ArticlePloS one2012
Transient focal cerebral ischemia/reperfusion induces early and chronic axonal changes in rats: its importance for the risk of Alzheimer's disease.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 47 citations in OpenAlex.
- Association between total-Tau and brain atrophy one year after first-ever stroke.BMC neurology · 2017Trial
- Axonal Energy Crisis and Calcium Phosphate Dysregulation as Pathogenesis of Optic Disc Drusen.Aging and disease · 2024Review
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- The interaction and pathogenesis between cognitive impairment and common cardiovascular diseases in the elderly.Therapeutic advances in chronic disease · 2022Review
- Expression and Clinical Value of miR-185 and miR-424 in Patients with Acute Ischemic Stroke.International journal of general medicine · 2022Article
- Privileged Quinolylnitrones for the Combined Therapy of Ischemic Stroke and Alzheimer's Disease.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Identification of the Hub Genes in Alzheimer's Disease.Computational and mathematical methods in medicine · 2021Article
- Characterization of Tauopathy in a Rat Model of Post-Stroke Dementia Combining Acute Infarct and Chronic Cerebral Hypoperfusion.International journal of molecular sciences · 2020Article
- Translating concepts of neural repair after stroke: Structural and functional targets for recovery.Restorative neurology and neuroscience · 2020Review
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- Cognitive Impairment and Brain and Peripheral Alterations in a Murine Model of Intraventricular Hemorrhage in the Preterm Newborn.Molecular neurobiology · 2018Article
- Thrombopoietin could protect cerebral tissue against ischemia-reperfusion injury by suppressing NF-κB and MMP-9 expression in rats.International journal of medical sciences · 2018Article
- Intranasal insulin reverts central pathology and cognitive impairment in diabetic mother offspring.Molecular neurodegeneration · 2017Article
- Comparison of the glycopattern alterations of mitochondrial proteins in cerebral cortex between rat Alzheimer's disease and the cerebral ischemia model.Scientific reports · 2017Article
- Selective astrocytic endothelin-1 overexpression contributes to dementia associated with ischemic stroke by exaggerating astrocyte-derived amyloid secretion.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2015Article
- Transient Cerebral Ischemia Promotes Brain Mitochondrial Dysfunction and Exacerbates Cognitive Impairments in Young 5xFAD Mice.PloS one · 2015Article
- 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.Journal of Alzheimer's disease : JAD · 2015Article
- The back and forth of axonal injury and repair after stroke.Current opinion in neurology · 2014Review
- Neurogenesis and inflammation after ischemic stroke: what is known and where we go from here.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2014Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The dementia of Alzheimer's type and brain ischemia are known to increase at comparable rates with age. Recent advances suggest that cerebral ischemia may contribute to the pathogenesis of Alzheimer's disease (AD), however, the neuropathological relationship between these two disorders is largely unclear. It has been demonstrated that axonopathy, mainly manifesting as impairment of axonal transport and swelling of the axon and varicosity, is a prominent feature in AD and may play an important role in the neuropathological mechanisms in AD. In this study, we investigated the early and chronic changes of the axons of neurons in the different brain areas (cortex, hippocampus and striatum) using in vivo tracing technique and grading analysis method in a rat model of transient focal cerebral ischemia/reperfusion (middle cerebral artery occlusion, MCAO). In addition, the relationship between the changes of axons and the expression of β-amyloid 42 (Aβ42) and hyperphosphorylated Tau, which have been considered as the key neuropathological processes of AD, was analyzed by combining tracing technique with immunohistochemistry or western blotting. Subsequently, we found that transient cerebral ischemia/reperfusion produced obvious swelling of the axons and varicosities, from 6 hours after transient cerebral ischemia/reperfusion even up to 4 weeks. We could not observe Aβ plaques or overexpression of Aβ42 in the ischemic brain areas, however, the site-specific hyperphosphorylated Tau could be detected in the ischemic cortex. These results suggest that transient cerebral ischemia/reperfusion induce early and chronic axonal changes, which may be an important mechanism affecting the clinical outcome and possibly contributing to the development of AD after stroke.
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