Control of Peripheral Nerve Myelination by the ß-Secretase BACE1

By M. Willem, A. Garratt, B. Novak, M. Citron, Steve Kaufmann, Andrea Rittger, B. Destrooper, P. Saftig, C. Birchmeier, Christian Haass. Science, 2006

740 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Developmental Neuroscience, Physiology

View Paper: https://www.semanticscholar.org/paper/d1a59e92996c00dbdf841a157ad00a060b5929ea

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In Cellular and Molecular Neuroscience

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Citations in the corpus

ADAM10 is the physiologically relevant, constitutive α‐secretase of the amyloid precursor protein in primary neurons (2010, background): “Although the b-secretase BACE1 is ubiquitously expressed, its expression is particularly high in neurons during embryonic development (such as the E16 neurons used here) and in the first 2 weeks after birth and then drops sharply (Willem et al, 2006).”
APP processing in Alzheimer's disease (2011, background): “BACE1, as neuregulin 1 is another substrate of BACE1 [85,86].”
The epidermal growth factor receptor family: Biology driving targeted therapeutics (2008, background): “Accumulation of unprocessed neuregulin-1 and defective myelination occurs within cells lacking β-amyloid cleaving enzyme-1 (BACE1), an enzyme thought important in the pathophysiology of the Alzheimer’s disease [141].”
An Overview of APP Processing Enzymes and Products (2010, neutral): “They show a rather severe hypo-myelination of peripheral nerves (Willem et al., 2006), but only modest hypo-myelination in the CNS (Hu et al., 2006).”
Alzheimer’s Disease: The Challenge of the Second Century (2011, background): “Although b-secretase knockout mice have defects in peripheral nerve myelination (113), BACE1 appears to be a potentially attractive therapeutic target for AD because inhibition of the enzyme in adults seems to have fewer side effects than inhibition of g-secretase, which has many substrates.”
The amyloid hypothesis of Alzheimer's disease at 25 years (2016, background): “…discovery of many new substrates of b-secretase, including some that are critical for signaling events in both the immature and mature nervous system (Willem et al, 2006; Hemming et al, 2009; Kuhn et al, 2012), raises the possibility of significant adverse events appearing over time in such trials.”
MicroRNAs in Common Human Diseases (2012, background): “miR-29a, miR-29b-1 and miR-9 was significantly decreased in AD patients [95], resulting in abnormally high expression of their target BACE1, a protein playing an important role in AD pathogenesis [96].”
Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019, neutral): “, 2010), myelination deficits (Willem et al., 2006), cognitive impairment (Laird et al.”
Trafficking and proteolytic processing of APP. (2012, background): “2A; Hu et al. 2006; Willem et al. 2006).”
Axon-glial signaling and the glial support of axon function. (2008, background): “NRG1 processing enzymes include the tumor-necrosis factoralpha-converting enzyme for NRG1 type I shedding and the beta-amyloid converting enzyme, which likely activates NRG1 type III (Horiuchi et al. 2005, Hu et al. 2006, Willem et al. 2006).”
Loss of microRNA cluster miR-29a/b-1 in sporadic Alzheimer's disease correlates with increased BACE1/β-secretase expression (2008, background): “5 A–C), suggesting a molecular mechanism for the previously noticed developmental regulation of BACE1 (28).”