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Diffusion tensor imaging detects and differentiates axon and myelin degeneration in mouse optic nerve after retinal ischemia
- Sheng-Kwei Song, S. Sun, W. Ju, Shiow J. Lin, A. Cross, A. Neufeld
- Medicine, Chemistry
- 1 November 2003
The hypothesis that lambdaparallel and lambdaperpendicular hold promise as specific markers of axonal and myelin injury, respectively, and, further, that the coexistence of axon andMyelin degeneration does not confound this utility, are supported. Expand
Autophagy and Exosomes in the Aged Retinal Pigment Epithelium: Possible Relevance to Drusen Formation and Age-Related Macular Degeneration
It is speculated that increased autophagy and the release of intracellular proteins via exosomes by the aged RPE may contribute to the formation of drusen. Expand
Inhibition of nitric-oxide synthase 2 by aminoguanidine provides neuroprotection of retinal ganglion cells in a rat model of chronic glaucoma.
- A. Neufeld, A. Sawada, B. Becker
- Proceedings of the National Academy of Sciences…
- 17 August 1999
Pharmacological neuroprotection by inhibition of NOS-2 may prove useful for the treatment of patients with glaucoma by quantitating retinal ganglion cell loss by retrograde labeling with Fluoro-Gold. Expand
Epidermal Growth Factor Receptor Activation: An Upstream Signal for Transition of Quiescent Astrocytes into Reactive Astrocytes after Neural Injury
It is found that upregulation and activation of the epidermal growth factor receptor (EGFR) occur in astrocytes after different injuries in optic nerves in vivo, and targeting EGFR activation using an EGFR tyrosine kinase inhibitor prevents the loss of retinal ganglion cells in a model of glaucomatous optic neuropathy. Expand
Nitric oxide synthase in the human glaucomatous optic nerve head.
The increased presence of NOS-1 and the induction of Nos-2 in astrocytes of the lamina cribrosa suggest that the glaucomatous optic nerve head is exposed to excessive levels of nitric oxide, which may be neurodestructive, locally, to the axons of the retinal ganglion cells. Expand
Changes in the extracellular matrix of the human optic nerve head in primary open-angle glaucoma.
- M. Hernandez, W. Andrzejewska, A. Neufeld
- Chemistry, Medicine
- American journal of ophthalmology
- 1 February 1990
The results indicate that changes in the extracellular matrix play an important role in the progression of the glaucomatous process and may be a causative agent of the disease. Expand
Microglia in the optic nerve head and the region of parapapillary chorioretinal atrophy in glaucoma.
- A. Neufeld
- Biology, Medicine
- Archives of ophthalmology
- 1 August 1999
The activity of microglia in the parapapillary chorioretinal region in glaucoma may be responsible for some of the biomicroscopic and histological changes that are associated with parapapillaris choraoretinal atrophy. Expand
Isoforms of nitric oxide synthase in the optic nerves of rat eyes with chronic moderately elevated intraocular pressure.
- S. Shareef, A. Sawada, A. Neufeld
- Biology, Medicine
- Investigative ophthalmology & visual science
- 1 November 1999
The cellular distributions of constitutive NOS isoforms in the rat optic nerve suggest physiological roles for NO in this tissue, and the excessive NO production that is associated with this isoform may contribute to the neurotoxicity of the retinal ganglion cells in eyes with chronic moderately elevated IOP. Expand
Cigarette smoking, oxidative stress, the anti-oxidant response through Nrf2 signaling, and Age-related Macular Degeneration
This review explores how cigarette smoking and oxidative stress to the retinal pigmented epithelium (RPE) might contribute to AMD, and how the transcription factor Nrf2 can activate a cytoprotective response. Expand
The Aged Retinal Pigment Epithelium/Choroid: A Potential Substratum for the Pathogenesis of Age-Related Macular Degeneration
These phenotypic changes indicate that the RPE/choroid in the normal, old mouse has become an immunologically active tissue and may provide the background for an error in regulation of immunological activity to cause AMD to appear in an elderly individual. Expand