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Cited by 175

The DOI matches its Crossref record; 15 of the 15 references it cites were found in a registry or an index.

Increased Alzheimer's disease–like pathology in the APP/ PS1ΔE9 mouse model lacking Nrf2 through modulation of autophagy

Open access
Joshi, Gururaj, Gan, Kok Ann, Johnson, Delinda A., Johnson, Jeffrey A.·2015·Neurobiology of Aging
DOI 10.1016/j.neurobiolaging.2014.09.004
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Abstract

The presence of senile plaques is one of the major pathological hallmarks of the Alzheimer’s disease (AD) brain. The plaques predominantly contain insoluble amyloid β-peptide; a cleavage product of the larger amyloid precursor protein (APP). Two enzymes named β and γ secretase generate the neurotoxic amyloid-β peptide from APP. Mature APP is also turnovered endogenously by autophagy, more specifically by the endosomal-lysosomal pathway. A defective lysosomal system is known to be pathogenic in AD. Modulation of NF-E2 related factor 2 (Nrf2) has been shown in several neurodegenerative disorders and Nrf2 has become a potential therapeutic target for various neurodegenerative disorders including AD, Parkinson’s disease, and amyotrophic lateral sclerosis. In the current study, we explored the effect of genetic ablation of Nrf2 on APP/Aβ processing and/or aggregation as well as changes in autophagic dysfunction in APP/PS1 mice. There was a significant increase in inflammatory response in APP/PS1 mice lacking Nrf2. This was accompanied by increased intracellular levels of APP, Aβ (1-42), and Aβ (1-40), without a change total full-length APP. There was a shift of APP and Aβ into the insoluble fraction, as well as increased poly-ubiquitin conjugated proteins in mice lacking Nrf2. APP/PS1-mediated autophagic dysfunction is also enhanced in Nrf2 deficient mice. Finally, neurons in the APP/PS1/Nrf2−/− mice had increased accumulation of multivesicular bodies, endosomes and lysosomes. These outcomes provide a better understanding of the role of Nrf2 in modulating autophagy in an AD mouse model and may help design better Nrf2 targeted therapeutics that could be efficacious in the treatment of AD.

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Metadata

Authors
Joshi, G., Gan, K. A., Johnson, D. A., & Johnson, J. A.
Venue
Neurobiology of Aging
Publisher
Elsevier BV
Published
2015-02
Volume
36
Issue
2
Pages
664-679
ISSN
0197-4580 (ISSN-L)
DOI
10.1016/j.neurobiolaging.2014.09.004
OpenAlex
W2071174827
Cited by
175
References
15
FWCI
7.58
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Increased Alzheimer's disease–like pathology in the APP/ PS1ΔE9 mouse model lacking Nrf2 through modulation of autophagy. https://app.cochat.ai/papers/10.1016/j.neurobiolaging.2014.09.004
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Joshi, G., Gan, K. A., Johnson, D. A., & Johnson, J. A. (2015). Increased Alzheimer's disease–like pathology in the APP/ PS1ΔE9 mouse model lacking Nrf2 through modulation of autophagy. Neurobiology of Aging. https://doi.org/10.1016/j.neurobiolaging.2014.09.004

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.