Pathological changes in human retinal ganglion cells associated with diabetic and hypertensive retinopathy

Meyer-Rüsenberg, Birthe; Pavlidis, Mitrofanis; Stupp, Tobias; Thanos, Solon

doi:10.1007/s00417-006-0489-x

Cited by 50 publications

(27 citation statements)

References 39 publications

(45 reference statements)

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“…There was also a significant increase in the density of dendrites in large ON-ganglion cells, measured by Scholl analysis (Figure 2). Similar pathological features were also described in a small study using DiI on postmortem human retinas [50]. The small amount of morphological data that is available suggests that diabetes leads to changes in the dendrite morphology of retinal ganglion cells, possibly as a precursor to cell death, and also appears to alter the content of certain synaptic proteins.…”

Section: Degenerative Changes In Synapses and Neuron Morphology Accomsupporting

confidence: 68%

Diabetic retinopathy: recent advances towards understanding neurodegeneration and vision loss

Barber

2015

Sci. China Life Sci.

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Diabetic retinopathy (DR) is one of the most common retinal diseases world-wide. It has a complex pathology that involves the vasculature of the inner retina and breakdown of the blood-retinal barrier. Extensive research has determined that DR is not only a vascular disease but also has a neurodegenerative component and that essentially all types of cells in the retina are affected, leading to chronic loss of visual function. A great deal of work using animal models of DR has established the loss of neurons and pathology of other cell types, including supporting glial cells. There has also been an increased emphasis on measuring retinal function in the models, as well as further validation and extension of the animal studies by clinical and translational research. This article will attempt to summarize the more recent developments in research towards understanding the complexities of retinal neurodegeneration and functional vision loss in DR. retina, diabetes, neurodegeneration, visual function, vascular function, apoptosis, synapse, dendrite Citation:Barber AJ. Diabetic retinopathy: recent advances towards understanding neurodegeneration and vision loss.

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Section: Degenerative Changes In Synapses and Neuron Morphology Accomsupporting

confidence: 68%

Diabetic retinopathy: recent advances towards understanding neurodegeneration and vision loss

Barber

2015

Sci. China Life Sci.

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“…These changes surprisingly were found limited to the large ON-RGCs in short-term diabetes and did not occur in any class of OFF-RGCs (Kern and Barber, 2008). Similar changes in RGC morphology have been observed in human retinas (Meyer-Rusenberg et al, 2007). This alteration in a subset of RGCs could alter the functional output of the certain subtypes of RGCs (Kern and Barber, 2008), leading to changes in VEPs (see later text).…”

Section: P0540supporting

confidence: 58%

Neuropeptides, Trophic Factors, and Other Substances Providing Morphofunctional and Metabolic Protection in Experimental Models of Diabetic Retinopathy

Szabadfi

Pintér

Reglődi

et al. 2014

International Review of Cell and Molecular Biology

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Any queries or remarks that have arisen during the processing of your manuscript are listed below and are highlighted by flags in the proof. (AU indicates author queries; ED indicates editor queries; and TS/TY indicates typesetter queries.) Please check your proof carefully and answer all AU queries. Mark all corrections and query answers at the appropriate place in the proof (e.g., by using on-screen annotation in the PDF file http:// www.elsevier.com/book-authors/science-and-technology-book-publishing/overviewof-the-publishing-process) or compile them in a separate list, and tick off below to indicate that you have answered the query. Please return your input as instructed by the project manager. Location in ChapterQuery / remark AU:1, page 47 Please check the change made in the table title. AU:2, page 57 Citation " Frank et al. (1997)" has not been found in the reference list. Please supply full details for this reference. AU:3, page 58Citation "Wang et al. (2004)" has not been found in the reference list. Please supply full details for this reference. AU:4, page 63The citation "Wang et al. (2010)" has been changed to " Wang et al. (2010)" to match the author name/date in the reference list. Please check here and in subsequent occurrences, and correct if necessary. AU:5, page 3The abbreviations IBA-1 and ZFDM are used only once in the text and they have been deleted in the text. Please consider deleting them from the abbreviation list. B978-0-12-800179-0.00001-5, 00001 IRCMB, 978-0-12-800179-0To protect the rights of the author(s) and publisher we inform you that this PDF is an uncorrected proof for internal business use only by the author(s), editor(s), reviewer(s), Elsevier and typesetter SPi. It is not allowed to publish this proof online or in print. This proof copy is the copyright property of the publisher and is confidential until formal publication. AU:6, page 3Please check if all occurrences of "interstitial cell adhesion molecule 1" should be changed to "intercellular adhesion molecule 1." AU:7, page 3Please check the change from "neural" to "neuronal" to match with the text.AU:8, page 3The abbreviation "PKCa" is not used in the text. Please check and delete from the abbreviation list. AU:9, page 9Please check if "retinal ganglion cells (RGCs)" is okay as edited.AU:10, page 13 Please check the change from "retinal circuity" to "retinal circuitry."AU:11, page 17 Please check if "polyamine catabolism" is okay as edited. AU:20, page 46 Please check if edit to sentence starting "The STZ-induced diabetic. . ." is okay. B978-0-12-800179-0.00001-5, 00001 IRCMB, 978-0-12-800179-0To protect the rights of the author(s) and publisher we inform you that this PDF is an uncorrected proof for internal business use only by the author(s), editor(s), reviewer(s), Elsevier and typesetter SPi. It is not allowed to publish this proof online or in print. This proof copy is the copyright property of the publisher and is confidential until formal publication. AU:21, page 72Please check if "SST" is okay as edited.AU:2...

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“…[21][22][23] As our study groups include presbiyopic and AMD patients, our age range is narrow, so it is possible no to be found a difference between the age and ganglion cell layer thickness.…”

Section: Discussionmentioning

confidence: 99%

Ganglion cell complex thickness in nonexudative age-related macular degeneration

Yenice

Şengün

Demirok

et al. 2015

Eye

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Purpose To evaluate ganglion cell complex (GCC) thickness with spectral domain optical coherence tomography (SD-OCT) in eyes with nonexudative age-related macular degeneration (NEAMD). Methods Forty-seven eyes of 28 patients with nonexudative age-related macular degeneration (NEAMD) and 54 eyes of 28 age-matched healthy subjects were enrolled. Each subject underwent a complete ophthalmic examination before SD-OCT were obtained. Macular scans were taken with software version 6.0 of the ganglion cell analysis (GCA) algorithm. GCC thickness was evaluated automatically as the average, minimum, temporal superior, superior, nasal superior, nasal inferior, inferior, and temporal-inferior segments by SD-OCT and parameters were compared between groups. Results The mean age was 68.7 ± 8.73 years in patient group, and 61.51 ± 5.66 years in control group. There were no significant differences in mean age, gender distribution, intraocular pressure, and sferic equivalent at imaging between the groups (P40.05). The mean (± SD) GCC thicknesses were as follows; average 71.53 ±16.53 μm, minumum 62.36 ± 21.51 μm, temporal superior 72.23 ± 14.60 μm, superior 72.76 ± 20.40 μm, nasal superior 72.31 ± 20.13 μm, nasal inferior 69.74 ± 20.51 μm, inferior 69.38 ± 19.03 μm, and temporal-inferior 73.12 ± 15.44 μm in patient group. Corresponding values in control group were 81.46 ± 4.90 μm, 78.66 ± 6.00 μm, 81.51 ± 4.66 μm, 82.94 ± 5.14 μm, 81.79 ± 5.86 μm, 80.94 ± 6.18 μm, 80.14 ± 6.30 μm, and 81.75 ± 5.26 μm, respectively. There were significant differences between two groups in each segments (Mann-Whitney U-test, Po0.05). Conclusion The average GCC thickness values (in all segments) of NEAMD patients were lower than control group. NEAMD, which is considered as a disease of outer layers of retina, may be accompanied with a decrease of ganglion cell thickness, so inner layers of retina may be affected.

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Pathological changes in human retinal ganglion cells associated with diabetic and hypertensive retinopathy

Cited by 50 publications

References 39 publications

Diabetic retinopathy: recent advances towards understanding neurodegeneration and vision loss

Diabetic retinopathy: recent advances towards understanding neurodegeneration and vision loss

Neuropeptides, Trophic Factors, and Other Substances Providing Morphofunctional and Metabolic Protection in Experimental Models of Diabetic Retinopathy

Ganglion cell complex thickness in nonexudative age-related macular degeneration

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