Amyloid-Peptide Vaccinations Reduce β-Amyloid Plaques but Exacerbate Vascular Deposition and Inflammation in the Retina of Alzheimer’s Transgenic Mice
Open accessAbstract
Alzheimer's disease (AD) is pathologically characterized by accumulation of beta-amyloid (Abeta) protein deposits and/or neurofibrillary tangles in association with progressive cognitive deficits. Although numerous studies have demonstrated a relationship between brain pathology and AD progression, the Alzheimer's pathological hallmarks have not been found in the AD retina. A recent report showed Abeta plaques in the retinas of APPswe/PS1DeltaE9 transgenic mice. We now report the detection of Abeta plaques with increased retinal microvascular deposition of Abeta and neuroinflammation in Tg2576 mouse retinas. The majority of Abeta-immunoreactive plaques were detected from the ganglion cell layer to the inner plexiform layer, and some plaques were observed in the outer nuclear layer, photoreceptor outer segment, and optic nerve. Hyperphosphorylated tau was labeled in the corresponding areas of the Abeta plaques in adjacent sections. Although Abeta vaccinations reduced retinal Abeta deposits, there was a marked increase in retinal microvascular Abeta deposition as well as local neuroinflammation manifested by microglial infiltration and astrogliosis linked with disruption of the retinal organization. These results provide evidence to support further investigation of the use of retinal imaging to diagnose AD and to monitor disease activity.
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pTau is observed from OPL to GCL in the retina of AD patients, and from ONL to GCL in transgenic mouse.
“In addition to Aβ plaques, pTau was observed from OPL to GCL in the retina of AD patients. Also, pTau has been found from the ONL to GCL in the transgenic mouse (Liu et al., 2009).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Liu et al., 2009
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- Authors
- Liu, B., Rasool, S., Yang, Z., Glabe, C. G., Schreiber, S. S., Ge, J., & Tan, Z.
- Affiliations
- Sun Yat-sen University (CN)
- University of California, Irvine (US)
- Corresponding author
- Ge, Jian
- Tan, Zhiqun
- Venue
- The American Journal of Pathology
- Publisher
- Elsevier BV
- Published
- 2009-11
- Volume
- 175
- Issue
- 5
- Pages
- 2099-2110
- ISSN
- 0002-9440 (ISSN-L)
- PMC
- PMC2774073
- OpenAlex
- W2095555365
- Cited by
- 182
- References
- 71
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 10 · 2023: 11 · 2022: 10 · 2021: 15 · 2020: 21 · 2019: 16 · 2018: 17 · 2017: 11 · 2016: 15 · 2015: 7 · 2014: 7 · 2013: 8 · 2012: 8
- FWCI
- 5.32
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- American Journal Of Pathology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Larry L. Hillblom Foundation
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, amyloid plaques, retinal neuroinflammation, microglial infiltration, astrocyte activation, hyperphosphorylated tau, retinal microvasculature, Tg2576 mice, APPswe/PS1ΔE9 mice, ganglion cell layer
- MeSH terms
- Alzheimer Disease, Animals, Brain, Humans, Inflammation, Mice, Transgenic, Peptide Fragments, Retinal Vessels, Vaccination, Amyloid beta-Peptides, Neurofibrillary Tangles, Mice
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