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Retinal amyloid peptides and complement factor H in transgenic models of Alzheimer's disease
Open accessAbstract
Murine transgenic models of Alzheimer's disease (Tg-AD) have been useful to analyze the contribution of β-amyloid precursor protein (βAPP), Aβ42 peptide deposition, and the proinflammatory mechanisms that characterize Alzheimer-type neuropathology. In this report, we have studied the levels of βAPP, Aβ40 and Aβ42 peptide, as well as the innate immune and inflammatory response-regulator complement factor H in the brain and retina in four different Tg-AD models including Tg2576, PSAPP, 3xTg-AD, and 5xFAD. Aged, symptomatic 5xFAD mice showed the highest retinal abundance of Aβ42 peptides and the highest deficits in complement factor H. This may be a useful model to study the mechanisms of amyloid-mediated inflammatory degeneration. The superior colliculus and retina obtained from late-stage Alzheimer's disease revealed upregulated amyloidogenic and inflammatory signaling along the anteroposterior axis of the retinal-primary visual cortex pathway.
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In the citing paper
“In AD patients, the alloform Aβ42 is increased (Alexandrov et al., 2011).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Alexandrov et al., 2011
In the citing paper
“In addition, in the retina of AD patients as well as AD human postmortem specimens the presence of Aβ plaques has been demonstrated.”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Alexandrov et al., 2011
In the citing paper
“Aβ deposition was observed from the outer nuclear layer (ONL) to nerve fiber layer (NFL), being more abundant in the superior region of the retina where greater neuronal degeneration has been detected (Hardy and Selkoe, 2002; Selkoe, 2004, 2008; Alexandrov et al., 2011; Ratnayaka et al., 2015; Hart et al., 2016; Table 1).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Alexandrov et al., 2011
In the citing paper
“Aβ42 peptide accumulation in the retina may contribute to retinal degeneration and visual impairment in AD (Hardy and Selkoe, 2002; Selkoe, 2004, 2008; Alexandrov et al., 2011; Ratnayaka et al., 2015; Hart et al., 2016; Figure 1A, Table 1).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Alexandrov et al., 2011
In the citing paper
“CFH functions as a cofactor in the inactivation of C3b in the alternative complement pathway, and thus low CFH levels result in complement activation, triggering inflammation in the retina and brain (Alexandrov et al., 2011).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Alexandrov et al., 2011
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Citations
Cites
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Metadata
- Authors
- Alexandrov, P. N., Pogue, A., Bhattacharjee, S., & Lukiw, W. J.
- Affiliations
- Louisiana State University Health Sciences Center New Orleans (US)
- Louisiana State University (US)
- Corresponding author
- Lukiw, Walter J.
- Venue
- Neuroreport
- Published
- 2011-08-24
- Volume
- 22
- Issue
- 12
- Pages
- 623-627
- ISSN
- 0959-4965 (ISSN-L)
- PMC
- PMC3719862
- OpenAlex
- W2336513583
- Cited by
- 128
- References
- 25
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 3 · 2023: 7 · 2022: 8 · 2021: 17 · 2020: 23 · 2019: 9 · 2018: 7 · 2017: 9 · 2016: 9 · 2015: 9 · 2014: 10 · 2013: 4 · 2012: 5
- FWCI
- 4.15
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neuroreport (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (P51OD011104)
- National Institute on Aging (P50 AG 16573, P50AG016573, R01AG038834, R01AG018031)
- National Eye Institute (P30EY002377)
- National Institute of General Medical Sciences (P30GM103340)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, complement factor H, amyloid-beta 42, Aβ40, amyloid precursor protein, transgenic mouse model, 5xFAD mice, Tg2576 mice, 3xTg-AD mice, innate immunity, neuroinflammation, superior colliculus, visual cortex
- MeSH terms
- Alzheimer Disease, Animals, Brain, Enzyme-Linked Immunosorbent Assay, Humans, Mice, Transgenic, Retina, Amyloid beta-Peptides, Complement Factor H, Mice
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