ArticleInternational journal of molecular sciences2023
The Rat Brain Transcriptome: From Infancy to Aging and Sporadic Alzheimer's Disease-like Pathology.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 13 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
- Increase in BACE1 Phosphorylation in the Rat Hippocampus and Phytosphingosine in Plasma After Chronic Administration of Scopolamine.International journal of molecular sciences · 2026Article
- A pan-cancer analysis of the oncogenic and immunological roles of THOC3 in human cancer.Scientific reports · 2025Article
- Alzheimer's disease, aging, and cannabidiol treatment: a promising path to promote brain health and delay aging.Molecular biology reports · 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
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2 authors at 1 institution in 1 country.
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Abstract
It has been suggested that functional traits of the adult brain-all of which are established early in life-may affect the brain's susceptibility to Alzheimer's disease (AD). Results of our previous studies on senescence-accelerated OXYS rats, a model of sporadic AD, support this hypothesis. Here, to elucidate the molecular genetic nature of the aberrations revealed during brain maturation, we analyzed transcriptomes (RNA-seq data) of the prefrontal cortex (PFC) and hippocampus of OXYS rats and Wistar (control) rats in the period of brain maturation critical for OXYS rats (ages P3 and P10; P: postnatal day). We found more than 1000 differentially expressed genes in both brain structures; functional analysis indicated reduced efficiency of the formation of neuronal contacts, presumably explained mainly by deficits of mitochondrial functions. Next, we compared differentially expressed genes in the rat PFC and hippocampus from infancy to the progressive stage of AD-like pathology (five ages in total). Three genes (
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