The DOI matches its Crossref record; 73 of the 73 references it cites were found in a registry or an index.
Amyloid generation and dysfunctional immunoproteasome activation with disease progression in animal model of familial Alzheimer’s disease
Open accessAbstract
Double-transgenic amyloid precursor protein/presenilin 1 (APP/PS1) mice express a chimeric mouse/human APP bearing the Swedish mutation (Mo/HuAPP695swe) and a mutant human PS1-dE9 both causative of familial Alzheimer's disease (FAD). Transgenic mice show impaired memory and learning performance from the age of 6 months onwards. Double-transgenic APP/PS1 mice express altered APP and PS1 mRNAs and proteins, reduced β-secretase 1 (BACE1) mRNA and normal BACE1 protein, all of which suggest a particular mechanism of amyloidogenesis when compared with sporadic AD. The first β-amyloid plaques in APP/PS1 mice appear at 3 months, and they increase in number and distribution with disease progression in parallel with increased levels of brain soluble β-amyloid 1-42 and 1-40, but also with reduced 1-42/1-40 ratio with age. Amyloid deposition in plaques is accompanied by altered mitochondria and increased oxidative damage, post-translational modifications and accumulation of altered proteins at the dystrophic neurites surrounding plaques. Degradation pathways are also modified with disease progression including activation of the immunoproteasome together with variable alterations of the different protease activities of the ubiquitin-proteasome system. Present observations show modifications in the production of β-amyloid and activation and malfunction of the subcellular degradation pathways that have general implications in the pathogenesis of AD and more particularly in specificities of FAD amyloidogenesis.
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“IHC for SOD1 labels areas of high oxidative stress, specifically around Aβ plaques, and is associated with dystrophic neurites [21,48].”
From Centella Asiatica Improves Memory and Promotes Antioxidative Signaling in 5XFAD Mice (2019) · cites this paper as [48]
In the citing paper
“Elevated SOD expression is indicative of the high levels of oxidative stress associated with Aβ plaques in Alzheimer’s disease brains [21,48,80,104].”
From Centella Asiatica Improves Memory and Promotes Antioxidative Signaling in 5XFAD Mice (2019) · cites this paper as [48]
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Metadata
- Authors
- Aso, E., Lomoio, S., López‐González, I., Joda, L., Carmona, M., Fernández‐Yagüe, N., Moreno, J., Juvés, S., Pujol, A., Pamplona, R., Portero‐Otin, M., Martín, V., Díaz, M., & Ferrer, I.
- Affiliations
- Bellvitge University Hospital (ES)
- University of Pavia (IT)
- Institució Catalana de Recerca i Estudis Avançats (ES)
- Universitat de Lleida (ES)
- Universidad de La Laguna (ES)
- Venue
- Brain Pathology
- Publisher
- Wiley
- Published
- 2012-01-13
- Volume
- 22
- Issue
- 5
- Pages
- 636-653
- ISSN
- 1015-6305 (ISSN-L)
- 1750-3639
- PMC
- PMC8057644
- OpenAlex
- W1869566076
- Cited by
- 118
- References
- 73
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 6 · 2023: 8 · 2022: 4 · 2021: 11 · 2020: 9 · 2019: 10 · 2018: 9 · 2017: 4 · 2016: 11 · 2015: 10 · 2014: 14 · 2013: 9 · 2012: 6
- FWCI
- 6.33
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain Pathology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion, cc-by-nc-nd)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, cc-by-nc-nd)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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
- familial Alzheimer's disease, APP/PS1 mice, amyloidogenesis, amyloid plaques, beta-secretase 1, BACE1, Swedish mutation, presenilin 1, proteasome, ubiquitin-proteasome system, mitochondrial dysfunction, oxidative damage, dystrophic neurites, post-translational modification, disease progression, memory impairment
- MeSH terms
- Superoxide Dismutase-1, Age Factors, Alzheimer Disease, Animals, Avoidance Learning, Brain, Cognition Disorders, Cysteine Endopeptidases, Disease Models, Animal, Gene Expression Regulation, Humans, Mice, Inbred C57BL, Mice, Transgenic, Mutation, Neuropsychological Tests, RNA, Messenger, Superoxide Dismutase, Signal Transduction, Amyloid beta-Peptides, Microscopy, Immunoelectron, Aspartic Acid Endopeptidases, Amyloid beta-Protein Precursor, tau Proteins, Disease Progression, Mitogen-Activated Protein Kinases, Recognition, Psychology, Ubiquitin Thiolesterase, Microscopy, Electron, Transmission, Proteasome Endopeptidase Complex, Mice, alpha-Synuclein, Presenilin-1, Plaque, Amyloid
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