In this study, we present a new molecule, Memoquin, designed to display a range of activities potentially beneficial at distinct levels of the AD neuropathology. In vitro, this compound is able not only to inhibit acetylcholinesterase (AChE) activity, but it is also able to block in vitro the Abeta aggregation induced by AChE and shows anti-oxidant activity. In vivo, Memoquin was able to rescue, at the behavioral level, cognitive deficits in mice in which amnesia was induced by scopolamine and in AD11 anti-NGF transgenic mice. From the neuropathological point of view, in this comprehensive model for sporadic AD-like neurodegeneration, the oral admistration of Memoquin causes an effective recovery from the observed cholinergic deficit, tau hyperphosphorylation, beta-amyloid deposition. These findings show that a multiple therapeutic approach can be realized through properly designed molecules.
Memoquin: a new therapeutic poly-agent for Alzheimer's disease / Cavalli A.; Bolognesi M.L.; Bartolini M.; Andrisano V.; Melchiorre C.; Recanatini M.; Margotti E.; Capsoni S.; Cattaneo A.. - In: NEUROBIOLOGY OF AGING. - ISSN 0197-4580. - STAMPA. - 25:(2004), pp. S194-S194. (Intervento presentato al convegno The 9th International Conference on Alzheimer's Disease and Related Disorders tenutosi a Philadelphia, Pennsylvania, U.S.A. nel 17-22 Luglio 2004).
Memoquin: a new therapeutic poly-agent for Alzheimer's disease
CAVALLI, ANDREA;BOLOGNESI, MARIA LAURA;BARTOLINI, MANUELA;ANDRISANO, VINCENZA;MELCHIORRE, CARLO;RECANATINI, MAURIZIO;
2004
Abstract
In this study, we present a new molecule, Memoquin, designed to display a range of activities potentially beneficial at distinct levels of the AD neuropathology. In vitro, this compound is able not only to inhibit acetylcholinesterase (AChE) activity, but it is also able to block in vitro the Abeta aggregation induced by AChE and shows anti-oxidant activity. In vivo, Memoquin was able to rescue, at the behavioral level, cognitive deficits in mice in which amnesia was induced by scopolamine and in AD11 anti-NGF transgenic mice. From the neuropathological point of view, in this comprehensive model for sporadic AD-like neurodegeneration, the oral admistration of Memoquin causes an effective recovery from the observed cholinergic deficit, tau hyperphosphorylation, beta-amyloid deposition. These findings show that a multiple therapeutic approach can be realized through properly designed molecules.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
