ArticleNeurobiology of disease2015
Differential roles of Aβ processing in hypoxia-induced axonal damage.
Article in Neurobiology of disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Rapid Functional Drug Screening of Passage-Zero Patient Brain Tumor Tissues Ex Vivo: Results from a Clinical Feasibility Study.Research square · 2025Article
- Dehydroepiandrosterone alleviates hypoxia-induced learning and memory dysfunction by maintaining synaptic homeostasis.CNS neuroscience & therapeutics · 2022Article
- Emerging Roles of Dyslipidemia and Hyperglycemia in Diabetic Retinopathy: Molecular Mechanisms and Clinical Perspectives.Frontiers in endocrinology · 2021Review
- The Roles of Microtubules and Membrane Tension in Axonal Beading, Retraction, and Atrophy.Biophysical journal · 2019Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Axonopathy is a common and early phase in neurodegenerative and traumatic CNS diseases. Recent work suggests that amyloid β (Aβ) produced from amyloid precursor protein (APP) may be a critical downstream mediator of CNS axonopathy in CNS diseases, particularly those associated with hypoxia. We critically tested this hypothesis in an adult retinal explant system that preserves the three-dimensional organization of the retina while permitting direct imaging of two cardinal features of early-stage axonopathy: axonal structural integrity and axonal transport capacity. Using this system, we found via pharmacological inhibition and genetic deletion of APP that production of Aβ is a necessary step in structural compromise of retinal ganglion cell (RGC) axons induced by the disease-relevant stressor hypoxia. However, identical blockade of Aβ production was not sufficient to protect axons from associated hypoxia-induced reduction in axonal transport. Thus, Aβ mediates distinct facets of hypoxia-induced axonopathy and may represent a functionally selective pharmacological target for therapies directed against early-stage axonopathy in CNS diseases.
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Registered trials
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