Ortiz, L. (Lourdes)

Filtering

2005 - 200912010 - 20181

Settings

Author search.filters.isAuthorOfPublication.8b0adbb3-2bda-40f4-a1b2-7e5d971155de

Search Results

Now showing 1 - 2 of 2
  • Thumbnail Image
    Interaction between an adcy3 genetic variant and two weight-lowering diets affecting body fatness and body composition outcomes depending on macronutrient distribution: a randomized trial
    (MDPI AG, 2018) Martinez, J.A. (José Alfredo); Riezu-Boj, J.I. (José Ignacio); Ortiz, L. (Lourdes); Corrales, F.J. (Fernando José); Goñi-Mateos, L. (Leticia); Milagro-Yoldi, F.I. (Fermín Ignacio); Cuervo, M. (Marta)
    The adenylate cyclase 3 (ADCY3) gene is involved in the regulation of several metabolic processes including the development and function of adipose tissue. The effects of the ADCY3 rs10182181 genetic variant on changes in body composition depending on the macronutrient distribution intake after 16 weeks of the dietary intervention were tested. The ADCY3 genetic variant was genotyped in 147 overweight or obese subjects, who were randomly assigned to one of the two diets varying in macronutrient content: a moderately-high-protein diet and a low-fat diet. Anthropometric and body composition measurements (DEXA scan) were recorded. Significant interactions between the ADCY3 genotype and dietary intervention on changes in weight, waist circumference, and body composition were found after adjustment for covariates. Thus, in the moderately-high-protein diet group, the G allele was associated with a lower decrease of fat mass, trunk and android fat, and a greater decrease in lean mass. Conversely, in the low-fat diet group carrying the G allele was associated with a greater decrease in trunk, android, gynoid, and visceral fat. Subjects carrying the G allele of the rs10182181 polymorphism may benefit more in terms of weight loss and improvement of body composition measurements when undertaking a hypocaloric low-fat diet as compared to a moderately-high-protein diet.
  • Thumbnail Image
    Accelerated amyloid deposition, neurofibrillary degeneration and neuronal loss in double mutant APP/tau transgenic mice
    (Elsevier, 2005) Ortiz, L. (Lourdes); Gomez-Isla, T. (Teresa); Avila, J. (Jesús); Perez-Mediavilla, L.A. (Luis Alberto); Ramos, P. (Pilar); Catena, S. (Silvia); Cabodevilla, F. (Felipe); Perez, M. (Mar); Samaranch, L. (Lluis); Ribe, E. (Elena M.); Ferrer, I. (Isidro); Nieto, M. (María); Puig, B. (Berta); Moran, M.A. (María Asunción); Cuadrado-Tejedor, M. (Mar); Sesma, T. (Teresa); Gich, I. (Ignasi); Sanchez, B. (Belén); Lim, F. (Filip)
    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.