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Neuroscience. 2013 Oct 10;250:309-19. doi: 10.1016/j.neuroscience.2013.07.014. Epub 2013 Jul 18.

Attenuating Aβ1-42-induced toxicity by a novel acetylcholinesterase inhibitor.

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1
Department of Pharmaceutical Sciences, Birla Institute of Technology, Mesra, 835215 Ranchi, India. Electronic address: nmishra@bitmesra.ac.in.

Erratum in

  • Neuroscience. 2013 Nov 12;252:526.

Abstract

We explored the attenuating effects of NP-9 on β-amyloid (Aβ) aggregation and amyloid-induced toxicity. NP-9 is a recently reported monoamine oxidase B (MAO-B), and acetylcholinesterase (AChE) inhibitor. In the present study, we found that NP-9 inhibited AChE activity in a dose-dependent manner with a maximal inhibition dose of 8 mg/kg, i.p. It inhibited Aβ aggregation, observed through thioflavin-T assay (IC50=60 μM) and scanning electron microscopy (S.E.M.) (no fibril formation). NP-9 has shown marked protection against scopolamine and Aβ1-42-induced memory impairments. It also minimized neuronal loss and amyloid plaque deposition in the brains of Aβ1-42-induced mice model. Therefore, NP-9 could be a promising lead molecule for AD, with effects against MAO-B, AChE, Aβ aggregation, and Aβ1-42 induced toxicity.

KEYWORDS:

3-(anthracen-10-yl)-5-(3-nitrophenyl)-4,5-dihydro-1H-pyrazole; AChE; AD; Alzheimer’s disease; Aβ; GSH; MAO; MTDL; Multi-target-directed ligand; NP-9; PAS; S.E.M.; Scopolamine; Th-T; acetylcholinesterase; acetylcholinesterase inhibitor; amnesia; glutathione; monoamine oxidase; multi-target-directed ligand; peripheral anionic site; scanning electron microscopy; thioflavin-T; β-amyloid

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