, non-aggregated fAß(1-40) and fAß(1-42) were obtained by extending sonicated fAß(1-40) or fAß(1-42) with fresh Aß(1-40) or Aß(1-42) solutions, respectively, just before the destabilization reaction (Ono et al, 2002a;2002b) . The reaction mixture was 600 µL and contained 10 µg/mL (2.3 µM) fAß(1-40) or fAß(1-42), 50 µM Aß(1-40) or Aß(1-42), 50 mM phosphate buffer, pH 7.5, and 100 mM NaCl.…”

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confidence: 99%

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

et al. 2005

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The pathogenesis of Alzheimer's disease (AD) is characterized by cerebral deposits of amyloid ß-peptides (Aß) and neurofibrillary tangles which are surrounded by inflammatory cells. Long-term uses of non-steroidal anti-inflammatory drugs (NSAIDs) reduce the risk of developing AD and delay the onset of the disease. In the present study, we used fluorescence spectroscopy with thioflavin T and electron microscopy to examine the effects of NSAIDs such as ibuprofen, aspirin, meclofenamic acid sodium salt, diclofenac sodium salt, ketoprofen, flurbiprofen, naproxen, sulindac sulfide and indomethacin on the formation, extension, and destabilization of ß-amyloid fibrils (fAß) at pH 7.5 at 37˚C in vitro. All examined NSAIDs dose-dependently inhibited formation of fAß from fresh Aß(1-40) and Aß(1-42), as well as their extension. Moreover, these NSAIDs dose-dependently destabilized preformed fAßs. The overall activity of the molecules examined was in the following order: ibuprofen ≈ sulindac sulfide ≥ meclofenamic acid sodium salt > aspirin ≈ ketoprofen ≥ flurbiprofen ≈ diclofenac sodium salt > naproxen ≈ indomethacin. Although the mechanisms by which these NSAIDs inhibit fAß formation from Aß, and destabilize preformed fAß in vitro are still unclear, NSAIDs may be promising for the prevention and treatment of AD.

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“…A polymerization assay was performed in the current study using a previously described procedure [15,16]. A reaction mixture containing 25 μM Aβ42 was mixed with different amounts (i.e., 0.3, 1.0, 3.0, 10, 30, 50 and 100 μM) of compounds 1, 2 and 6, as well as 1% DMSO, 50 mM phosphate buffer (pH 7.5) and 100 mM NaCl.…”

Section: Polymerization Assaymentioning

confidence: 99%

Quantitative Analysis of the Flavonoid Glycosides and Terpene Trilactones in the Extract of Ginkgo biloba and Evaluation of Their Inhibitory Activity towards Fibril Formation of β-Amyloid Peptide

et al. 2014

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Abstract:The standard extract of Ginkgo biloba leaves (EGb761) is used clinically in Europe for the symptomatic treatment of impaired cerebral function in primary degenerative dementia syndromes, and the results of numerous in vivo and in vitro studies have supported such clinical use. The abnormal production and aggregation of amyloid β peptide (Aβ) and the deposition of fibrils in the brain are regarded as key steps in the onset of Alzheimer's Disease (AD), and the inhibition of Aβ aggregation and destabilization of the preformed fibrils represent viable approaches for the prevention and treatment of AD. Flavonoid glycosides and terpene trilactones (TTLs) are the two main components of EGb761 which represent 24 and 6% of the overall content, respectively. In our research, seven abundant flavonoid glycosides 1-7 were isolated from the extract of Ginkgo biloba leaves and characterized by spectroscopic analysis. Furthermore, an ultra-high performance liquid chromatography method was established for the simultaneous quantification of these seven flavonoids. The inhibitory activities of these flavonoids, as well as four TTLs, i.e., ginkgolides A, B, and C and bilobalide (compounds 8-11), were evaluated towards Aβ42 fibril formation using a thioflavin T fluorescence assay. It was found that three flavonoids 1, 3 and 4 exhibited moderate inhibitory activities, whereas the other four flavonoids 2, 5, 6 OPEN ACCESSMolecules 2014, 19 4467 and 7, as well as the four terpene trilactones, showed poor activity. This is the first report of the inhibition of Aβ fibril formation of two characteristic acylated flavonoid glycosides 6, 7 in Ginkgo leaves, on the basis of which the structure-activity relationship of these flavonoids 1-7 was discussed.

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Nicotine breaks down preformed Alzheimer’s β-amyloid fibrils in vitro

Cited by 110 publications

References 29 publications

Alpha7 nicotinic acetylcholine receptor: A link between inflammation and neurodegeneration

Alpha7 nicotinic acetylcholine receptor: A link between inflammation and neurodegeneration

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

Quantitative Analysis of the Flavonoid Glycosides and Terpene Trilactones in the Extract of Ginkgo biloba and Evaluation of Their Inhibitory Activity towards Fibril Formation of β-Amyloid Peptide

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