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Accelerated amyloid deposition, neurofibrillary degeneration and neuronal loss in double mutant APP/tau transgenic mice

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Accelerated amyloid deposition, neurofibrillary degeneration and neuronal loss in double mutant APP/tau transgenic mice. / Ribé, Elena M; Pérez, Mar; Puig, Berta; Gich, Ignasi; Lim, Filip; Cuadrado, Mar; Sesma, Teresa; Catena, Silvia; Sánchez, Belén; Nieto, María; Gómez-Ramos, Pilar; Morán, M Asunción; Cabodevilla, Felipe; Samaranch, Lluis; Ortiz, Lourdes; Pérez, Alberto; Ferrer, Isidro; Avila, Jesús; Gómez-Isla, Teresa; Puig Martorell, Berta.

In: NEUROBIOL DIS, Vol. 20, No. 3, 01.12.2005, p. 814-22.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Ribé, EM, Pérez, M, Puig, B, Gich, I, Lim, F, Cuadrado, M, Sesma, T, Catena, S, Sánchez, B, Nieto, M, Gómez-Ramos, P, Morán, MA, Cabodevilla, F, Samaranch, L, Ortiz, L, Pérez, A, Ferrer, I, Avila, J, Gómez-Isla, T & Puig Martorell, B 2005, 'Accelerated amyloid deposition, neurofibrillary degeneration and neuronal loss in double mutant APP/tau transgenic mice', NEUROBIOL DIS, vol. 20, no. 3, pp. 814-22. https://doi.org/10.1016/j.nbd.2005.05.027

APA

Ribé, E. M., Pérez, M., Puig, B., Gich, I., Lim, F., Cuadrado, M., Sesma, T., Catena, S., Sánchez, B., Nieto, M., Gómez-Ramos, P., Morán, M. A., Cabodevilla, F., Samaranch, L., Ortiz, L., Pérez, A., Ferrer, I., Avila, J., Gómez-Isla, T., & Puig Martorell, B. (2005). Accelerated amyloid deposition, neurofibrillary degeneration and neuronal loss in double mutant APP/tau transgenic mice. NEUROBIOL DIS, 20(3), 814-22. https://doi.org/10.1016/j.nbd.2005.05.027

Vancouver

Ribé EM, Pérez 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 1;20(3):814-22. https://doi.org/10.1016/j.nbd.2005.05.027

Bibtex

@article{b3626fe9150341ee95dc73b16a4a8f44,
title = "Accelerated amyloid deposition, neurofibrillary degeneration and neuronal loss in double mutant APP/tau transgenic mice",
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.",
keywords = "Alzheimer Disease, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Animals, Brain, Cell Death, Disease Models, Animal, Female, Humans, Male, Mice, Mice, Knockout, Mice, Transgenic, Mutation, Nerve Degeneration, Neurofibrillary Tangles, Neurons, Plaque, Amyloid, tau Proteins",
author = "Rib{\'e}, {Elena M} and Mar P{\'e}rez and Berta Puig and Ignasi Gich and Filip Lim and Mar Cuadrado and Teresa Sesma and Silvia Catena and Bel{\'e}n S{\'a}nchez and Mar{\'i}a Nieto and Pilar G{\'o}mez-Ramos and Mor{\'a}n, {M Asunci{\'o}n} and Felipe Cabodevilla and Lluis Samaranch and Lourdes Ortiz and Alberto P{\'e}rez and Isidro Ferrer and Jes{\'u}s Avila and Teresa G{\'o}mez-Isla and {Puig Martorell}, Berta",
year = "2005",
month = dec,
day = "1",
doi = "10.1016/j.nbd.2005.05.027",
language = "English",
volume = "20",
pages = "814--22",
journal = "NEUROBIOL DIS",
issn = "0969-9961",
publisher = "Academic Press Inc.",
number = "3",

}

RIS

TY - JOUR

T1 - Accelerated amyloid deposition, neurofibrillary degeneration and neuronal loss in double mutant APP/tau transgenic mice

AU - Ribé, Elena M

AU - Pérez, Mar

AU - Puig, Berta

AU - Gich, Ignasi

AU - Lim, Filip

AU - Cuadrado, Mar

AU - Sesma, Teresa

AU - Catena, Silvia

AU - Sánchez, Belén

AU - Nieto, María

AU - Gómez-Ramos, Pilar

AU - Morán, M Asunción

AU - Cabodevilla, Felipe

AU - Samaranch, Lluis

AU - Ortiz, Lourdes

AU - Pérez, Alberto

AU - Ferrer, Isidro

AU - Avila, Jesús

AU - Gómez-Isla, Teresa

AU - Puig Martorell, Berta

PY - 2005/12/1

Y1 - 2005/12/1

N2 - 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.

AB - 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.

KW - Alzheimer Disease

KW - Amyloid beta-Peptides

KW - Amyloid beta-Protein Precursor

KW - Animals

KW - Brain

KW - Cell Death

KW - Disease Models, Animal

KW - Female

KW - Humans

KW - Male

KW - Mice

KW - Mice, Knockout

KW - Mice, Transgenic

KW - Mutation

KW - Nerve Degeneration

KW - Neurofibrillary Tangles

KW - Neurons

KW - Plaque, Amyloid

KW - tau Proteins

U2 - 10.1016/j.nbd.2005.05.027

DO - 10.1016/j.nbd.2005.05.027

M3 - SCORING: Journal article

C2 - 16125396

VL - 20

SP - 814

EP - 822

JO - NEUROBIOL DIS

JF - NEUROBIOL DIS

SN - 0969-9961

IS - 3

ER -