Amyloid-β, the Retina, and Mouse Models of Alzheimer Disease

Abstract

This Correspondence relates to Vaccinations reduce β-amyloid plaques but exacerbate vascular deposition and inflammation in the retina of Alzheimer’s transgenic mice. (Am J Pathol 2009, 175:2099–2110).

To the Editor-in-Chief:

In our recent publication, “Vaccinations Reduce β-Amyloid Plaques but Exacerbate Vascular Deposition and Inflammation in the Retina of Alzheimer’s Transgenic Mice,”1 we cited work by Ning et al2 describing retinal degeneration in a mouse model of Alzheimer disease. It has been brought to our attention that some of our statements regarding the work by Ning et al are incorrect.

On page 2107 of the Discussion, we stated, “Interestingly, although intraneuronal accumulation of Aβ was reported in association with ganglion cell degeneration in Tg2576 mice, no Aβ-associated plaques were found in their retinas in the previous studies (Ning et al2).” This is not correct, as the publication by Ning et al demonstrates immunoreactivity for Aβ as an extracellular deposit in the retinas of the transgenic mice. Importantly, the two transgenic mouse strains examined by Ning et al were APP/PS1-bitransgenic, not of Tg2576. Further, our statement about intraneuronal accumulation of Aβ is also incorrect as the authors demonstrated cytoplasmic staining of APP (amyloid precursor protein), not Aβ.

We apologize to Ning et al2 for these misstatements, as well as to the readers of either article for any confusion we may have caused.