| It is estimated that nearly 160 million people worldwide suffer from significant visual impairment. Some of these cases require surgery, some are possibly preventable, while others are incurable. Many diseased states of the eye have been dutifully investigated to see changes in inflammatory markers, growth factor expression and various other protein expression associated with the particular ailment. While we now have a working paradigm of some of these illnesses, we do not have a great understanding of what is to be expected in the normal aging process. This thesis examines some of the changes seen in the normal aging retina and choroid in order to aid in the explanation of the difference between normal ocular aging and ocular diseased states.; Retinal and choroidal research was conducted on 8, 22, and 32 month F344 x BN F1 hybrid male rats. Real time PCR was conducted to check for changes in mRNA, while either immunohistochemistry or Western blot densitometry was conducted for changes in protein expression with age. A decrease in sympathetic neurotransmission of both dopamine beta-hydroxylase and norepinephrine was found with age that may parallel other aging organs. In order to compensate for the decreases seen, the sympathetic receptor, beta1-adrenergic receptor was found to significantly increase with age due to denervation supersensitivity.; Many changes are seen in various states of ocular diseases. However, what changes of growth factor expression are seen in normal aging is unknown. Using the same strain of rats and the same techniques, we investigated changes in growth factor expression in normal aging rat retina. We found an increased expression of the VEGF and its receptor KDR which could lead to angiogenesis, but a decrease in Tie-s which would lead to vessel stabilization. At the same time, the retina was expressing less PEDF. PEDF has not only protective effects on photoreceptor cells, but also slows angiogenesis. The data collected suggests that the retina creates an environment well suited for angiogenesis, and that some diseased states may only be an acceleration of normal aging. |