Decelerated neurodegeneration after intravitreal injection of α-synuclein antibodies in a glaucoma animal model

Abstract Although elevated intraocular pressure (IOP) remains the major risk factor in glaucoma, neurodegenerative processes continue despite effective IOP lowering. Altered α-synuclein antibody (Abs) levels have been reported to play a crucial role. This study aimed at identifying whether α-synucle...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	J. Teister, F. Anders, S. Beck, S. Funke, H. von Pein, V. Prokosch, N. Pfeiffer, F. Grus
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/58bd9281a7ea40119c5225aca32f1ff5
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:58bd9281a7ea40119c5225aca32f1ff5
record_format	dspace
spelling	oai:doaj.org-article:58bd9281a7ea40119c5225aca32f1ff52021-12-02T15:05:28ZDecelerated neurodegeneration after intravitreal injection of α-synuclein antibodies in a glaucoma animal model10.1038/s41598-017-06702-12045-2322https://doaj.org/article/58bd9281a7ea40119c5225aca32f1ff52017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-06702-1https://doaj.org/toc/2045-2322Abstract Although elevated intraocular pressure (IOP) remains the major risk factor in glaucoma, neurodegenerative processes continue despite effective IOP lowering. Altered α-synuclein antibody (Abs) levels have been reported to play a crucial role. This study aimed at identifying whether α-synuclein Abs are capable to decelerate neuronal decay while providing insights into proteomic changes. Four groups of Sprague Dawley rats received episcleral vein occlusion: (1) CTRL, no intravitreal injection, n = 6, (2) CTRL IgG, intravitreal injection of unspecific IgG, n = 5, (3) Buffer, intravitreal injection of buffer, n = 6, (4), α-synuclein Ab, intravitreal injection of α-synuclein Ab, n = 5. IOP and retinal nerve fiber layer thickness (RNFLT) were monitored and immunohistochemistry, microarray and proteomic analysis were performed. RNFLT was reduced in CTRL, CTRL IgG and Buffer group (all p < 0.01) and α-synuclein Ab group (p = 0.17). Axon and RGC density showed an increased neurodegeneration in CTRL, CTRL IgG and Buffer group (all p < 0.01) and increased neuronal survival in α-synuclein Ab group (p = 0.38 and 0.06, respectively) compared with fellow eyes. Proteomic analysis revealed alterations of cofilin 1 and superoxide dismutase 1 expression. This data indicate that α-synuclein Ab might indirectly modulate the actin cytoskeleton organization and negatively regulate apoptotic processes via cofilin 1 and superoxide dismutase 1.J. TeisterF. AndersS. BeckS. FunkeH. von PeinV. ProkoschN. PfeifferF. GrusNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-16 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q J. Teister F. Anders S. Beck S. Funke H. von Pein V. Prokosch N. Pfeiffer F. Grus Decelerated neurodegeneration after intravitreal injection of α-synuclein antibodies in a glaucoma animal model
description	Abstract Although elevated intraocular pressure (IOP) remains the major risk factor in glaucoma, neurodegenerative processes continue despite effective IOP lowering. Altered α-synuclein antibody (Abs) levels have been reported to play a crucial role. This study aimed at identifying whether α-synuclein Abs are capable to decelerate neuronal decay while providing insights into proteomic changes. Four groups of Sprague Dawley rats received episcleral vein occlusion: (1) CTRL, no intravitreal injection, n = 6, (2) CTRL IgG, intravitreal injection of unspecific IgG, n = 5, (3) Buffer, intravitreal injection of buffer, n = 6, (4), α-synuclein Ab, intravitreal injection of α-synuclein Ab, n = 5. IOP and retinal nerve fiber layer thickness (RNFLT) were monitored and immunohistochemistry, microarray and proteomic analysis were performed. RNFLT was reduced in CTRL, CTRL IgG and Buffer group (all p < 0.01) and α-synuclein Ab group (p = 0.17). Axon and RGC density showed an increased neurodegeneration in CTRL, CTRL IgG and Buffer group (all p < 0.01) and increased neuronal survival in α-synuclein Ab group (p = 0.38 and 0.06, respectively) compared with fellow eyes. Proteomic analysis revealed alterations of cofilin 1 and superoxide dismutase 1 expression. This data indicate that α-synuclein Ab might indirectly modulate the actin cytoskeleton organization and negatively regulate apoptotic processes via cofilin 1 and superoxide dismutase 1.
format	article
author	J. Teister F. Anders S. Beck S. Funke H. von Pein V. Prokosch N. Pfeiffer F. Grus
author_facet	J. Teister F. Anders S. Beck S. Funke H. von Pein V. Prokosch N. Pfeiffer F. Grus
author_sort	J. Teister
title	Decelerated neurodegeneration after intravitreal injection of α-synuclein antibodies in a glaucoma animal model
title_short	Decelerated neurodegeneration after intravitreal injection of α-synuclein antibodies in a glaucoma animal model
title_full	Decelerated neurodegeneration after intravitreal injection of α-synuclein antibodies in a glaucoma animal model
title_fullStr	Decelerated neurodegeneration after intravitreal injection of α-synuclein antibodies in a glaucoma animal model
title_full_unstemmed	Decelerated neurodegeneration after intravitreal injection of α-synuclein antibodies in a glaucoma animal model
title_sort	decelerated neurodegeneration after intravitreal injection of α-synuclein antibodies in a glaucoma animal model
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/58bd9281a7ea40119c5225aca32f1ff5
work_keys_str_mv	AT jteister deceleratedneurodegenerationafterintravitrealinjectionofasynucleinantibodiesinaglaucomaanimalmodel AT fanders deceleratedneurodegenerationafterintravitrealinjectionofasynucleinantibodiesinaglaucomaanimalmodel AT sbeck deceleratedneurodegenerationafterintravitrealinjectionofasynucleinantibodiesinaglaucomaanimalmodel AT sfunke deceleratedneurodegenerationafterintravitrealinjectionofasynucleinantibodiesinaglaucomaanimalmodel AT hvonpein deceleratedneurodegenerationafterintravitrealinjectionofasynucleinantibodiesinaglaucomaanimalmodel AT vprokosch deceleratedneurodegenerationafterintravitrealinjectionofasynucleinantibodiesinaglaucomaanimalmodel AT npfeiffer deceleratedneurodegenerationafterintravitrealinjectionofasynucleinantibodiesinaglaucomaanimalmodel AT fgrus deceleratedneurodegenerationafterintravitrealinjectionofasynucleinantibodiesinaglaucomaanimalmodel
_version_	1718388831015665664

Decelerated neurodegeneration after intravitreal injection of α-synuclein antibodies in a glaucoma animal model

Ejemplares similares