Browsing by Subject "Optical coherence tomography"

Now showing 1 - 3 of 3
  • Thumbnail Image
    Publication
    Restricted
    ¿Hasta dónde llega la precocidad de la tomografía de coherencia óptica en el deterioro cognitivo?
    (Viguera editores, 2016-07-01) Giménez Castejón, Domingo; Martínez Martínez, María de los LLanos; Dudekova, Mirka; Lajara Blesa, Jerónimo; Gómez Gallego, María; Atención Sociosanitaria
    Introducción. La enfermedad de Alzheimer (EA) es la primera causa de demencia mundial. Cada vez son más los esfuerzos para lograr una detección temprana del deterioro cognitivo y surgen en el panorama científico entidades diagnósticas como el deterioro cognitivo leve (DCL) y las quejas subjetivas de memoria (QSM). Debido a ello, aparecen numerosos biomarcadores estudiados para conseguir dicho objetivo, entre ellos la tomografía de coherencia óptica. Sujetos y métodos. Se ha realizado un estudio que utiliza la tomografía de coherencia óptica para medir el grosor macular y la capa de fibras nerviosas de la retina en pacientes diagnosticados de EA (n = 36), pacientes con DCL (n = 33), en individuos con QSM (n = 24) y en sujetos control (n = 45). Resultados. Se han encontrado diferencias estadísticamente significativas en cuanto al grosor macular entre todos los grupos estudiados (QSM: 261,8 ± 25,88 μm; DCL: 259,19 ± 22,582 μm; EA leve: 258,53 ± 14,804 μm; EA moderada: 249,32 ± 18,467 μm) y sujetos control (271,96 ± 15,57 μm). Respecto a la capa de fibras nerviosas de la retina, ocurre de igual manera, y la diferencia es estadísticamente significativa frente al grupo control (94,51 ± 9,203 μm) de todos los grupos (QSM: 90,44 ± 9,059 μm; DCL: 89,4 ± 10,421 μm; EA leve: 87,12 ± 10,279 μm; EA moderada: 82,25 ± 10,636 μm). Conclusión. La tomografía de coherencia óptica podría situarse como un futuro biomarcador y una herramienta de apoyo para facilitar el diagnóstico precoz del deterioro cognitivo y de la EA.
  • Thumbnail Image
    Publication
    Open Access
    The aging rat retina: from function to anatomy
    (Elsevier, 2018-01-01) Nadal-Nicolás, Francisco Manuel; Vidal Sanz, Manuel; Agudo Barriuso, Marta; Oftalmología, Optometría, Otorrinolaringología y Anatomía Patológica; Facultad de Medicina
    In healthy beings, age is the ultimate reason of cellular malfunction and death. In the rat retina, age causes a functional decline and loss of specific neuronal populations. In this regard, controversial conclusions have been reported for the innermost retina. Here, we have studied the albino and pigmented retina for the duration of the rat life-span. Independent of age (21 dayse22 months), the electroretinographic recordings and the volume of the retina and its layers are smaller in albinos. Functionally, aging causes in both strains a loss of cone- and rod-mediated responses. Anatomically, cell density decreases with age because the retina grows linearly with time; no cell loss is observed in the ganglion cell layer; and only in the pigmented rat, there is a decrease in cone photoreceptors. In old animals of both strains, there is gliosis in the superior colliculi and a diminution of the area innervated by retinal ganglion cells. In conclusion, this work provides the basis for further studies linking senescence to neurodegenerative retinal diseases.
  • Thumbnail Image
    Publication
    Open Access
    Topical Treatment With Bromfenac Reduces Retinal Gliosis and Inflammation After Optic Nerve Crush
    (Association for Research in Vision and Ophthalmology, 2016-11) Rovere, Giuseppe ; Nadal-Nicolás, Francisco Manuel; Sobrado Calvo, Paloma; García Bernal, David; Villegas Pérez, Maria Paz; Vidal Sanz, Manuel; Agudo Barriuso, Marta; Oftalmología, Optometría, Otorrinolaringología y Anatomía Patológica; Facultad de Medicina
    Purpose: To study the effect of topical administration of bromfenac, a nonsteroidal anti-inflammatory drug (NSAID), on retinal gliosis and levels of prostaglandin E2 (PGE2) after complete optic nerve crush (ONC). Methods: Adult albino rats were divided into the following groups (n = 8 retinas/group): (1) intact, (2) intact and bromfenac treatment (twice a day during 7 days), (3) ONC (7 days), and (4) ONC (7 days) + bromfenac treatment (twice a day during 7 days). Animals from groups 3 and 4 were imaged in vivo with spectral-domain optical coherence tomography (SD-OCT) before the procedure and 15 minutes, 3, 5, or 7 days later. Retinas from all groups were analyzed by immunodetection, Western blotting, or enzyme-linked immunoabsorbent assay (ELISA). Results: Quantification of Brn3a (brain-specific homeobox/POU domain protein 3A) +RGCs (retinal ganglion cells) in cross sections showed that bromfenac treatment does not accelerate ONC-induced degeneration. Cellular retinaldehyde binding protein 1 regulation indicated that bromfenac improves retinal homeostasis in injured retinas. Spectral-domain OCT showed that the thickness of the retina and the retinal nerve fiber layer at 7 days post ONC was significantly reduced in bromfenac-treated animals when compared to untreated animals. In agreement with these data, hypertrophy of astrocytes and Müller cells and expression of glial fibrillary acidic protein and vimentin were greatly diminished by bromfenac treatment. While no changes in cyclooxygenase (COX) enzyme COX1 and COX2 expression were observed, there was a significant increase of PGE2 after ONC that was controlled by bromfenac treatment. Conclusions: Topical administration of bromfenac is an efficient and noninvasive treatment to control the retinal gliosis and release of proinflammatory mediators that follow a massive insult to the RGC population.