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Purpose Amyloid beta, the main protein component of Alzheimer (AD) plaques and tangles, is characterized by high levels of beta‐sheets. Raman microspectroscopy allows quantitative analysis of this specific molecular conformation. We compared the beta‐sheet levels in lens opacities and in plaques and tangles in the hippocampus of AD patients. Methods We obtained 14 lenses from 7 post‐mortem donors , neuropathologically confirmed as having advanced or moderate AD. From 3 of these donors, we also obtained hippocampus tissue. Protein and lipid conformations were analysed in the 500‐1800 cm‐1 fingerprint region. The ratio of the beta‐sheet peak at 1668 cm‐1 and the protein peak at 1450 cm‐1 is a quantitative measure for the beta‐sheet content. Additionally, histological sections were stained using a standard Congo red protocol and amyloid beta immunohistochemistry. Results The 1668cm‐1/1450cm‐1 ratio, quantitatively reflecting the beta‐sheet content, is 1.28 for clear and cataractous regions in the lens.For the plaques and tangles in the hippocampus the ratio is 1.62 and 1.23 for non‐affected regions. When corrected for the presence of lipids in plaques and tangles this ratio is 2.64. Congo red and amyloid beta immunohistochemistry is positive for AD plaques and tangles but is negative for all lenses studied. Conclusion In contrast with a previous study (Goldstein et al. 2003) we conclude that proteins in opaque regions of lenses and in hippocampal plaques and tangles are fully different species. Moreover opacification is not accompanied by changes in the beta‐sheet configuration of lens proteins. This means that cortical cataract cannot be considered as an indicator and predictor of AD.

Purpose Eye lenses from human donors with and without Alzheimer's disease (AD) were studied to evaluate the presence of amyloid in cortical cataract. Methods We obtained 39 lenses from 21 postmortem donors with AD and 15 lenses from age‐matched controls. For 17 donors, AD was clinically diagnosed by general physicians and for 4 donors the AD diagnosis was neuropathologically confirmed. As controls, 7 donors with pronounced cortical opacities and 8 donors with almost transparent lenses were selected. All lenses were photographed in a dark field stereomicroscope. Histological sections were analyzed using a standard and a more sensitive Congo red protocol, thioflavin staining and beta‐amyloid immunohistochemistry. Results Of the 21 donors with AD, 6 had pronounced bilateral cortical lens opacities and 15 only minor or no cortical opacities. Thioflavin, standard and modified Congo red staining were positive in the control brain tissues and in the dystrophic cornea. Beta‐amyloid immunohistochemistry was positive in the brain tissues but not in the cornea sample. Lenses from control and AD donors were, without exception, negative after Congo red, thioflavin, and beta‐amyloid immunohistochemical staining. Conclusion The absence of staining in AD and control lenses with the techniques employed lead us to conclude that there is no beta‐amyloid in lenses from donors with AD or in control cortical cataracts.