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 Rac1 Guides Porf-2 to Wnt Pathway to Mediate Neural Stem Cell Proliferation. Front Mol Neurosci. 2017;10:172 Authors: Yang XT, Huang GH, Li HJ, Sun ZL, Xu NJ, Feng DF Abstract The molecular and cellular mechanisms underlying the anti-proliferative effects of preoptic regulator factor 2 (Porf-2) on neural stem cells (NSCs) remain largely unknown. Here, we found that Porf-2 inhibits the activity of ras-related C3 botulinum toxin substrate 1 (Rac1) protein in hippocampus-derived rat NSCs. Reduced Rac1 activity impaired the nuclear translocation of β-catenin, ultimately causing a repression of NSCs proliferation. Porf-2 knockdown enhanced NSCs proliferation but not in the presence of small molecule inhibitors of Rac1 or Wnt. At the same time, the repression of NSCs proliferation caused by Porf-2 overexpression was counteracted by small molecule activators of Rac1 or Wnt. By using a rat optic nerve crush model, we observed that Porf-2 knockdown enhanced the recovery of visual function. In particular, optic nerve injury in rats led to increased Wnt family member 3a (Wnt3a) protein expression, which we found responsible for enhancing Porf-2 knockdown-induced NSCs proliferation. These findings suggest that Porf-2 exerts its inhibitory effect on NSCs proliferation via Rac1-Wnt/β-catenin pathway. Porf-2 may therefore represent and interesting target for optic nerve injury recovery and therapy. PMID: 28626389 [PubMed - in process]
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