ArticleMolecular neurobiology2020
Expression of the Tau Protein and Amyloid Protein Precursor Processing Genes in the CA3 Area of the Hippocampus in the Ischemic Model of Alzheimer's Disease in the Rat.
Article in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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48 citing papers in PubMed, 55 citations in OpenAlex.
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- The Role of Sphingosine-1-Phosphate Signaling in Cerebral Ischemia/Reperfusion Injury and Alzheimer's Disease Pathology.International journal of molecular sciences · 2026Review
- Ellagic acid can improve stroke by regulating gut microbiota.Metabolic brain disease · 2026Review
- Genomic and proteomic conversion of brain ischemia to Alzheimer's disease.Frontiers in cell and developmental biology · 2026Review
- Direct and indirect role of non-coding RNAs in company with amyloid and tau protein in promoting neuroinflammation in post-ischemic brain neurodegeneration.Frontiers in cellular neuroscience · 2025Review
- Strategic delivery of omega-3 fatty acids for modulating inflammatory neurodegenerative diseases.Frontiers in aging neuroscience · 2025Article
- Decoding TMAO in the Gut-Organ Axis: From Biomarkers and Cell Death Mechanisms to Therapeutic Horizons.Drug design, development and therapy · 2025Review
- Melatonin Inhibits Hypoxia-Induced Alzheimer's Disease Pathogenesis by Regulating the Amyloidogenic Pathway in Human Neuroblastoma Cells.International journal of molecular sciences · 2024Article
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- Ischemia-Reperfusion Programming of Alzheimer's Disease-Related Genes-A New Perspective on Brain Neurodegeneration after Cardiac Arrest.International journal of molecular sciences · 2024Article
- Alpha-, Beta-, and Gamma-Secretase, Amyloid Precursor Protein, and Tau Protein Genes in the Hippocampal CA3 Subfield in an Ischemic Model of Alzheimer's Disease with Survival up to 2 Years.Journal of Alzheimer's disease : JAD · 2024Article
- A Look at the Etiology of Alzheimer's Disease based on the Brain Ischemia Model.Current Alzheimer research · 2024Review
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- Vitamin D Improves Cognitive Impairment and Alleviates Ferroptosis via the Nrf2 Signaling Pathway in Aging Mice.International journal of molecular sciences · 2023Article
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- Apitherapy in Post-Ischemic Brain Neurodegeneration of Alzheimer's Disease Proteinopathy: Focus on Honey and Its Flavonoids and Phenolic Acids.Molecules (Basel, Switzerland) · 2023Review
- Network pharmacology to explore the mechanism of scutellarin in the treatment of brain ischaemia and experimental verification of JAK2/STAT3 signalling pathway.Scientific reports · 2023Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Understanding the mechanisms underlying the selective susceptibility to ischemia of the CA3 region is very important to explain the neuropathology of memory loss after brain ischemia. We used a rat model to study changes in gene expression of the amyloid protein precursor and its cleaving enzymes and tau protein in the hippocampal CA3 sector, after transient 10-min global brain ischemia with survival times of 2, 7, and 30 days. The expression of the α-secretase gene was below control values at all times studied. But, the expression of the β-secretase gene was below the control values at 2-7 days after ischemia and the maximal increase in its expression was observed on day 30. Expression of the presenilin 1 gene was significantly elevated above the control values at 2-7 days after ischemia and decreased below the control values at day 30. Expression of the presenilin 2 gene showed an opposite trend to the expression of presenilin 1. Expression of the amyloid protein precursor gene after ischemia was at all times above the control values with a huge significant overexpression on day 7. Additionally, the expression of the tau protein gene was below the control values 2 days after ischemia, but the significant increase in its expression was observed on days 7-30. Data show that brain ischemia activates neuronal changes and death in the CA3 region of the hippocampus in a manner dependent on amyloid and tau protein, thus determining a new and important way to regulate the survival and/or death of ischemic neurons.
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