Myelinated axon number in the optic nerve is unaffected by Alzheimer's disease.

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Abstract
AIMS/BACKGROUND--Visual symptoms are a common but not invariable feature of Alzheimer's disease (AD) and such symptoms appear to become more pronounced as the severity of the dementia increases. Pathology in both the pregeniculate and cortical parts of the visual system has been suggested to underlie the visual deficits in AD. In order to investigate the former possibility, the effect of AD on the optic nerve was investigated. METHODS--Intraorbital segments of optic nerve were taken at autopsy from nine patients with AD and seven patients with no history of psychiatric or neurological disease and no abnormal neuropathology. All patients had functional vision before death and appeared free of retinal, optic nerve, or microvascular disease. The optic nerves were processed into resin, semi-thin sections cut perpendicular to the long axis of each optic nerve, and stained with paraphenylenediamine. The sections were then investigated using an image analysis system and standard morphometric techniques. RESULTS--There was no significant difference in the mean cross sectional neural area of AD compared with control optic nerves. Neither were there any significant differences between myelinated axon surface density, total axon number, or mean cross sectional axon area in AD compared with control optic nerves. CONCLUSION--These results indicate that optic nerve degeneration is not a feature of AD and suggest that the visual deficits in the disease result from cortical dysfunction. This view is supported by the fact that visuospatial dysfunction appears to be the most common visual problem in AD.