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Cited by 155

The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.

Genetic deletion of BACE1 in mice affects remyelination of sciatic nerves

Hu, Xiangyou, He, Wanxia, Diaconu, Claudiu, Tang, Xiaoying, Kidd, Grahame J., Macklin, Wendy B., Trapp, Bruce D., Yan, Riqiang·2008·The FASEB Journal
DOI 10.1096/fj.08-106666
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Abstract

BACE1 is a promising therapeutic and preventive target for Alzheimer's disease because it is essential for amyloid deposition. However, the recent demonstration of BACE1 in modulating developmental myelination in both peripheral and central nervous systems raises a concern of its effect on myelin maintenance or remyelination, and inhibition of these processes will potentially be detrimental to the BACE1 inhibitor users who are susceptible to myelination diseases such as adult peripheral nerve injury or multiple sclerosis. In this report, we investigated the role of BACE1 during peripheral nerve remyelination in wildtype (WT) and BACE1‐null mice. We show here that genetic deletion of BACE1 affects sciatic nerve remyelination. The impaired remyelination appears to stem from the loss of neuregulin‐1 cleavage by BACE1. To demonstrate a direct cleavage of neuregulin‐1 by BACE1, we have identified a BACE1 cleavage site that turns out be highly conserved among neuregulin‐1 paralogues. Moreover, we show that neuregulin‐1 family member neuregulin‐3 is also cleavable by BACE1. We hypothesize that the BACE1‐cleaved extracellular domain of axonal neuregulin‐1, perhaps neuregulin‐3 as well, binds to Schwann cell ErbB receptors, which in turn regulate remyelination. Pharmacological inhibition of BACE1 should be carefully monitored to avoid alteration of signaling pathway that regulates remyelination.—Hu, X., He, W., Diaconu, C., Tang, X., Kidd, G. J., Macklin, W. B., Trapp, B. D., Yan, R. Genetic deletion of BACE1 in mice affects remyelination of sciatic nerves. FASEB J. 22, 2970–2980 (2008)

Overview

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Crossref · 10.1096/fj.08-106666

Cites

7 of 7 references verified0 citation errors · 0 not checkable

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Claims other papers make about this one

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  • BACE1 knockout mice display reduced birth weight, hypomyelination, memory deficits, behavioral alterations, axon guidance impairment, impaired midbrain dopaminergic signaling, seizures, and abnormal electroencephalograms.

    “Conversely, BACE1 knockout mice display reduced birth weight, hypomyelination, memory deficits, behavioral alterations, axon guidance impairment, impaired midbrain dopaminergic signaling, seizures, and abnormal electroencephalograms (EEGs).”

    From BACE1: More than just a β‐secretase (2022) · cites this paper as [42]

Citations

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Metadata

Authors
Hu, X., He, W., Diaconu, C., Tang, X., Kidd, G. J., Macklin, W. B., Trapp, B. D., & Yan, R.
Affiliations
Department of Neurosciences Lerner Research Institute, Cleveland Clinic Foundation Cleveland Ohio USA
Venue
The FASEB Journal
Publisher
Wiley
Published
2008-04-15
Volume
22
Issue
8
Pages
2970-2980
ISSN
  • 0892-6638
  • 1530-6860
DOI
10.1096/fj.08-106666
Cited by
155
References
7
Language
en
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Funders
  • National Institutes of Health (AG025493)
  • National Multiple Sclerosis Society

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