Anavex 2-73 and/or Anavex 3-71 could be used to prevent blindness!!!
The role of sigma 1 receptor (Sig1R) in rescuing cone photoreceptor function was investigated in Pde6ßrd10 (rd10) mice, a model of severe retinal degeneration. Sig1R, a putative molecular chaperone, is implicated in several human neurodegenerative diseases. We administered (+)-pentazocine, a high-affinity Sig1R ligand, to rd10 mice, which lose rod and subsequently cone photoreceptor cells (PRC) within the first few weeks of life, rendering them completely blind. Regular administration of (+)-pentazocine rescued cone PRC responses, which were markedly preserved and were similar to those in wild-type mice. To our knowledge, this is the first demonstration of significant preservation of retinal function as a consequence of Sig1R activation. The data are highly relevant to potential therapeutic interventions in human retinal disease.
The major cause of untreatable blindness worldwide is retinal degenerative disease. The retinal cells most affected are photoreceptor cells (PRC) and ganglion cells (RGC) (1). PRCs degenerate in retinitis pigmentosa (RP), macular degeneration, and cone-rod dystrophies; RGCs die in glaucoma, optic neuropathies, and diabetic retinopathy. There is great heterogeneity underlying retinal degenerative diseases. Thousands of mutations in >200 genes have been identified that lead to blindness in humans (2). In developing therapeutic strategies to treat blindness, it may not be practical to target each genetic defect; however targeting common disease mechanisms holds promise for the development of realistic treatment for patients suffering from retinal disease. Pathogenic features common to retinal diseases, i.e., oxidative damage, endoplasmic reticulum (ER) stress, inflammation, and apoptosis (3?–5), are implicated in neurodegenerative diseases.
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