Person:
Triviño Casado, Alberto

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First Name
Alberto
Last Name
Triviño Casado
URI
https://hdl.handle.net/20.500.14352/79594
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Medicina
Department
Inmunología, Oftalmología y ORL
Area
Oftalmología
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2017 - 20203
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Author: López Cuenca, Inés × Subject: 611.8.018.84 ×

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Now showing 1 - 3 of 3
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    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.
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    Microglial changes in the early aging stage in a healthy retina and an experimental glaucoma model
    (Glaucoma: A Neurodegenerative Disease of the Retina and Beyond - Part A, 2020) Ramírez Sebastián, Ana Isabel; Fernández Albarral, José Antonio; Hoz Montañana, Rosa de; López Cuenca, Inés; García Martín, Elena Salobrar; Rojas Lozano, Pilar; Valiente Soriano, Francisco Javier; Avilés Trigueros, Marcelino; Villegas Pérez, María Paz; Vidal Sanz, Manuel; Triviño Casado, Alberto; Salazar Corral, Juan José; Ramirez Sebastian, Jose Manuel; Bagetta, Giacinto; Nucci, Carlo
    Glaucoma is an age-related neurodegenerative disease that begins at the onset of aging. In this disease, there is an involvement of the immune system and therefore of the microglia. The purpose of this study is to evaluate the microglial activation using a mouse model of ocular hypertension (OHT) at the onset of aging. For this purpose, we used both naive and ocular hypertensives of 15-month-old mice (early stage of aging). In the latter, we analyzed the OHT eyes and the eyes contralateral to them to compare them with their aged controls. In the eyes of aged naive, aged OHT and aged contralateral eyes, microglial changes were observed compared to the young mice, including: (i) aged naive vs young naive: An increased soma size and vertical processes; (ii) aged OHT eyes vs young OHT eyes: A decrease in the area of the retina occupied by Iba-1 cells and in vertical processes; and (iii) aged contralateral vs young contralateral: A decrease in the soma size and arbor area and an increase in the number of microglia in the outer segment layer. Aged OHT eyes and the eyes contralateral to them showed an up-regulation of the CD68 expression in the branched microglia and a down-regulation in the MHCII and P2RY12 expression with respect to the eyes of young OHT mice. Conclusion: in the early phase of aging, morphological microglial changes along with changes in the expression of MHCII, CD68 and P2RY12, in both naive and OHT mice. These changes appear in aged OHT eyes and the eyes contralateral to them eyes.
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    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 Manuel
    Microglia, 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.