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Originally published In Press as doi:10.1167/iovs.08-2384 on September 12, 2008
 (Investigative Ophthalmology and Visual Science. 2009;50:793-800.)
© 2009 by The Association for Research in Vision and Ophthalmology, Inc.
doi:10.1167/iovs.08-2384
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β-Amyloid Deposition and Functional Impairment in the Retina of the APPswe/PS1{Delta}E9 Transgenic Mouse Model of Alzheimer’s Disease

Sylvia E. Perez,1 Stephen Lumayag,1,2 Beatrix Kovacs,1,2 Elliott J. Mufson,*,1 and Shunbin Xu*,1,2

1From the Departments of Neurological Sciences and 2Ophthalmology, Rush University Medical Center, Chicago, Illinois.

PURPOSE. To determine whether β-amyloid (Aβ) deposition affects the structure and function of the retina of the APPswe/PS1{Delta}E9 transgenic (tg) mouse model of Alzheimer’s disease.

METHODS. Retinas from 12- to 19-month old APPswe/PS1{Delta}E9 tg and age-matched non-transgenic (ntg) littermates were single or double stained with thioflavine-S and antibodies against Aβ, glial fibrilar acidic protein (GFAP), microglial marker F4/80, choline acetyltransferase (ChAT), and syntaxin 1. Quantification of thioflavine-S positive plaques and retinal layer thickness was analyzed semi-quantitatively, whereas microglial cell size and levels of F4/80 immunoreactivity were evaluated using a densitometry program. Scotopic electroretinogram (ERG) recording was used to investigate retinal physiology in these mice.

RESULTS. Thioflavine-S positive plaques appeared at 12 months in the retinas of APPswe/PS1{Delta}E9 tg mice with the majority of plaques in the outer and inner plexiform layers. Plaques were embedded in the inner plexiform layer strata displaying syntaxin 1 and ChAT. The number and size of the plaques in the retina increased with age. Plaques appeared earlier and in greater numbers in females than in male tg littermate mice. Microglial activity was significantly increased in the retinas of APPswe/PS1{Delta}E9 tg mice. Although we did not detect neuronal degeneration in the retina, ERG recordings revealed a significant reduction in the amplitudes of a- and b-waves in aged APPswe/PS1{Delta}E9 tg compared to ntg littermates.

CONCLUSIONS. The present findings suggest that Aβ deposition disrupts retinal structure and may contribute to the visual deficits seen in aged APPswe/PS1{Delta}E9 tg mice. Whether Aβ is involved in other forms of age-related retinal dysfunction is unclear.




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