ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
Axonal and Schwann cell BACE1 is equally required for remyelination of peripheral nerves.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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, 39 citations in OpenAlex.
- Molecular Mediators Associated With Myelination, Demyelination, and Remyelination in the Peripheral Nervous System.Journal of the peripheral nervous system : JPNS · 2026Review
- The dual roles of chemokines in peripheral nerve injury and repair.Inflammation and regeneration · 2025Review
- A Novel RAGE Modulator Induces Soluble RAGE to Reduce BACE1 Expression in Alzheimer's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Oligodendrocytes produce amyloid-β and contribute to plaque formation alongside neurons in Alzheimer's disease model mice.Nature neuroscience · 2024Article
- Stimulating myelin restoration with BDNF: a promising therapeutic approach for Alzheimer's disease.Frontiers in cellular neuroscience · 2024Review
- Myelin repair in Alzheimer's disease: a review of biological pathways and potential therapeutics.Translational neurodegeneration · 2022Review
- Physiological Roles of Monomeric Amyloid-β and Implications for Alzheimer's Disease Therapeutics.Experimental neurobiology · 2022Review
- Enhanced Nerve Regeneration by Exosomes Secreted by Adipose-Derived Stem Cells with or without FK506 Stimulation.International journal of molecular sciences · 2021Article
- The influence of BACE1 on macrophage recruitment and activity in the injured peripheral nerve.Journal of neuroinflammation · 2021Review
- Blood-brain barrier-penetrating siRNA nanomedicine for Alzheimer's disease therapy.Science advances · 2020Article
- The physiological roles of tau and Aβ: implications for Alzheimer's disease pathology and therapeutics.Acta neuropathologica · 2020Review
- Penetrating Ballistic-Like Brain Injury Leads to MicroRNA Dysregulation, BACE1 Upregulation, and Amyloid Precursor Protein Loss in Lesioned Rat Brain Tissues.Frontiers in neuroscience · 2020Article
- The Complex Work of Proteases and Secretases in Wallerian Degeneration: Beyond Neuregulin-1.Frontiers in cellular neuroscience · 2019Review
- CA1 pyramidal neuron gene expression mosaics in the Ts65Dn murine model of Down syndrome and Alzheimer's disease following maternal choline supplementation.Hippocampus · 2018Article
- Article
- Beta secretase activity in peripheral nerve regeneration.Neural regeneration research · 2017Review
- Article
- Dysregulation of ErbB Receptor Trafficking and Signaling in Demyelinating Charcot-Marie-Tooth Disease.Molecular neurobiology · 2017Review
- Physiological Functions of the β-Site Amyloid Precursor Protein Cleaving Enzyme 1 and 2.Frontiers in molecular neuroscience · 2017Review
- SCY1-Like 1-Binding Protein 1 (SCYL1BP1) Suppressed Sciatic Nerve Regeneration by Enhancing the RhoA Pathway.Molecular neurobiology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
Inhibition of β-site APP cleaving enzyme 1 (BACE1) is being pursued as a therapeutic target for treating patients with Alzheimer's disease because BACE1 is the sole β-secretase for generating β-amyloid peptide. Knowledge regarding the other cellular functions of BACE1 is therefore critical for the safe use of BACE1 inhibitors in human patients. BACE1 deficiency in mice causes hypomyelination during development and impairs remyelination in injured sciatic nerves. Since BACE1 is expected to be ubiquitously expressed, we asked whether axonal or Schwann cell BACE1 is required for optimal remyelination. By swapping sciatic nerve segments from BACE1-null mice with the corresponding wild-type nerve segments or vice versa, we tested how a deficiency of BACE1 in Schwann cells or axons affects remyelination. Our results show that BACE1 in axons and Schwann cells is similarly important for remyelination of regenerated axons. Nerve injury induces BACE1 transcription and protein levels are elevated in Schwann cells. Expression of type I neuregulin 1 (Nrg1), rather than type III Nrg1, was induced by Schwann cells, and the abolished Nrg1 cleavage in BACE1-null Schwann cells contributed to decreased remyelination of regenerated axons. Hence, this study is the first to demonstrate the equal importance of axonal and Schwann cell BACE1 for remyelination of injured nerves.
Indexed as
Identifiers
What OpenQuestion holds
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.