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1 General aspects (0)   1.1 Epidemiology (8)   1.2 Population genetics (0)   1.3 Pathogenesis (0)   1.4 Quality of life (9)   1.5 Glaucomas as cause of blindness (3)   1.6 Prevention and screening (6) 2 Anatomical structures in glaucoma (0)   2.1 Conjunctiva (3)   2.2 Cornea (12)   2.3 Sclera (3)   2.4 Anterior chamber angle (1)   2.5 Meshwork (0)     2.5.1 Trabecular meshwork (5)     2.5.2 Schlemms canal (1)     2.5.3 Scleral outlet channels (0)   2.6 Aqueous humor dynamics (1)     2.6.1 Production (0)     2.6.2 Outflow (1)       2.6.2.1 Trabecular meshwork (3)       2.6.2.2 Uveoscleral (0)     2.6.3 Compostion (0)   2.7 Episcleral veins and venous pressure (1)   2.8 Iris (1)   2.9 Ciliary body (2)   2.10 Lens (0)   2.11 Vitreous body (0)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (14)   2.13 Retina and retinal nerve fibre layer (17)   2.14 Optic disc (23)   2.15 Optic nerve (3)   2.16 Chiasma and retrochiasmal central nervous system (3)   2.17 Stem cells (1)   2.20 Other (0) 3 Laboratory methods (0)   3.1 Microscopy (1)   3.2 Electron microscopy (0)   3.3 Immunohistochemistry (3)   3.4 Molecular genetics (0)     3.4.1 Linkage studies (2)     3.4.2 Gene studies (17)   3.5 Molecular biology incl. SiRNA (5)   3.6 Cellular biology (20)   3.7 Biochemistry (3)   3.8 Pharmacology (12)   3.9 Pathophysiology (11)   3.10 Immunobiology (2)   3.11 Pharmacogenetics (0)   3.12 Proteomics (0)   3.13 In vivo imaging (0)     3.13.1 Laser Scanning (0)       3.13.1.1 Confocal Scanning Laser Ophthalmoscopy (0)       3.13.1.2 Confocal Scanning Laser Polarimetry (0)     3.13.2 Optical Coherence Tomography (0)       3.13.2.1 Anterior Segment (0)       3.13.2.2 Posterior Segment (0)     3.13.3 RGC Imaging (5)     3.13.4 Other (1)   3.20 Other (0) 4 Tissue culture of ocular cells (0) 5 Experimental glaucoma; animal models (2)   5.1 Rodent (21)   5.2 Primates (1)   5.3 Other (3) 6 Clinical examination methods (0)   6.1 Intraocular pressure measurement; factors affecting IOP (0)     6.1.1 Devices, techniques (6)     6.1.2 Fluctuation, circadian rhythms (2)     6.1.3 Factors affecting IOP (11)   6.2 Tonography, aqueous flow measurement (see also 2.6) (0)   6.3 Biomicroscopy (slitlamp) (0)     6.3.1 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8 Refractive errors in relation to glaucoma (2)   8.1 Myopia (10)   8.2 Hypermetropia (0)   8.3 Contact lenses (0)   8.4 Refractive surgical procedures (0)   8.5 Other (0) 9 Clinical forms of glaucomas (0)   9.1 Developmental glaucomas (0)     9.1.1 Congenital glaucoma, Buphthalmos (8)     9.1.2 Juvenile glaucoma (7)     9.1.3 Syndromes of Axenfeld, Rieger, Peters, aniridia (3)     9.1.4 Other (0)   9.2 Primary open angle glaucomas (0)     9.2.1 Ocular hypertension (7)     9.2.2 Other risk factors for glaucoma (3)     9.2.3 Open angle glaucoma with elevated IOP (0)     9.2.4 Normal pressure glaucoma (11)   9.3 Primary angle closure glaucomas (0)     9.3.1 Acute primary angle closure glaucoma (pupillary block) (8)     9.3.2 Chronic primary angle closure glaucoma (pupillary block) (4)     9.3.3 Plateau iris syndrome (1)     9.3.4 Primary angle closure suspect (3)     9.3.5 Primary angle closure (2)     9.3.10 Other (0)   9.4 Glaucomas associated with other ocular and systemic disorders 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associated with intraocular tumors (1)     9.4.9 Glaucomas associated with elevated episcleral venous pressure (1)       9.4.10 Glaucomas associated with hemorrhage (7)     9.4.11 Glaucomas following intraocular surgery (0)       9.4.11.1 Ciliary block (malignant) glaucoma (2)       9.4.11.2 Glaucomas in aphakia and pseudophakia (4)       9.4.11.3 Epithelial, fibrous, and endothelial proliferation (0)       9.4.11.4 Glaucomas associated with corneal surgery (2)       9.4.11.5 Glaucomas associated with vitreoretinal surgery (3)     9.4.15 Glaucoma in relation to systemic disease (20)     9.4.20 Other (3) 10 Differential diagnosis e.g. anterior and posterior ischemic optic neuropathy (0) 11 Medical treatment (0)   11.1 General management, indication (3)   11.2 Cholinergic drugs (0)   11.3 Adrenergic drugs (0)     11.3.1 Epinephrine (0)     11.3.2 Thymoxamine, dapiprazole (0)     11.3.3 Apraclonidine, brimonidine (4)     11.3.4 Betablocker (3)     11.3.5 Other (0)   11.4 Prostaglandins 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    12.8.1 Without tube implant (11)     12.8.2 With tube implant or other drainage devices (29)     12.8.3 Non-perforating (7)     12.8.4 Using laser (0)     12.8.5 Other (0)     12.8.10 Woundhealing antifibrosis (12)     12.8.11 Complications, endophthalmitis (7)   12.9 Trabeculotomy, goniotomy (2)   12.10 Cyclodestruction (1)   12.11 Cyclodialysis (0)   12.12 Cataract extraction (0)     12.12.1 Intracapsular (0)     12.12.2 Extracapsular (0)     12.12.3 Phacoemulsification (4)   12.14 Combined cataract extraction and glaucoma surgery (0)     12.14.1 Intracapsular (0)     12.14.2 Extracapsular (1)     12.14.3 Phacoemulsification (6)   12.15 Capsulotomy (0)   12.16 Vitrectomy (6)   12.17 Anesthesia (1)   12.20 Other (2) 13 Therapeutic prognosis and outcome (0)   13.1 Prognostic factors (0)   13.2 Outcome (0)     13.2.1 IOP (0)     13.2.2 Visual field (0)       13.2.2.1 Progression (0)       13.2.2.2 Improvement (1)     13.2.3 Other (0) 14 Costing studies; pharmacoeconomics (3) 15 Miscellaneous (17)

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Abstract #75226 Published in IGR 19-2

Neurotrophin-conjugated nanoparticles prevent retina damage induced by oxidative stress

Giannaccini M; Usai A; Chiellini F; Guadagni V; Andreazzoli M; Ori M; Pasqualetti M; Dente L; Raffa V
Cellular and Molecular Life Sciences 2018; 75: 1255-1267

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Glaucoma and other optic neuropathies are characterized by a loss of retinal ganglion cells (RGCs), a cell layer located in the posterior eye segment. Several preclinical studies demonstrate that neurotrophins (NTs) prevent RGC loss. However, NTs are rarely investigated in the clinic due to various issues, such as difficulties in reaching the retina, the very short half-life of NTs, and the need for multiple injections. We demonstrate that NTs can be conjugated to magnetic nanoparticles (MNPs), which act as smart drug carriers. This combines the advantages of the self-localization of the drug in the retina and drug protection from fast degradation. We tested the nerve growth factor and brain-derived neurotrophic factor by comparing the neuroprotection of free versus conjugated proteins in a model of RGC loss induced by oxidative stress. Histological data demonstrated that the conjugated proteins totally prevented RGC loss, in sharp contrast to the equivalent dose of free proteins, which had no effect. The overall data suggest that the nanoscale MNP-protein hybrid is an excellent tool in implementing ocular drug delivery strategies for neuroprotection and therapy.

Department of Biology, Università di Pisa, 56127, Pisa, Italy.

Full article

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Classification:

11.8 Neuroprotection (Part of: 11 Medical treatment)
3.6 Cellular biology (Part of: 3 Laboratory methods)
11.14 Investigational drugs; pharmacological experiments (Part of: 11 Medical treatment)
11.16 Vehicles, delivery systems, pharmacokinetics, formulation (Part of: 11 Medical treatment)

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