Person: López Cuenca, Inés
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First Name
Inés
Last Name
López Cuenca
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Medicina
Department
Inmunología, Oftalmología y ORL
Area
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Item Situs inversus del nervio óptico. A propósito de un caso(Revista de Neurología, 2017) López Cuenca, Inés; Hoz Montañana, Rosa de; García Martín, Elena Salobrar; Rojas López, Blanca; Ramírez Sebastián, Ana Isabel; Salazar Corral, Juan José; Triviño Casado, Alberto; Ramirez Sebastian, Jose ManuelIntroducción. El situs inversus del nervio óptico es una anomalía congénita caracterizada por la emergencia de los vasos de la retina en dirección nasal en lugar de temporal. Es causado por una anómala inserción del tallo óptico en la vesícula óptica que da lugar a la variación de disposición de la cabeza del nervio óptico. No es una condición aislada y suele aparecer junto con el síndrome del disco inclinado y en pacientes con miopía. Se caracteriza por la presencia de un cono de atrofia inferior, defectos en el campo visual temporal, defectos de refracción y ambliopía. Caso clínico. Mujer de 22 años, que acude a revisión oftalmológica por presentar fuertes cefaleas frontales acompañadas de halos y pérdida de nitidez en la visión. Tras un examen optométrico y oftalmológico se llega al juicio clínico de que padece un cuadro compatible con esta anomalía anatómica congénita. Conclusiones. El situs inversus del nervio óptico es una condición rara que puede aparecer aislada o acompañada de otras patologías. La aplicación de la campimetría y de nuevas técnicas diagnósticas, como la tomografía de coherencia óptica, facilita el diagnóstico diferencial de esta situación. No se conoce su prevalencia, pues no se encuentra en el registro de las enfermedades raras. Además, el escaso número de pacientes estudiados y la exigua bibliografía existente sobre esta anomalía no permiten conocer si los defectos causados progresan en el tiempo, por lo que sería importante realizar un seguimiento oftalmológico de los pacientes con situs inversus del nervio óptico.Item Ocular Exploration in the Diagnosis and Follow-Up of the Alzheimer’s Dementia(Alzheimer’s Disease, 2019) García Martín, Elena Salobrar; Hoz Montañana, María Rosa de; Ramírez Sebastián, Ana Isabel; Salazar Corral, Juan José; Rojas Lozano, Pilar; López Cuenca, Inés; Fernández Albarral, José Antonio; Ramirez Sebastian, Jose ManuelThe retina is part of the central nervous system (CNS), and therefore, in Alzheimer’s disease (AD), retinal and optic nerve degeneration could take place. This degeneration leads to neurofunctional changes that can be detected early and followed up throughout the evolution of the disease. As opposed to other CNS structures, the eye is easily accessible for in vivo observation. Retinal organization allows for the identification of its different neurons, and in consequence, detection of minimal changes taking place during neurodegeneration is possible. Functional vision studies performed on AD patients in recent years have shown how visual acuity, contrast sensitivity, color vision, and visual integration vary with the progression of neurodegeneration. The development of optical coherence tomography in ophthalmology has meant a breakthrough in retinal exploratory techniques, allowing the obtention of high-resolution images using light. This technique enables retinal analysis in the earliest stages of AD, being considered as a biomarker of neuronal damage. Given AD’s high prevalence and its expected increase, it is important to perform easy tests that cause minimal discomfort to the patients at a low cost while offering abundant information on the stage of the disease.Item The role of microglia in retinal neurodegeneration: Alzheimer’s disease, Parkinson, and glaucoma(Frontiers in Aging Neuroscience, 2017) Daniel Ajoy; Ramírez Sebastián, José Manuel; Hoz Montañana, María Rosa De; García Martín, Elena Salobrar; Salazar Corral, Juan José; Rojas López, María Blanca; López Cuenca, Inés; Rojas Lozano, María Del Pilar; Triviño Casado, Alberto; Ramírez Sebastián, Ana IsabelMicroglia, the immunocompetent cells of the central nervous system (CNS), act as neuropathology sensors and are neuroprotective under physiological conditions. Microglia react to injury and degeneration with immune-phenotypic and morphological changes, proliferation, migration, and inflammatory cytokine production. An uncontrolled microglial response secondary to sustained CNS damage can put neuronal survival at risk due to excessive inflammation. A neuroinflammatory response is considered among the etiological factors of the major aged-related neurodegenerative diseases of the CNS, and microglial cells are key players in these neurodegenerative lesions. The retina is an extension of the brain and therefore the inflammatory response in the brain can occur in the retina. The brain and retina are affected in several neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), and glaucoma. AD is an age-related neurodegeneration of the CNS characterized by neuronal and synaptic loss in the cerebral cortex, resulting in cognitive deficit and dementia. The extracellular deposits of beta-amyloid (Aβ) and intraneuronal accumulations of hyperphosphorylated tau protein (pTau) are the hallmarks of this disease. These deposits are also found in the retina and optic nerve. PD is a neurodegenerative locomotor disorder with the progressive loss of dopaminergic neurons in the substantia nigra. This is accompanied by Lewy body inclusion composed of α-synuclein (α-syn) aggregates. PD also involves retinal dopaminergic cell degeneration. Glaucoma is a multifactorial neurodegenerative disease of the optic nerve, characterized by retinal ganglion cell loss. In this pathology, deposition of Aβ, synuclein, and pTau has also been detected in retina. These neurodegenerative diseases share a common pathogenic mechanism, the neuroinflammation, in which microglia play an important role. Microglial activation has been reported in AD, PD, and glaucoma in relation to protein aggregates and degenerated neurons. The activated microglia can release pro-inflammatory cytokines which can aggravate and propagate neuroinflammation, thereby degenerating neurons and impairing brain as well as retinal function. The aim of the present review is to describe the contribution in retina to microglial-mediated neuroinflammation in AD, PD, and glaucomatous neurodegeneration.Item Anatomy of the Human Optic Nerve: Structure and Function(Optic Nerve, 2018) Salazar Corral, Juan José; Ramírez Sebastián, Ana Isabel; Hoz Montañana, María Rosa De; García Martín, Elena Salobrar; Rojas Lozano, María Del Pilar; Fernández Arrabal, José A.; López Cuenca, Inés; Rojas López, María Blanca; Triviño Casado, Alberto; Ramírez Sebastián, José Manuel; Ferreri, Felicia M.The optic nerve (ON) is constituted by the axons of the retinal ganglion cells (RGCs). These axons are distributed in an organized pattern from the soma of the RGC to the lateral geniculated nucleus (where most of the neurons synapse). The key points of the ON are the optic nerve head and chiasm. This chapter will include a detailed and updated review of the ON different parts: RGC axons, glial cells, connective tissue of the lamina cribrosa and the septum and the blood vessels derivate from the central retina artery and from the ciliary system. There will be an up-to-date description about the superficial nerve fibre layer, including their organization, and about prelaminar, laminar and retrolaminar regions, emphasizing the axoplasmic flow, glial barriers, biomechanics of the lamina cribrosa and the role of the macro- and microglia in their working.Item Changes in visual function and retinal structure in the progression of Alzheimer's disease(PLoS ONE, 2019) García Martín, Elena Salobrar; Hoz Montañana, Rosa de; Ramírez Sebastián, Ana Isabel; López Cuenca, Inés; Rojas Lozano, Pilar; Vazirani Ballesteros, Ravi; Amarante Cuadrado, Carla; Yubero Pancorbo, Raquel; Gil Gregorio, Pedro; Pinazo Durán, Mª Dolores; Salazar Corral, Juan José; Ramirez Sebastian, Jose ManuelBackground: Alzheimer’s Disease (AD) can cause degeneration in the retina and optic nerve either directly, as a result of amyloid beta deposits, or secondarily, as a result of the degradation of the visual cortex. These effects raise the possibility that tracking ophthalmologic changes in the retina can be used to assess neurodegeneration in AD. This study aimed to detect retinal changes and associated functional changes in three groups of patients consisting of AD patients with mild disease, AD patients with moderate disease and healthy controls by using non-invasive psychophysical ophthalmological tests and optical coherence tomography (OCT). Methods: We included 39 patients with mild AD, 21 patients with moderate AD and 40 age-matched healthy controls. Both patients and controls were ophthalmologically healthy. Visual acuity, contrast sensitivity, colour perception, visual integration, and choroidal thicknesses were measured. In addition, OCT and OCT angiography (OCTA) were applied. Findings: Visual acuity, contrast sensitivity, colour perception, and visual integration were significantly lower in AD patients than in healthy controls. Compared to healthy controls, macular thinning in the central region was significant in the mild AD patients, while macular thickening in the central region was found in the moderate AD group. The analysis of macular layers revealed significant thinning of the retinal nerve fibre layer, the ganglion cell layer and the outer plexiform layer in AD patients relative to controls. Conversely, significant thickening was observed in the outer nuclear layer of the patients. However, mild AD was associated with significant thinning of the subfovea and the nasal and inferior sectors of the choroid. Significant superonasal and inferotemporal peripapillary thinning was observed in patients with moderate disease. Conclusions: The first changes in the mild AD patients appear in the psychophysical tests and in the central macula with a decrease in the central retinal thickness. When there was a disease progression to moderate AD, psychophysical tests remained stable with respect to the decrease in mild AD, but significant thinning in the peripapillary retina and thickening in the central retina appeared. The presence of AD is best indicated based on contrast sensitivity.Item The Role of Microglia in Retinal Neurodegeneration: Alzheimer's Disease, Parkinson, and Glaucoma(Frontiers in Aging Neuroscience, 2017) Ramírez Sebastián, Ana Isabel; Hoz Montañana, María Rosa de; García Martín, Elena Salobrar; Salazar Corral, Juan José; Rojas López, Blanca; Ajoy, Daniel; López Cuenca, Inés; Rojas, Pilar; Triviño Casado, Alberto; Ramirez Sebastian, Jose ManuelMicroglia, the immunocompetent cells of the central nervous system (CNS), act as neuropathology sensors and are neuroprotective under physiological conditions. Microglia react to injury and degeneration with immune-phenotypic and morphological changes, proliferation, migration, and inflammatory cytokine production. An uncontrolled microglial response secondary to sustained CNS damage can put neuronal survival at risk due to excessive inflammation. A neuroinflammatory response is considered among the etiological factors of the major aged-related neurodegenerative diseases of the CNS, and microglial cells are key players in these neurodegenerative lesions. The retina is an extension of the brain and therefore the inflammatory response in the brain can occur in the retina. The brain and retina are affected in several neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), and glaucoma. AD is an age-related neurodegeneration of the CNS characterized by neuronal and synaptic loss in the cerebral cortex, resulting in cognitive deficit and dementia. The extracellular deposits of beta-amyloid (Aβ) and intraneuronal accumulations of hyperphosphorylated tau protein (pTau) are the hallmarks of this disease. These deposits are also found in the retina and optic nerve. PD is a neurodegenerative locomotor disorder with the progressive loss of dopaminergic neurons in the substantia nigra. This is accompanied by Lewy body inclusion composed of α-synuclein (α-syn) aggregates. PD also involves retinal dopaminergic cell degeneration. Glaucoma is a multifactorial neurodegenerative disease of the optic nerve, characterized by retinal ganglion cell loss. In this pathology, deposition of Aβ, synuclein, and pTau has also been detected in retina. These neurodegenerative diseases share a common pathogenic mechanism, the neuroinflammation, in which microglia play an important role. Microglial activation has been reported in AD, PD, and glaucoma in relation to protein aggregates and degenerated neurons. The activated microglia can release pro-inflammatory cytokines which can aggravate and propagate neuroinflammation, thereby degenerating neurons and impairing brain as well as retinal function. The aim of the present review is to describe the contribution in retina to microglial-mediated neuroinflammation in AD, PD, and glaucomatous neurodegeneration.Item Neuroprotective and Anti-Inflammatory Effects of a Hydrophilic Saffron Extract in a Model of Glaucoma(International Journal of Molecular Sciences, 2019) Fernández Albarral, José Antonio; Ramírez Sebastián, Ana Isabel; Hoz Montañana, Rosa de; López Villarín, Nerea; García Martín, Elena Salobrar; López Cuenca, Inés; Licastro, Ester; Inarejos García, Antonio M.; Almodóvar, Paula; Pinazo Durán, Mª Dolores; Ramirez Sebastian, Jose Manuel; Salazar Corral, Juan JoséGlaucoma is a neurodegenerative disease characterized by the loss of retinal ganglion cells (RGCs). An increase in the intraocular pressure is the principal risk factor for such loss, but controlling this pressure does not always prevent glaucomatous damage. Activation of immune cells resident in the retina (microglia) may contribute to RGC death. Thus, a substance with anti-inflammatory activity may protect against RGC degeneration. This study investigated the neuroprotective and anti-inflammatory effects of a hydrophilic saffron extract standardized to 3% crocin content in a mouse model of unilateral, laser-induced ocular hypertension (OHT). Treatment with saffron extract decreased microglion numbers and morphological signs of their activation, including soma size and process retraction, both in OHT and in contralateral eyes. Saffron extract treatment also partially reversed OHT-induced down-regulation of P2RY12. In addition, the extract prevented retinal ganglion cell death in OHT eyes. Oral administration of saffron extract was able to decrease the neuroinflammation associated with increased intraocular pressure, preventing retinal ganglion cell death. Our findings indicate that saffron extract may exert a protective effect in glaucomatous pathology.