PHYSL405 Lecture Notes - Lecture 16: Trabecular Meshwork, Retinitis Pigmentosa, Glaucoma
7 Nov 2016
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Most striking feature in transgenic models with mutated rhodopsin is misfolding of mutant rhodopsin, lack of maturation and lack of vectorial transport to the os. Not all loss of fu(cid:374)(cid:272)tio(cid:374) (cid:894)too (cid:862)easy(cid:863) for s(cid:272)ie(cid:374)tists(cid:863)(cid:895); mo t (cid:272)ases = common do(cid:449)(cid:374)strea(cid:373) effe(cid:272)ts. = death of photoreceptors and rpe (same thing for rp) So far, ~270 mutations found to cause blindness (albeit, not all in different genes) Most, but not all, forms of glaucoma are characterized by high intraocular pressure. All forms of glaucoma have in common: death of rgcs. Rgcs die b/c of damage to their axons (axotomy) In open angle glaucoma, fluid can not flow effectively through the trabecular meshwork, and this causes an increase in intraocular p causing damage to optic nerve and leading to vision loss. Treatment: 1) drops (6 different classes) 2) laser to trabecular meshwork (argon laser trabeculoplasty, alt) Vulnerability of rgcs to axotomy depends on subtypes and varies b/w indivs.
