ArticlePloS one2015
Transient Cerebral Ischemia Promotes Brain Mitochondrial Dysfunction and Exacerbates Cognitive Impairments in Young 5xFAD Mice.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 34 citations in OpenAlex.
- Mito-TEMPO improves survival rates inScience advances · 2026Article
- Possible Engagement of Nicotinic Acetylcholine Receptors in Pathophysiology of Brain Ischemia-Induced Cognitive Impairment.Journal of molecular neuroscience : MN · 2022Review
- ROS scavengers decrease γH2ax spots in motor neuronal nuclei of ALS model miceFrontiers in cellular neuroscience · 2022Article
- Mito-Tempo suppresses autophagic flux via the PI3K/Akt/mTOR signaling pathway in neuroblastoma SH-SY5Y cells.Heliyon · 2021Article
- Combustion-derived particles from biomass sources differently promote epithelial-to-mesenchymal transition on A549 cells.Archives of toxicology · 2021Article
- Modulation of OSCP mitigates mitochondrial and synaptic deficits in a mouse model of Alzheimer's pathology.Neurobiology of aging · 2021Article
- Cerebral artery dilation during transient ischemia is impaired by amyloid β deposition around the cerebral artery in Alzheimer's disease model mice.The journal of physiological sciences : JPS · 2020Article
- Deterioration of cognitive function after transient cerebral ischemia with amyloid-β infusion-possible amelioration of cognitive function by ATJournal of neuroinflammation · 2020Article
- Triheptanoin Mitigates Brain ATP Depletion and Mitochondrial Dysfunction in a Mouse Model of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2020Article
- Disrupted hippocampal growth hormone secretagogue receptor 1α interaction with dopamine receptor D1 plays a role in Alzheimer's disease.Science translational medicine · 2019Article
- Association among plasma lactate, systemic inflammation, and mild cognitive impairment: a community-based study.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2019Article
- Effects of Acupuncture on Alzheimer's Disease: Evidence from Neuroimaging Studies.Chinese journal of integrative medicine · 2019Review
- MK0677, a Ghrelin Mimetic, Improves Neurogenesis but Fails to Prevent Hippocampal Lesions in a Mouse Model of Alzheimer's Disease Pathology.Journal of Alzheimer's disease : JAD · 2019Article
- Oxidative Stress: A Major Player in Cerebrovascular Alterations Associated to Neurodegenerative Events.Frontiers in physiology · 2018Review
- Genetic ablation of the p66Molecular psychiatry · 2017Article
- The protective effects of propofol against CoClBMC anesthesiology · 2017Article
- Mitochondrial Dysfunction and Synaptic Transmission Failure in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2017Review
- Deregulation of mitochondrial F1FO-ATP synthase via OSCP in Alzheimer's disease.Nature communications · 2016Article
- Sevoflurane Post-conditioning Enhanced Hippocampal Neuron Resistance to Global Cerebral Ischemia Induced by Cardiac Arrest in Rats through PI3K/Akt Survival Pathway.Frontiers in cellular neuroscience · 2016Article
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Alzheimer's disease (AD) is heterogeneous and multifactorial neurological disorder; and the risk factors of AD still remain elusive. Recent studies have highlighted the role of vascular factors in promoting the progression of AD and have suggested that ischemic events increase the incidence of AD. However, the detailed mechanisms linking ischemic insult to the progression of AD is still largely undetermined. In this study, we have established a transient cerebral ischemia model on young 5xFAD mice and their non-transgenic (nonTg) littermates by the transient occlusion of bilateral common carotid arteries. We have found that transient cerebral ischemia significantly exacerbates brain mitochondrial dysfunction including mitochondrial respiration deficits, oxidative stress as well as suppressed levels of mitochondrial fusion proteins including optic atrophy 1 (OPA1) and mitofusin 2 (MFN2) in young 5xFAD mice resulting in aggravated spatial learning and memory. Intriguingly, transient cerebral ischemia did not induce elevation in the levels of cortical or mitochondrial Amyloid beta (Aβ)1-40 or 1-42 levels in 5xFAD mice. In addition, the glucose- and oxygen-deprivation-induced apoptotic neuronal death in Aβ-treated neurons was significantly mitigated by mitochondria-targeted antioxidant mitotempo which suppresses mitochondrial superoxide levels. Therefore, the simplest interpretation of our results is that young 5xFAD mice with pre-existing AD-like mitochondrial dysfunction are more susceptible to the effects of transient cerebral ischemia; and ischemic events may exacerbate dementia and worsen the outcome of AD patients by exacerbating mitochondrial dysfunction.
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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.