ReviewInternational journal of molecular sciences2020
Participation of Amyloid and Tau Protein in Neuronal Death and Neurodegeneration after Brain Ischemia.
Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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
25 citing papers in PubMed, 34 citations in OpenAlex.
- Differences in gut microbiota composition between ischemic stroke patients and healthy individuals.BMC neurology · 2026Article
- The Role of Sphingosine-1-Phosphate Signaling in Cerebral Ischemia/Reperfusion Injury and Alzheimer's Disease Pathology.International journal of molecular sciences · 2026Review
- New Advances in the Mechanisms and Therapeutic Strategies of Gut Microbiota in Regulating Glycolipid Metabolism to Combat Atherosclerosis.Journal of cardiovascular translational research · 2026Review
- Ellagic acid can improve stroke by regulating gut microbiota.Metabolic brain disease · 2026Review
- Mitochondria as a Therapeutic Target in Neurodegeneration: Strategies for Restoring Cellular Homeostasis.Current neuropharmacology · 2026Review
- Gut Acetic Acid Alleviates Cognitive Impairment by Inhibiting Tau Hyperphosphorylation via Regulating FFAR3/Erk Pathway in Chronic Cerebral Ischemia Mice.Molecular neurobiology · 2025Article
- FeInternational journal of molecular sciences · 2025Article
- The relationship between estimated glucose disposal rate and cognitive function in older individuals.Scientific reports · 2025Article
- Decoding TMAO in the Gut-Organ Axis: From Biomarkers and Cell Death Mechanisms to Therapeutic Horizons.Drug design, development and therapy · 2025Review
- Essential New Complexity-Based Themes for Patient-Centered Diagnosis and Treatment of Dementia and Predementia in Older People: Multimorbidity and Multilevel Phenomenology.Journal of clinical medicine · 2024Review
- Melatonin Inhibits Hypoxia-Induced Alzheimer's Disease Pathogenesis by Regulating the Amyloidogenic Pathway in Human Neuroblastoma Cells.International journal of molecular sciences · 2024Article
- White matter hyperintensities influence distal cortical β-amyloid accumulation in default mode network pathways.Brain and behavior · 2023Article
- Preservation of Biomarkers Associated with Alzheimer's Disease (Amyloid Peptides 1-38, 1-40, 1-42, Tau Protein, Beclin 1) in the Blood of Neonates after Perinatal Asphyxia.International journal of molecular sciences · 2023Article
- Apitherapy in Post-Ischemic Brain Neurodegeneration of Alzheimer's Disease Proteinopathy: Focus on Honey and Its Flavonoids and Phenolic Acids.Molecules (Basel, Switzerland) · 2023Review
- Cell Death and Neurodegenerative Diseases: Mechanisms and Cytoprotective Molecules.International journal of molecular sciences · 2023Article
- Article
- 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
- Nicotinic receptor components of amyloid beta 42 proteome regulation in human neural cells.PloS one · 2022Article
- On the Common Journey of Neural Cells through Ischemic Brain Injury and Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Alzheimer's Disease AssociatedInternational journal of molecular sciences · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Current evidence indicates that postischemic brain injury is associated with the accumulation of folding proteins, such as amyloid and tau protein, in the intra- and extracellular spaces of neuronal cells. In this review, we summarize protein changes associated with Alzheimer's disease and their gene expression (amyloid protein precursor and tau protein) after brain ischemia, and their roles in the postischemic period. Recent advances in understanding the postischemic mechanisms in development of neurodegeneration have revealed dysregulation of amyloid protein precursor, α-, β- and γ-secretase and tau protein genes. Reduced expression of the α-secretase gene after brain ischemia with recirculation causes neuronal cells to be less resistant to injury. We present the latest data that Alzheimer's disease-related proteins and their genes play a crucial role in postischemic neurodegeneration. Understanding the underlying processes of linking Alzheimer's disease-related proteins and their genes in development of postischemic neurodegeneration will provide the most significant goals to date for therapeutic development.
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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.