ReviewCell cycle (Georgetown, Tex.)2014
Senescence-accelerated OXYS rats: a model of age-related cognitive decline with relevance to abnormalities in Alzheimer disease.
Review in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 95 citations in OpenAlex.
- Features of Alteration in MAPK Pathway Activity in the Postnatal Brain of a Rat Model of Sporadic Alzheimer's Disease.International journal of molecular sciences · 2026Article
- Disruption of electrophysiological rhythms and memory impairment in an Alzheimer's transgenic rat model.Alzheimer's research & therapy · 2025Article
- Experimental modeling of Alzheimer's disease: Translational lessons from cross-taxon analyses.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Quantitative analysis of serum metabolites in a rat model of Alzheimer's disease.Frontiers in aging neuroscience · 2025Article
- Emerging insights in senescence: pathways from preclinical models to therapeutic innovations.npj aging · 2024Review
- The Expression of GenesBiomedicines · 2024Article
- Adenylyl cyclase 2 expression and function in neurological diseases.CNS neuroscience & therapeutics · 2024Review
- Postnatal Maturation of the Blood-Brain Barrier in Senescence-Accelerated OXYS Rats, Which Are Prone to an Alzheimer's Disease-like Pathology.International journal of molecular sciences · 2023Article
- The Rat Brain Transcriptome: From Infancy to Aging and Sporadic Alzheimer's Disease-like Pathology.International journal of molecular sciences · 2023Article
- Calorie Restriction Provides Kidney Ischemic Tolerance in Senescence-Accelerated OXYS Rats.International journal of molecular sciences · 2022Article
- Stress Reactivity, Susceptibility to Hypertension, and Differential Expression of Genes in Hypertensive Compared to Normotensive Patients.International journal of molecular sciences · 2022Article
- Protein degradation-associated mechanisms that are affected in Alzheimer´s disease.Molecular and cellular biochemistry · 2022Review
- Changes in Glial Support of the Hippocampus during the Development of an Alzheimer's Disease-like Pathology and Their Correction by Mitochondria-Targeted Antioxidant SkQ1.International journal of molecular sciences · 2022Article
- Glia Not Neurons: Uncovering Brain Dysmaturation in a Rat Model of Alzheimer's Disease.Biomedicines · 2021Article
- MEK1/2-ERK Pathway Alterations as a Therapeutic Target in Sporadic Alzheimer's Disease: A Study in Senescence-Accelerated OXYS Rats.Antioxidants (Basel, Switzerland) · 2021Article
- Review
- Cognitive Training as a Potential Activator of Hippocampal Neurogenesis in the Rat Model of Sporadic Alzheimer's Disease.International journal of molecular sciences · 2020Article
- SkQ1 Suppresses the p38 MAPK Signaling Pathway Involved in Alzheimer's Disease-Like Pathology in OXYS Rats.Antioxidants (Basel, Switzerland) · 2020Article
- Mitochondrial Dysfunction: a Potential Therapeutic Target to Treat Alzheimer's Disease.Molecular neurobiology · 2020Review
- Contrast-enhanced plane-wave ultrasound imaging of the rat eye.Experimental eye research · 2020Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Senescence-accelerated OXYS rats are an experimental model of accelerated aging that was established from Wistar stock via selection for susceptibility to cataractogenic effects of a galactose-rich diet and via subsequent inbreeding of highly susceptible rats. Currently, we have the 102nd generation of OXYS rats with spontaneously developing cataract and accelerated senescence syndrome, which means early development of a phenotype similar to human geriatric disorders, including accelerated brain aging. In recent years, our group found strong evidence that OXYS rats are a promising model for studies of the mechanisms of brain aging and neurodegenerative processes similar to those seen in Alzheimer disease (AD). The manifestation of behavioral alterations and learning and memory deficits develop since the fourth week of age, i.e., simultaneously with first signs of neurodegeneration detectable on magnetic resonance imaging and under a light microscope. In addition, impaired long-term potentiation has been demonstrated in OXYS rats by the age of 3 months. With age, neurodegenerative changes in the brain of OXYS rats become amplified. We have shown that this deterioration happens against the background of overproduction of amyloid precursor protein (AβPP), accumulation of β-amyloid (Aβ), and hyperphosphorylation of the tau protein in the hippocampus and cortex. The development of AMD-like retinopathy in OXYS rats is also accompanied by increased accumulation of Aβ in the retina. These published data suggest that the OXYS strain may serve as a spontaneous rat model of AD-like pathology and could help to decipher the pathogenesis of AD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.