ArticleOncotarget2015
Amyloid accumulation is a late event in sporadic Alzheimer's disease-like pathology in nontransgenic rats.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed.
- Quantitative analysis of serum metabolites in a rat model of Alzheimer's disease.Frontiers in aging neuroscience · 2025Article
- Invisible but Insidious Effects of Microplastics.Molecules (Basel, Switzerland) · 2024Article
- 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
- Targeting the cannabinoid system to counteract the deleterious effects of stress in Alzheimer's disease.Frontiers in aging neuroscience · 2022Review
- Glia Not Neurons: Uncovering Brain Dysmaturation in a Rat Model of Alzheimer's Disease.Biomedicines · 2021Article
- Review
- Review
- Personalizing the Care and Treatment of Alzheimer's Disease: An Overview.Pharmacogenomics and personalized medicine · 2021Review
- The pleiotropic role of p53 in functional/dysfunctional neurons: focus on pathogenesis and diagnosis of Alzheimer's disease.Alzheimer's research & therapy · 2020Review
- Neuroprotective Effects of Salidroside in a Mouse Model of Alzheimer's Disease.Cellular and molecular neurobiology · 2020Article
- 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
- Tau and Alpha Synuclein Synergistic Effect in Neurodegenerative Diseases: When the Periphery Is the Core.International journal of molecular sciences · 2020Review
- Mitochondrial Dysfunction: a Potential Therapeutic Target to Treat Alzheimer's Disease.Molecular neurobiology · 2020Review
- Features of Postnatal Hippocampal Development in a Rat Model of Sporadic Alzheimer's Disease.Frontiers in neuroscience · 2020Article
- Retinal Vascular Pathology in a Rat Model of Cerebral Small Vessel Disease.Frontiers in neurology · 2020Article
- BACE1 Translation: At the Crossroads Between Alzheimer's Disease Neurodegeneration and Memory Consolidation.Journal of Alzheimer's disease reports · 2019Review
- Suppression of Alzheimer's Disease-Like Pathology Progression by Mitochondria-Targeted Antioxidant SkQ1: A Transcriptome Profiling Study.Oxidative medicine and cellular longevity · 2019Article
- Modulation of the expression of genes related to the system of amyloid-beta metabolism in the brain as a novel mechanism of ceftriaxone neuroprotective properties.BMC neuroscience · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The amyloid cascade hypothesis posits that deposition of the amyloid β (Aβ) peptide in the brain is a key event in the initiation of Alzheimer's disease (AD). Nonetheless, it now seems increasingly unlikely that amyloid toxicity is the cause of sporadic AD, which leads to cognitive decline. Here, using accelerated-senescence nontransgenic OXYS rats, we confirmed that aggregation of Aβ is a later event in AD-like pathology. We showed that an age-dependent increase in the levels of Aβ₁₋₄₂ and extracellular Aβ deposits in the brain of OXYS rats occur later than do synaptic losses, neuronal cell death, mitochondrial structural abnormalities, and hyperphosphorylation of the tau protein. We identified the variants of the genes that are strongly associated with the risk of either late-onset or early-onset AD, including App, Apoe4, Bace1, Psen1, Psen2, and Picalm. We found that in OXYS rats nonsynonymous SNPs were located only in the genes Casp3 and Sorl1. Thus, we present proof that OXYS rats may be a model of sporadic AD. It is possible that multiple age-associated pathological processes may precede the toxic amyloid accumulation, which in turn triggers the final stage of the sporadic form of AD and becomes a hallmark event of the disease.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.