Optic Nerve Injury Stem Cell Treatment

Stem Cell Treatments for Optic Nerve Injury

Stem Cell Treatmet for Optic Nerve Injuries

Stem Cell Treatment for Optic Nerve Injuries

Optic Nerve Injury Treatments using Stem Cells is now an option...

Via IV and Retrobulbar injections of the patient's own Mesenchymal Stem Cells, we strive to give patients an option where there was none before. The optic nerve is composed of retinal ganglion cell axons and support cells. It leaves the orbit (eye socket) via the optic canal, running postero-medially towards the optic chiasm, where there is a partial decussation (crossing) of fibres from the nasal visual fields of both eyes. The optic nerve is the second of twelve paired cranial nerves but is considered to be part of the central nervous system, as it is derived from an outpouching of the diencephalon during embryonic development. As a consequence, the fibres are covered with myelin produced by oligodendrocytes, rather than Schwann cells, which are found in the peripheral nervous system, and are encased within the meninges.

Damage to the optic nerve typically causes permanent and potentially severe loss of vision, as well as an abnormal pupillary reflex, which is diagnostically important. The type of visual field loss will depend on which portions of the optic nerve were damaged. In general:

  • Damage proximal to the optic chiasm causes loss of vision in the visual field of the same side only.
  • Damage in the chiasm causes loss of vision laterally in both visual fields (bitemporal hemianopia). It may occur in large pituitary adenomata.
  • Damage distal to the chiasm causes loss of vision in one eye but affecting both visual fields: The visual field affected is located on the opposite side of the lesion.

Injury to the optic nerve can be the result of congenital or inheritable problems like Leber's Hereditary Optic Neuropathy, glaucoma, trauma, toxicity, inflammation, ischemia, infection (very rarely), or compression from tumors or aneurysms. By far, the three most common injuries to the optic nerve are from glaucoma, optic neuritis (especially in those younger than 50 years of age), and anterior ischemic optic neuropathy (usually in those older than 50).

  • Glaucoma is a group of diseases involving loss of retinal ganglion cells causing optic neuropathy in a pattern of peripheral vision loss, initially sparing central vision.
  • Optic neuritis is inflammation of the optic nerve. It is associated with a number of diseases, the most notable one being multiple sclerosis.
  • Anterior Ischemic Optic Neuropathy is a particular type of infarct that affects patients with an anatomical predisposition and cardiovascular risk factors.
  • Optic nerve hypoplasia is the under-development of the optic nerve causing little to no vision in the affected eye.

Our goal is to overcome the limitations that Optic Nerve Injuries have placed on our patients using Autologous Stem Cell Therapies.

Stem Cell Treatments for Optic Nerve Injury and Damage

Streaming NIH Search and Results:

Related Articles Effect of human umbilical cord blood mesenchymal stem cells administered by intravenous or intravitreal routes on cryo-induced retinal injury. IUBMB Life. 2017 Mar;69(3):188-201 Authors: Mohamed EM, Abdelrahman SA, Hussein S, Shalaby SM, Mosaad H, Awad AM Abstract Traumatic optic neuropathy is an important cause of severe vision loss. So, many attempts were performed to transplant stem cells systemically or locally to regenerate the injured retina. In this study, we investigated the effect of human umbilical cord blood mesenchymal stem cells (hUBMSCs) on histological structure, apoptotic, antiapoptotic, oxidant and antioxidant markers in an experimental model of cryo-induced retinal damage in mice. Forty-eight mice were included with 4 major groups; group I contained 18 mice as controls. The others included 30 mice exposed to cryo-induced retinal injury and were subdivided into three equal groups: group II received no treatment after injury. Group III was intravenously injected with hUCBMSCs after injury and group IV received an intravitreal injection with hUCBMSCs into both eyes. Retinal tissues were used for histopathological, immunological and gene expression studies. Real time-PCR was performed to assess B-cell lymphoma 2 (bcl2), Bcl2-associated X protein (bax), heme oxygenase-1 (hmox-1) and thioredoxin-2 (tnx-2) expression and to assess the differentiation of the stem cells into the retinal tissue. Immunohistochemical analysis was performed to assess caspase-3, 3-nitrotyrosine (3-NT) and basic fibroblast growth factor (bFGF). Disturbed retinal structure was seen in cryo-injured mice while hUCBMSCs treated groups showed nearly normal structure. By real time-PCR, significantly reduced mRNA expressions of Bax and notably enhanced mRNA expression of Bcl-2, hmox-1 and txn-2 were demonstrated in retinal injured mice with hUCBMSCs treatment compared to those without. In addition, immunohistochemical analysis confirmed downregulation of 3-NT and caspase-3 and upregulation of bFGF after hUCBMSCs injection in injured retina. Furthermore, there was no differentiation of transplanted stem cells into the retinal tissue. In conclusions, hUCBMSCs could improve the morphological retinal structure in cryo-induced retinal damage model by modulation of the oxidant-apoptotic status and by increased the expression of bFGF. © 2017 IUBMB Life, 69(3):188-201, 2017. PMID: 28164440 [PubMed - indexed for MEDLINE]

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