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e experiments, Li and colleagues identified cone outer segments by peanut agglutinin labeling or by antibodies against cone opsins. Moreover, antibodies against cone arrestin were applied to determine the cell bodies of cone photoreceptors. Loss of COS, an early DBeQ sign of cone degeneration, was detected as early as PD12, at the peak of rod degeneration. The loss of COS was not evenly distributed. Rather, DBeQ it was concentrated in numerous smaller patches that were negatively stained for PNA. The PNA damaging locations expanded with age, indicating progressive loss of COS. Intravitreal injection of recombinant CNTF protein dramatically changed the PNA damaging locations. They became significantly smaller and in several instances entirely resolved. The reappearance of PNA staining within the prior PNA damaging locations suggests regeneration of COS.
To prove that CNTF therapy induces regeneration of COS, the investigators compared the COS densities before and after CNTF therapy. They demonstrated that COS density was greater in CNTF treated retina than before the therapy, confirming that CNTF therapy did promote regeneration of COS. PluriSln 1 Because loss of COS is an early sign of cone degeneration, regeneration of COS might be considered as reversal with the degenerative process. This result indicates that CNTF therapy may not only slow or quit degeneration, but might also reverse the degeneration process. Given that COS is part of the functional organelles of cone photoreceptors for light detection, the regeneration of COS could translate into functional improvement of cones.
In an additional experiment, significant long term protection of cone cells and cone ERG were achieved by using CNTF secreting implants for sustained delivery of CNTF towards the retina of S334ter rats. 6. 2. Protection of cones in Human musculoskeletal system human by CNTF As already described, the first indication of a neurotrophic effect of CNTF on cones came from a smaller open label clinical trial of CNTF secreting implants in patients with advanced RP. Despite the fact that the trial objective was to decide the safety with the CNTF implants as well as the surgical procedure, the results showed that three patients knowledgeable an increase of 10 15 letters over baseline in visual acuity whereas no increase was observed within the untreated fellow eyes among the seven study eyes that might be tracked for visual acuity.
The improvement of visual acuity is most likely to have resulted from the improvement of cone function, since visual acuity tests the function with the fovea, which has only cones, and in patients with advanced RP, almost all rod photoreceptors have degenerated. PluriSln 1 The protective effect of CNTF on cone photoreceptors was objectively demonstrated in human patients utilizing a potent imaging technology known as the adaptive optics scanning laser ophthalmoscopy. Talcott and colleagues observed cones in three patients over a 2 year period and discovered a progressive cone density decreased in sham treated eyes. Nevertheless, the cone density remained stable in CNTF treated eyes. Moreover, a recent clinical trial of CNTF secreting implants in patients with geographic atrophy showed a stabilization of visual acuity in eyes treated with high dose CNTF secreting implants.
Together, these findings indicate that CNTF is neuroprotective for cone photoreceptors. 6. 3. Restoration of cone function in dogs with CNGB3 mutations by CNTF Kom romy and colleagues DBeQ lately discovered that a single intravitreal injection of recombinant CNTF protein in adult dogs with CNGB3 mutations, which causes day blindness in dogs, induced a transient restoration of cone function and vision. The cone ERGs became detectable for up to 4 weeks after injection. The treated animals also showed improved performance in navigating an obstacle course in bright light, indicating restoration of cone vision. There was in addition a transient decrease in rod ERG, which is consistent with the prior findings in rat and mice.
There's no functional B subunit with the cone cyclic nucleotide gated channel in CNGB3 dogs as well as the mechanism with the restored cone function is unknown. The transient PluriSln 1 nature of these adjustments DBeQ is most likely because of the clearance with the injected CNTF protein. 7. CNTF and retinal ganglion cells 7. 1. Neuroprotection CNTF serves a neurotrophic function for RGCs. A single injection of CNTF protein into PluriSln 1 the vitreous significantly protected RGCs in an optic nerve axotomy rat model, whereas brain derived neurotrophic element did not. RGC protection by CNTF was also noticed in nitric oxide induced cell death. CNTF therapy 2 days prior to injection with the nitric oxide donor significantly protected RGCs from cell death. In culture, CNTF promoted the survival of purified rat RGCs within the presence of forskolin. CNTF gene transfer by way of Ad vectors also protects retinal ganglion cells from degeneration. RGC density within the eyes treated with intravitreal Ad CNTF 1 2 hours after optic nerve axotomy was significantly greater than within the controls when examined 14 days later. Similar protection