Ocular changes in TgF344-AD rat model of Alzheimer's disease
Open accessAbstract
PURPOSE: Alzheimer's disease (AD) is the most common neurodegenerative disorder characterized by progressive decline in learning, memory, and executive functions. In addition to cognitive and behavioral deficits, vision disturbances have been reported in early stage of AD, well before the diagnosis is clearly established. To further investigate ocular abnormalities, a novel AD transgenic rat model was analyzed. METHODS: Transgenic (Tg) rats (TgF344-AD) heterozygous for human mutant APPswe/PS1ΔE9 and age-matched wild type (WT) rats, as well as 20 human postmortem retinal samples from both AD and healthy donors were used. Visual function in the rodent was analyzed using the optokinetic response and luminance threshold recording from the superior colliculus. Immunohistochemistry on retinal and brain sections was used to detect various markers including amyloid-β (Aβ) plaques. RESULTS: As expected, Aβ plaques were detected in the hippocampus, cortex, and retina of Tg rats. Plaque-like structures were also found in two AD human whole-mount retinas. The choroidal thickness was significantly reduced in both Tg rat and in AD human eyes when compared with age-matched controls. Tg rat eyes also showed hypertrophic retinal pigment epithelial cells, inflammatory cells, and upregulation of complement factor C3. Although visual acuity was lower in Tg than in WT rats, there was no significant difference in the retinal ganglion cell number and retinal vasculature. CONCLUSIONS: In this study, we observed pathological changes in the choroid and in RPE cells in the TgF344-AD rat model; choroidal thinning was observed further in human AD retina. Along with Ab deposition, the inflammatory response was manifested by microglial recruitment and complement activation. Further studies are needed to elucidate the significance and mechanisms of these pathological changes [corrected].
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In TgF344-AD transgenic rat model, Aβ deposition, microglial recruitment, and complement activation are associated with decline in visual function.
“In the transgenic rat model (TgF344-AD) also has been observed, along with Aβ deposition, microglial recruitment, and complement activation in association with a decline in visual function (Tsai et al., 2014; Table 1).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Tsai et al., 2014
Abundant evidence from animal and clinical studies shows a correlation between ocular pathology and AD development.
“Abundant evidence from animal and clinical studies shows a correlation between ocular pathology and AD development.553–555”
From Amyloid β-based therapy for Alzheimer’s disease: Challenges, successes and future (2023) · cites this paper as [553]
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References 99 · Cited by 153
Research works printed but not linked: 2
- Liu B, Rasool S, Yang Z, et al. Amyloid-peptide vaccinations reduce beta-amyloid plaques but exacerbate vascular deposi- tion and inflammation in the retina of Alzheimer's transgenic mice. Am J Pathol. 2009;175:2099-2110.
- Querques G, Lattanzio R, Querques L, et al. Enhanced depth imaging optical coherence tomography in type 2 diabetes. Invest Ophthalmol Vis Sci. 2012;53:6017-6024.
- Authors
- Tsai, Y., Lu, B., Ljubimov, A. V., Girman, S., Ross-Cisneros, F. N., Sadun, A. A., Svendsen, C. N., Cohen, R. M., & Wang, S.
- Affiliations
- Cedars-Sinai Regenerative Medicine Institute, Los Angeles, California
- University of California, Los Angeles (US)
- Cedars-Sinai Medical Center (US)
- Doheny Eye Institute and Department of Ophthalmology, Keck School of Medicine, University of Southern California, Los Angeles, California
- University of Southern California (US)
- Emory University (US)
- Corresponding author
- Wang, Shaomei
- ORCID
- Venue
- Investigative Opthalmology & Visual Science
- Published
- 2014-01-29
- Volume
- 55
- Issue
- 1
- Pages
- 523
- ISSN
- 0146-0404 (ISSN-L)
- 1552-5783
- PMC
- PMC3907137
- OpenAlex
- W1975040154
- Cited by
- 153
- References
- 99
- Citations by year
- 2026: 2 · 2025: 17 · 2024: 5 · 2023: 7 · 2022: 17 · 2021: 17 · 2020: 20 · 2019: 14 · 2018: 15 · 2017: 10 · 2016: 15 · 2015: 9 · 2014: 5
- FWCI
- 8.64
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Investigative Ophthalmology & Visual Science (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Defense (W81XWH)
- University of Southern California
- Lincy Foundation
- Cedars-Sinai Medical Center
- National Institutes of Health (NIH-R01, W81XWH, AG05142, EY-03040)
- National Institute on Aging (P50-AG05142, P50AG005142)
- National Eye Institute (P30EY003040, R01-EY-03040, R01EY020488)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, TgF344-AD rat model, choroidal thinning, complement C3, microglial inflammation, visual function, optokinetic response, superior colliculus, visual acuity
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Amyloid, Animals, Cell Count, Choroid, Disease Models, Animal, Female, Humans, Immunohistochemistry, Male, Middle Aged, Rats, Inbred F344, Retinal Diseases, Visual Acuity, Rats, Retinal Pigment Epithelium
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