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1.
CNS Neurol Disord Drug Targets ; 15(2): 135-40, 2016.
Artículo en Inglés | MEDLINE | ID: mdl-26831264

RESUMEN

Retinal adhesion mechanisms in mammals are quite complex and multifactorial in nature. To date, these mechanisms are incompletely understood due to a variety of chemical, physical, and physiological forces impinging upon retinal tissue: retinal pigment epithelium, nearby tissues as sclera and vitreous, the subretinal space, and the highly complex interphotoreceptor matrix that fills subretinal space. The adhesion of the retina to the choroid, rather than anatomical, is a dynamic process, as the retina detaches a few minutes after life ceases. The adhesion mechanisms described in the literature, such as intraocular pressure and the oncotic pressure of the choroid that seems to push the retina towards the choroid, the delicate anatomical relationships between the rod and cone photoreceptors, the retinal pigment epithelium, the existence of a complex material called interphotoreceptor matrix, as well as other metabolic and structural factors, still cannot explain the remarkable features observed in the adhesion mechanisms between the photoreceptor layer and retinal pigment epithelium cells. The unexpected intrinsic property of melanin to absorb light energy and transform it into chemically based free energy can explain normal adhesion of the sensory retina to the pigment epithelium. In this article, we explore and highlight this explanation, which states that it is definitely able to provide a new treatment avenue against devastating neurodegenerative properties.


Asunto(s)
Enfermedades del Sistema Nervioso Central/metabolismo , Melaninas/metabolismo , Melaninas/uso terapéutico , Retina/metabolismo , Agua/metabolismo , Animales , Enfermedades del Sistema Nervioso Central/tratamiento farmacológico , Humanos , Melaninas/farmacología , Retina/efectos de los fármacos , Resultado del Tratamiento
2.
CNS Neurol Disord Drug Targets ; 14(9): 1235-42, 2015.
Artículo en Inglés | MEDLINE | ID: mdl-26295828

RESUMEN

One of the biggest problems and challenges for the development of new drugs and treatment strategies against Alzheimer Disease (AD) is the crossing of target drugs into the blood brain barrier. The use of nanoparticles in drug delivery therapy holds much promise in targeting remote tissues, and as a result many studies have attempted to study the ultrastructural localization of nanoparticles in various tissues. However, there are currently no in vivo studies demonstrating the ultrastructural distribution of nanoparticles in the brain. The aim of this study was to address how intraperitoneal injection of silver nanoparticles in the brain leads to leaking on the inter-endothelial contact and luminal plasma membrane, thus elucidating the possibility of penetrating into the most affected areas in the Alzheimer brain (vascular endothelium, perivascular, neuronal and glial cells). Our results show that the silver nanoparticles reached the brain and were found in hippocampal areas, indicating that they can be conjugated and used to deliver the drugs into the cell cytoplasm of the damaged brain cells. The present study can be useful for the development of novel drug delivering therapy and useful in understanding the delivery, distribution and effects of silver nanoparticles in AD brain tissue at cellular and subcellular level.


Asunto(s)
Enfermedad de Alzheimer/tratamiento farmacológico , Encéfalo/efectos de los fármacos , Sistemas de Liberación de Medicamentos/métodos , Nanopartículas del Metal , Fármacos Neuroprotectores/administración & dosificación , Compuestos de Plata , Enfermedad de Alzheimer/patología , Animales , Barrera Hematoencefálica/efectos de los fármacos , Barrera Hematoencefálica/ultraestructura , Encéfalo/irrigación sanguínea , Encéfalo/ultraestructura , Femenino , Inyecciones Intraperitoneales , Masculino , Microscopía Electrónica , Microvasos/efectos de los fármacos , Microvasos/ultraestructura , Modelos Animales , Neuronas/efectos de los fármacos , Neuronas/ultraestructura , Ratas Wistar
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