Evidence map›Paper›PMID 25917367›Full record

ArticleMolecular psychiatry2015

p75NTR ectodomain is a physiological neuroprotective molecule against amyloid-beta toxicity in the brain of Alzheimer's disease.

X-Q Yao, S-S Jiao, K Saadipour, F Zeng, Q-H Wang, C Zhu, L-L Shen, G-H Zeng, C-R Liang, J Wang and 15 more

Erratum issuedOpen access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.

  1. Pooled it
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  6. Review
  7. Review
  8. Review
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  11. Article
  12. Article
  13. Article
  14. Article
  15. The Nerve Growth Factor Receptor (NGFR/p75International journal of molecular sciences · 2023
    Review
  16. Deletion of p75Frontiers in molecular neuroscience · 2023
    Article
  17. Review
  18. Up-Regulation of ProBDNF/p75Journal of inflammation research · 2023
    Article
  19. Article
  20. Finding New Ways How to Control BACE1.The Journal of membrane biology · 2022
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

25 authors at 5 institutions in 3 countries.

X-Q YaoDepartment of Neurology, Daping Hospital, Third Military Medical University, Chongqing, China.
S-S JiaoDepartment of Neurology, Daping Hospital, Third Military Medical University, Chongqing, China.
K SaadipourNeuroregeneration Laboratory, School of Pharmacy and Medical Sciences and Sansom Institute, Division of Health Sciences, University of South Australia, Adelaide, SA, Australia.
F ZengDepartment of Neurology, Daping Hospital, Third Military Medical University, Chongqing, China.
Q-H WangDepartment of Neurology, Daping Hospital, Third Military Medical University, Chongqing, China.
C ZhuDepartment of Neurology, Daping Hospital, Third Military Medical University, Chongqing, China.
L-L ShenDepartment of Neurology, Daping Hospital, Third Military Medical University, Chongqing, China.
G-H ZengDepartment of Neurology, Daping Hospital, Third Military Medical University, Chongqing, China.
C-R LiangDepartment of Neurology, Daping Hospital, Third Military Medical University, Chongqing, China.
J WangNeuroregeneration Laboratory, School of Pharmacy and Medical Sciences and Sansom Institute, Division of Health Sciences, University of South Australia, Adelaide, SA, Australia.ORCID http://orcid.org/0000-0002-6227-6112
Y-H LiuDepartment of Neurology, Daping Hospital, Third Military Medical University, Chongqing, China.
H-Y HouRashid Laboratory for Developmental Neurobiology, Silver Child Development Center, Morsani College of Medicine, University of South Florida, Tampa, FL, USA.
X XuFirst Department, Research Institute of Surgery, Daping Hospital, Third Military Medical University, Chongqing, China.
Y-P SuInstitute of Combined Injury, College of Preventive Medicine, Third Military Medical University, Chongqing, China.
X-T FanThird Military Medical University, Chongqing, China.
H-L XiaoDepartment of Pathology, Daping Hospital, Third Military Medical University, Chongqing, China.
L-F LueLaboratory of Neuroinflammation, Sun Health Research Institute, Sun City, AZ, USA.
Y-Q ZengKey Laboratory of Stem Cells and Regenerative Medicine, Institute of Molecular and Clinical Medicine, Kunming Medical University, Kunming, China.
B GiuntaRashid Laboratory for Developmental Neurobiology, Silver Child Development Center, Morsani College of Medicine, University of South Florida, Tampa, FL, USA.
J-H ZhongNeuroregeneration Laboratory, School of Pharmacy and Medical Sciences and Sansom Institute, Division of Health Sciences, University of South Australia, Adelaide, SA, Australia.
D G WalkerLaboratory of Neuroinflammation, Sun Health Research Institute, Sun City, AZ, USA.
H-D ZhouDepartment of Neurology, Daping Hospital, Third Military Medical University, Chongqing, China.
J TanRashid Laboratory for Developmental Neurobiology, Silver Child Development Center, Morsani College of Medicine, University of South Florida, Tampa, FL, USA.
X-F ZhouNeuroregeneration Laboratory, School of Pharmacy and Medical Sciences and Sansom Institute, Division of Health Sciences, University of South Australia, Adelaide, SA, Australia.
Y-J WangDepartment of Neurology, Daping Hospital, Third Military Medical University, Chongqing, China.
Army Medical University · CNUniversity of South Australia · AUUniversity of South Florida · USBanner Sun Health Research Institute · USKunming Medical University · CN

Funding

The impact of HAART on HIV-1 Tat induced brain agingR01MH098737 · NIMH · UNIVERSITY OF SOUTH FLORIDA · PI GIUNTA, BRIAN · 2012 to 2015
$1.3M
NIMH NIH HHS R01 MH098737
6 · The paper itself

Abstract

In Alzheimer's disease (AD), neurodegenerative signals such as amyloid-beta (Aβ) and the precursors of neurotrophins, outbalance neurotrophic signals, causing synaptic dysfunction and neurodegeneration. The neurotrophin receptor p75 (p75NTR) is a receptor of Aβ and mediates Aβ-induced neurodegenerative signals. The shedding of its ectodomain from the cell surface is physiologically regulated; however, the function of the diffusible p75NTR ectodomain (p75ECD) after shedding remains largely not known. Here, we show that p75ECD levels in cerebrospinal fluid and in the brains of Alzheimer's patients and amyloid-beta precursor protein (APP)/PS1 transgenic mice were significantly reduced, due to inhibition of the sheddase-tumor necrosis factor-alpha-converting enzyme by Aβ. Restoration of p75ECD to the normal level by brain delivery of the gene encoding human p75ECD before or after Aβ deposition in the brain of APP/PS1 mice reversed the behavioral deficits and AD-type pathologies, such as Aβ deposit, apoptotic events, neuroinflammation, Tau phosphorylation and loss of dendritic spine, neuronal structures and synaptic proteins. Furthermore, p75ECD can also reduce amyloidogenesis by suppressing β-secretase expression and activities. Our data demonstrate that p75ECD is a physiologically neuroprotective molecule against Aβ toxicity and would be a novel therapeutic target and biomarker for AD.

Indexed as

ADAM17 ProteinADAM ProteinsAge FactorsAlzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsApoptosisBrainCase-Control StudiesCognition DisordersDisease Models, AnimalDown-RegulationHumansMaze LearningMiceADAM17 ProteinADAM ProteinsAmyloid beta-PeptidesAmyloid beta-Protein PrecursorNerve Tissue ProteinsNGFR protein, humanPresenilin-1Receptors, Nerve Growth FactorRecombinant Proteins

Identifiers

PMID25917367
PMCPMC4759103
OpenAlexW2022980912

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.