Retinal amyloid peptides and complement factor H in transgenic models of Alzheimer's disease

Alexandrov, Peter N.; Pogue, Aileen; Bhattacharjee, Surjyadipta; Lukiw, Walter J.

doi:10.1097/wnr.0b013e3283497334

Cited by 128Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

Retinal amyloid peptides and complement factor H in transgenic models of Alzheimer's disease

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Alexandrov, Peter N., Pogue, Aileen, Bhattacharjee, Surjyadipta, Lukiw, Walter J.·2011·Neuroreport

DOI 10.1097/wnr.0b013e3283497334PMC PMC3719862

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Abstract

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 AD patients, alloform Aβ42 is increased.
“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
Aβ plaques are present in the retina of AD patients and AD human postmortem specimens.
“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
Aβ deposition in AD retina is observed from ONL to NFL, more abundant in superior region where greater neuronal degeneration is detected.
“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
Aβ42 peptide accumulation in the retina may contribute to retinal degeneration and visual impairment in AD.
“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
CFH functions as a cofactor in inactivation of C3b in alternative complement pathway, and low CFH levels result in complement activation, triggering inflammation in retina and brain.
“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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알쯔하이머병 모델 쥐의 망막색소상피에서 아밀로이드 베타 42의 세포 내 발현에 관한 연구
박성욱 (2012) · Seoul National University Open Repository (Seoul National University)

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.
ORCID: Bhattacharjee, Surjyadipta
Lukiw, Walter J.
Venue: Neuroreport
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2011-08-24
Volume: 22
Issue: 12
Pages: 623-627
ISSN: 0959-4965 (ISSN-L)
DOI: 10.1097/wnr.0b013e3283497334
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: Health Sciences › Medicine › Physiology › 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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Retinal amyloid peptides and complement factor H in transgenic models of Alzheimer's disease

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