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Dadun > Depósito Académico > CIMA (Centro de Investigación Médica Aplicada) > Área de Neurociencias > Neurofarmacología y conducta > DA - CIMA - Neurociencias - Neurofarmacología y conducta - Artículos de Revista >

Accelerated amyloid deposition, neurofibrillary degeneration and neuronal loss in double mutant APP/tau transgenic mice
Authors: Ribe, E. (Elena M.)
Perez, M. (Mar)
Puig, B. (Berta)
Gich, I. (Ignasi)
Lim, F. (Filip)
Cuadrado-Tejedor, M. (Mar)
Sesma, T. (Teresa)
Catena, S. (Silvia)
Sanchez, B. (Belén)
Nieto, M. (María)
Gomez-Ramos, P. (Pilar)
Moran, M.A. (María Asunción)
Cabodevilla, F. (Felipe)
Samaranch, L. (Lluis)
Ortiz, L. (Lourdes)
Perez-Mediavilla, L.A. (Luis Alberto)
Ferrer, I. (Isidro)
Avila, J. (Jesús)
Gomez-Isla, T. (Teresa)
Keywords: APP
Beta-amyloid
Tau
Lisosomes
Stereology
Neuronal loss
Transgenic mice
Alzheimer’s disease
Issue Date: 2005
Publisher: Elsevier
Publisher version: http://dx.doi.org/10.1016/j.nbd.2005.05.027
ISSN: 0969-9961
Citation: Ribe EM, Perez M, Puig B, Gich I, Lim F, Cuadrado M, et al. Accelerated amyloid deposition, neurofibrillary degeneration and neuronal loss in double mutant APP/tau transgenic mice. Neurobiol Dis 2005 Dec;20(3):814-22.
Abstract
Even though the idea that amyloid beta peptide accumulation is the primary event in the pathogenesis of Alzheimer's disease has become the leading hypothesis, the causal link between aberrant amyloid precursor protein processing and tau alterations in this type of dementia remains controversial. We further investigated the role of beta-amyloid production/deposition in tau pathology and neuronal cell death in the mouse brain by crossing Tg2576 and VLW lines expressing human mutant amyloid precursor protein and human mutant tau, respectively. The resulting double transgenic mice showed enhanced amyloid deposition accompanied by neurofibrillary degeneration and overt neuronal loss in selectively vulnerable brain limbic areas. These findings challenge the idea that tau pathology in Alzheimer's disease is merely a downstream effect of amyloid production/deposition and suggest that reciprocal interactions between beta-amyloid and tau alterations may take place in vivo.
Permanent link: http://hdl.handle.net/10171/19659
Appears in Collections:DA - CIMA - Neurociencias - Neurofarmacología y conducta - Artículos de Revista

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