ArticleJournal of Alzheimer's disease : JAD2015
Dysregulation of Amyloid-β Protein Precursor, β-Secretase, Presenilin 1 and 2 Genes in the Rat Selectively Vulnerable CA1 Subfield of Hippocampus Following Transient Global Brain Ischemia.
Article in Journal of Alzheimer's disease : JAD, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.
What it found
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Who cites it
50 citing papers in PubMed, 2 syntheses or guidelines pooled it, 71 citations in OpenAlex.
- The causative role of amyloidosis in the cardiac complications of Alzheimer's disease: a comprehensive systematic review.The Journal of physiology · 2026Pooled it
- Association of Blood Amyloid Beta-Protein 1-42 with Poststroke Cognitive Impairment: A Systematic Review and Meta-Analysis.BioMed research international · 2022Pooled it
- Article
- The Anticonvulsant Effect of Long-Term Valproate Might Be Attributable to Altered Expression of Selected Genes in Mice.International journal of molecular sciences · 2026Article
- Genomic and proteomic conversion of brain ischemia to Alzheimer's disease.Frontiers in cell and developmental biology · 2026Review
- Alterations of Apolipoprotein A1, E, and J Genes in the Frontal Cortex in an Ischemic Model of Alzheimer's Disease with 2-Year Survival.International journal of molecular sciences · 2025Article
- Profiling the Expression Level of a Gene from the Caspase Family in Triple-Negative Breast Cancer.International journal of molecular sciences · 2025Article
- Role of autophagy in neurotoxic protein's clearance following post-ischemic stroke: where we are and what we know?Molecular brain · 2025Review
- 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
- Alterations ofCurrent Alzheimer research · 2025Article
- Article
- Ischemia-Reperfusion Programming of Alzheimer's Disease-Related Genes-A New Perspective on Brain Neurodegeneration after Cardiac Arrest.International journal of molecular sciences · 2024Article
- A Look at the Etiology of Alzheimer's Disease based on the Brain Ischemia Model.Current Alzheimer research · 2024Review
- Development of capillary dysfunction in Alzheimer's disease.Frontiers in aging neuroscience · 2024Review
- Blood and Brain Metabolites after Cerebral Ischemia.International journal of molecular sciences · 2023Review
- Apitherapy in Post-Ischemic Brain Neurodegeneration of Alzheimer's Disease Proteinopathy: Focus on Honey and Its Flavonoids and Phenolic Acids.Molecules (Basel, Switzerland) · 2023Review
- Alzheimer's Disease Connected Genes in the Post-Ischemic Hippocampus and Temporal Cortex.Genes · 2022Review
- Molecular Hydrogen Neuroprotection in Post-Ischemic Neurodegeneration in the Form of Alzheimer's Disease Proteinopathy: Underlying Mechanisms and Potential for Clinical Implementation-Fantasy or Reality?International journal of molecular sciences · 2022Review
- Brain ischemia as a bridge to Alzheimer's disease.Neural regeneration research · 2022Article
- Cross-Talk between Amyloid, Tau Protein and Free Radicals in Post-Ischemic Brain Neurodegeneration in the Form of Alzheimer's Disease Proteinopathy.Antioxidants (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The interaction between brain ischemia and Alzheimer's disease (AD) has been intensively investigated recently. Nevertheless, we have not yet understood the nature and mechanisms of the ischemic episodes triggering the onset of AD and how they influence its slow progression. The assumed connection between brain ischemia and the accumulation of amyloid-β (Aβ) peptide awaits to be clearly explained. In our research, we employed a rat cardiac arrest model to study the changes in gene expression of amyloid-β protein precursor (AβPP) and its cleaving enzymes, β- and γ-secretases (including presenilins) in hippocampal CA1 sector, following transient 10-min global brain ischemia. The quantitative reverse-transcriptase PCR assay demonstrated that the expression of all above genes that contribute to Aβ peptide generation was dysregulated during 30 days in postischemic hippocampal CA1 area. It suggests that studied Aβ peptide generation-related genes can be involved in AβPP metabolism, following global brain ischemia and will be useful to identify the molecular mechanisms underpinning that cerebral ischemia might be an etiological cause of AD via dysregulation of AβPP and its cleaving enzymes, β- and γ-secretases genes, and subsequently, it may increase Aβ peptide production and promote the gradual and slow development of AD neuropathology. Our data demonstrate that brain ischemia activates delayed neuronal death in hippocampus in an AβPP-dependent manner, thus defining a new and important mode of ischemic cell death.
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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.