Unmet need for corrective eyeglasses: results from a Los Angeles County Hospital survey.

To investigate the socioeconomic challenges encountered by patients from Los Angeles County Ophthalmology Clinic, California, United States, in obtaining prescription eyeglasses. A retrospective survey study. Patients sent for refraction in June 2009 were asked to rate their satisfaction with their eyeglasses. If they did not obtain eyeglasses, they were asked the reason e.g., cost, lost prescription, etc. Fifty-five percent (54/99) of patients who received a prescription did not obtain eyeglasses. The most common reason was cost (67 %). Eighty-eight percent of patients had some form of health insurance; however, 100 % were lacking eyeglasses coverage. The mean visual acuity pre-refraction was 20/80 versus 20/30 post-refraction (p < 0.001). It is well known that refractive error is a major cause of blindness worldwide, which negatively impacts the patient and their community. However, it is infrequently addressed that these conditions persist in parts of the develop world, including the United States. Los Angeles County Hospital is an example of an environment with many low-income patients in need of refractive correction who are limited mainly by cost in attaining eyeglasses. Furthermore, insurance organizations that cover low-income patients provide minimal or no coverage for prescription eyeglasses.

Low-density lipoprotein receptor-related protein is decreased in optic neuropathy of Alzheimer disease.

BACKGROUND: Alzheimer disease (AD) is associated with optic nerve degeneration, yet the underlying pathophysiology of this disease and the optic nerve disorder remain poorly understood. Low-density lipoprotein receptor-related protein (LRP) is implicated in the pathogenesis of AD by mediating the transport of amyloid-ß (Aß) out of the brain into the systemic circulation. As a key player in the reaction to central nervous system injury, astrocytes associate with LRP in AD. This study investigates the role of LRP and astrocytes in the pathogenesis of AD optic neuropathy. METHODS: To investigate the role of LRP and astrocytes in the pathogenesis of AD optic neuropathy, we conducted immunohistochemical studies on postmortem optic nerves in AD patients (n = 11) and age-matched controls (n = 10) to examine the presence of LRP. Quantitative analyses using imaging software were used to document the extent of LRP in neural tissues. Axonal integrity was assessed by performing immunohistochemistry on the subjects' optic nerves with an antibody to neurofilament (NF) protein. Double-immunofluorescence labeling was performed to investigate whether LRP colocalized with astrocytes, expressing glial fibrillary acidic protein. RESULTS: LRP expression was decreased in AD optic nerves compared to that in controls (P < 0.001). LRP immunoreactivity was observed in the microvasculature and perivascularly in close proximity to the astrocytic processes. Colocalization of LRP in the astrocytes of optic nerves was also demonstrated. The presence of optic neuropathy was confirmed in the AD optic nerves by demonstrating greatly reduced immunostaining for NF protein as compared to controls. CONCLUSIONS: The reduction of LRP in the AD degenerative optic nerves supports the hypothesis that LRP may play a role in the pathophysiology of AD optic neuropathy.