Evidence map›Paper›PMID 28191691›Full record

ArticleGlia2017

BACE1 regulates the proliferation and cellular functions of Schwann cells.

Xiangyou Hu, Hailong Hou, Chinthasagar Bastian, Wanxia He, Shupeng Qiu, Yingying Ge, Xinhua Yin, Grahame J Kidd, Sylvain Brunet, Bruce D Trapp and 2 more

Abstract read
In one paragraph

Article in Glia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 17% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Evaluation and Comparison of the Effects of Mature Silkworm (Iranian journal of pharmaceutical research : IJPR · 2022
    Article
  6. BACE1: More than just a β-secretase.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2022
    Review
  7. Review
  8. Review
  9. Article
  10. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 2 countries.

Xiangyou HuDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, 44195.
Hailong HouDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, 44195.
Chinthasagar BastianDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, 44195.
Wanxia HeDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, 44195.
Shupeng QiuDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, 44195.
Yingying GeDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, 44195.
Xinhua YinDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, 44195.
Grahame J KiddDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, 44195.
Sylvain BrunetDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, 44195.
Bruce D TrappDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, 44195.
Selva BaltanDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, 44195.
Riqiang YanDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, 44195.ORCID 0000-0001-7195-7617
Cleveland Clinic Lerner College of Medicine · USAnhui Medical University · CN

Funding

Roles of reticulon proteins in neurodegenerative disordersR01AG025493 · NIA · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI YAN, RIQIANG · 2005 to 2024
$5.9M
Supplement for BACE1 in neurodegeneration and neuronal dysfunctionR01NS074256 · NINDS · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI RIQIANG YAN · 2011 to 2026
$5.8M
Inhibition of BACE1 for benefiting Alzheimer's patientsR01AG046929 · NIA · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI RIQIANG YAN · 2013 to 2026
$3.9M
Inhibition of BACE1 for benefiting Alzheimer's patientsRF1AG046929 · NIA · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI YAN, RIQIANG · 2018 to 2018
$3.3M
Vulnerability of Aging White Matter to IschemiaR01AG033720 · NIA · UNIVERSITY OF WASHINGTON · PI BALTAN, SELVA · 2010 to 2021
$2.7M
BACE1 in neurodegeneration and neurological dysfunctionRF1NS074256 · NINDS · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI YAN, RIQIANG · 2021 to 2021
$2.1M
The secreted form of Neuregulin-1 in schizophreniaR21MH103942 · NIMH · CLEVELAND CLINIC LERNER COM-CWRU · PI YAN, RIQIANG · 2014 to 2015
$436k
Vulnerability of Aging White Matter to IschemiaR56AG033720 · NIA · CLEVELAND CLINIC LERNER COM-CWRU · PI BALTAN, SELVA · 2016 to 2016
$396k
NIA NIH HHS R01 AG025493NIA NIH HHS R01 AG033720NIA NIH HHS R01 AG046929NIA NIH HHS R56 AG033720NIA NIH HHS RF1 AG046929NIMH NIH HHS R21 MH103942NINDS NIH HHS R01 NS074256NINDS NIH HHS RF1 NS074256
6 · The paper itself

Abstract

BACE1 is an indispensable enzyme for generating β-amyloid peptides, which are excessively accumulated in brains of Alzheimer's patients. However, BACE1 is also required for proper myelination of peripheral nerves, as BACE1-null mice display hypomyelination. To determine the precise effects of BACE1 on myelination, here we have uncovered a role of BACE1 in the control of Schwann cell proliferation during development. We demonstrate that BACE1 regulates the cleavage of Jagged-1 and Delta-1, two membrane-bound ligands of Notch. BACE1 deficiency induces elevated Jag-Notch signaling activity, which in turn facilitates proliferation of Schwann cells. This increase in proliferation leads to shortened internodes and decreased Schmidt-Lanterman incisures. Functionally, evoked compound action potentials in BACE1-null nerves were significantly smaller and slower, with a clear decrease in excitability. BACE1-null nerves failed to effectively use lactate as an alternative energy source under conditions of increased physiological activity. Correlatively, BACE1-null mice showed reduced performance on rotarod tests. Collectively, our data suggest that BACE1 deficiency enhances proliferation of Schwann cell due to the elevated Jag1/Delta1-Notch signaling, but fails to myelinate axons efficiently due to impaired the neuregulin1-ErbB signaling, which has been documented.

Indexed as

Amyloid Precursor Protein SecretasesAnimalsAspartic Acid EndopeptidasesAxonsCell ProliferationMice, KnockoutMyelin SheathNeurogenesisSchwann CellsSciatic NerveSignal TransductionAmyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesBace1 protein, mouseAlzheimer's β-secretaseBACE1Jaggedmyelinationmyelin sheathnode of RanvierNotchSchmidt-Lanterman clefts

Identifiers

PMID28191691
PMCPMC5357169
OpenAlexW2588011852

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.