. Absence of beta-amyloid in cortical cataracts of donors with and without Alzheimer's disease. Exp Eye Res. 2013 Jan;106:5-13. PubMed.


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  1. There appear to be major differences in the quality of the stained images between the two papers, suggesting perhaps that the reasons lie in the particular staining technique used (Bennhold's technique used by Goldstein et al. and Moncaster et al. vs. Puchtler's technique used by Michael et al., who also used a different immunostaining antibody).

    This raises the following question: If the goal was to replicate the results of Goldstein et al., 2003, in AD, and Moncaster et al., 2010, in Down's syndrome, does it perhaps make sense to use the identical staining technique? It may be worth noting that Frederikse, 2000, was also successful in immunostaining and Congo red staining of Aβ in human lenses. There is also a chance that differences in postmortem interval and in handling specimens could have contributed to the observed differences in results.

    From my perspective as a clinician, the upshot is that there are potentially crucial technical differences among the studies in question. However, there appear to be sufficient in-vitro data to justify in-vivo studies in humans. Our site participates in the ongoing Cognoptix study; I have also served as a consultant to them on study design. I also note that Cognoptix announced that, by detecting a specific fluorescent signature of ligand-marked β amyloid in the supranucleus region of the human lens, their so-called SAPPHIRE II system showed a twofold differentiation factor between small groups of five healthy volunteers and five patients diagnosed with probable Alzheimer s disease in a recent proof-of-concept clinical trial. I do not believe that these data have been published.


    . Amyloid-like protein structure in mammalian ocular lenses. Curr Eye Res. 2000 Jun;20(6):462-8. PubMed.

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  1. Not Seeing Eye to Eye: Do Lenses Accumulate Aβ?