ReviewMolecular neurobiology
Hypoxia signaling to genes: significance in Alzheimer's disease.
Review in Molecular neurobiology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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.
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Who cites it
36 citing papers in PubMed, 88 citations in OpenAlex.
- Trial
- Recent Advances in Nose-to-Brain Gene Delivery for Central Nervous System Disorders.Pharmaceutics · 2025Review
- Cognition as mediator of pulmonary function and risk of sarcopenia among older adults.BMC public health · 2024Article
- Neuroprotective effects of crude extracts, compounds, and isolated molecules obtained from plants in the central nervous system injuries: a systematic review.Frontiers in neuroscience · 2023Review
- HIF activation enhances FcγRIIb expression on mononuclear phagocytes impeding tumor targeting antibody immunotherapy.Journal of experimental & clinical cancer research : CR · 2022Article
- Neuroimmunometabolism: A New Pathological Nexus Underlying Neurodegenerative Disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Review
- PROTACs technology for treatment of Alzheimer's disease: Advances and perspectives.Acta materia medica · 2022Article
- Heart failure impairs mood and memory in male rats and down-regulates the expression of numerous genes important for synaptic plasticity in related brain regions.Behavioural brain research · 2021Article
- Role of GluN2A NMDA receptor in homocysteine-induced prostaglandin E2 release from neurons.Journal of neurochemistry · 2019Article
- Understanding the Role of Hypoxia Inducible Factor During Neurodegeneration for New Therapeutics Opportunities.Current neuropharmacology · 2018Review
- Functional analyses of major cancer-related signaling pathways in Alzheimer's disease etiology.Biochimica et biophysica acta. Reviews on cancer · 2017Review
- The impact of hypoxia on tumor-associated macrophages.The Journal of clinical investigation · 2016Review
- Reduced miR-659-3p Levels Correlate with Progranulin Increase in Hypoxic Conditions: Implications for Frontotemporal Dementia.Frontiers in molecular neuroscience · 2016Article
- CD36 upregulation mediated by intranasal LV-NRF2 treatment mitigates hypoxia-induced progression of Alzheimer's-like pathogenesis.Antioxidants & redox signaling · 2014Article
- Valproic acid reduces neuritic plaque formation and improves learning deficits in APP(Swe) /PS1(A246E) transgenic mice via preventing the prenatal hypoxia-induced down-regulation of neprilysin.CNS neuroscience & therapeutics · 2014Article
- Amyloid-clearing proteins and their epigenetic regulation as a therapeutic target in Alzheimer's disease.Frontiers in aging neuroscience · 2014Review
- Disruption of neurogenesis by hypothalamic inflammation in obesity or aging.Reviews in endocrine & metabolic disorders · 2013Review
- Neurotoxic saboteurs: straws that break the hippo's (hippocampus) back drive cognitive impairment and Alzheimer's Disease.Neurotoxicity research · 2013Review
- Hypoxia-triggered m-calpain activation evokes endoplasmic reticulum stress and neuropathogenesis in a transgenic mouse model of Alzheimer's disease.CNS neuroscience & therapeutics · 2013Article
- Hypoxia increases Aβ-induced tau phosphorylation by calpain and promotes behavioral consequences in AD transgenic mice.Journal of molecular neuroscience : MN · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Aberrations in neural signaling, converging to and diverging from oxidative metabolism and blood supply, contribute to the initiation and maintenance of inflammatory responses, neuronal degeneration, and age-related cognitive decline in Alzheimer's disease (AD). Hypoxia/ischemia triggers phospholipase A2, leading to the accumulation of free arachidonic and docosahexaenoic acids (AA, DHA), as well as that of lysophospholipids. Some of these bioactive lipid messengers in turn give rise to several downstream lipid messengers, such as platelet-activating factor (PAF) and ecosanoids (prostaglandins and leukotrienes). Eicosanoid synthesis is highly regulated in hypoxia and in reperfusion subsequent to ischemia. As one of the consequences, mitochondrial function is disrupted and reactive oxygen species (ROS) both contribute to the expansion of cellular inflammatory responses and reduce the expression of genes required to maintain synaptic structure and function. On the other hand, pro-inflammatory genes are up-regulated. One of these, the inducible cyclooxygenase-2 (COX-2), along with oxygen-starved mitochondria, comprise the major sources of ROS in the brain during hypoxia, ischemia, and reperfusion. One outcome is a sustained metabolic stress that drives progressive dysfunction, apoptosis and/or necrosis, and brain cell death. How hypoxia modulates oxygen-sensitive gene expression is not well understood. Pro-inflammatory gene families that contribute to neurodegeneration are transiently activated in part by the heterodimeric oxygen-sensitive DNA-binding proteins nuclear factor for kappa B (NF-kappaB) and hypoxia-inducible factor-alpha (HIF-1alpha). Here the authors summarize current studies supporting the hypothesis that synaptically-derived lipid messengers play significant roles in ischemic stroke and that hypoxia is an important contributor to the onset and progression of AD neurodegeneration.
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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.