Evidence map›Paper›PMID 27531392›Full record

ReviewJournal of neuroscience research2017

Restoring Soluble Amyloid Precursor Protein α Functions as a Potential Treatment for Alzheimer's Disease.

Ahsan Habib, Darrell Sawmiller, Jun Tan

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of neuroscience research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
–field-weighted citation impact
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

46 citing papers in PubMed.

  1. Review
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  6. Therapeutic effects of a novel synthetic α-secretase.Frontiers in aging neuroscience · 2024
    Article
  7. Review
  8. Article
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  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Amyloid, APP, and Electrical Activity of the Brain.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2020
    Review
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

3 authors.

Ahsan HabibRashid Laboratory for Developmental Neurobiology, Silver Child Development Center, Department of Psychiatry and Behavioral Neurosciences, Morsani College of Medicine, University of South Florida, Tampa, Florida, USA.
Darrell SawmillerRashid Laboratory for Developmental Neurobiology, Silver Child Development Center, Department of Psychiatry and Behavioral Neurosciences, Morsani College of Medicine, University of South Florida, Tampa, Florida, USA.
Jun TanRashid Laboratory for Developmental Neurobiology, Silver Child Development Center, Department of Psychiatry and Behavioral Neurosciences, Morsani College of Medicine, University of South Florida, Tampa, Florida, USA.

Funding

LISPRO, an ionic cocrystal of lithium, as a potential novel treatment for Alzheimer's diseaseR01AG050253 · NIA · UNIVERSITY OF SOUTH FLORIDA · PI TAN, JUN · 2016 to 2019
$1.5M
Implication of HUCBC: a novel therapeutic strategy for Alzheimer's diseaseR01AG032432 · NIA · UNIVERSITY OF SOUTH FLORIDA · PI TAN, JUN · 2009 to 2013
$1.4M
Flavonoid-diosmin modulation of Abeta and tau pathologies through GSK-3 signalingR01AT007411 · NCCIH · UNIVERSITY OF SOUTH FLORIDA · PI TAN, JUN · 2014 to 2015
$663k
Identification of novel APP-specific alpha secretase in human umbilical cord blood seraR21AG055116 · NIA · UNIVERSITY OF SOUTH FLORIDA · PI TAN, JUN · 2017 to 2018
$411k
NCCIH NIH HHS R01 AT007411NIA NIH HHS R01 AG032432NIA NIH HHS R01 AG050253NIA NIH HHS R21 AG055116
6 · The paper itself

Abstract

Soluble amyloid precursor protein α (sAPPα), a secreted proteolytic fragment of nonamyloidogenic amyloid precursor protein (APP) processing, is known for numerous neuroprotective functions. These functions include but are not limited to proliferation, neuroprotection, synaptic plasticity, memory formation, neurogenesis, and neuritogenesis in cell culture and animal models. In addition, sAPPα influences amyloid-β (Aβ) production by direct modulation of APP β-secretase proteolysis as well as Aβ-related or unrelated tau pathology, hallmark pathologies of Alzheimer's disease (AD). Thus, the restoration of sAPPα levels and functions in the brain by increasing nonamyloidogenic APP processing and/or manipulation of its signaling could reduce AD pathology and cognitive impairment. It is likely that identification and characterization of sAPPα receptors in the brain, downstream effectors, and signaling pathways will pave the way for an attractive therapeutic target for AD prevention or intervention. © 2016 Wiley Periodicals, Inc.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsBrainDisease Models, AnimalHumansAmyloid beta-PeptidesAmyloid beta-Protein PrecursoragingAlzheimer's diseaseAPPAβbiomarkercognitive impairmentmemoryneurogenesisneuroprotectionreceptorsAPPαsynaptic plasticityTautherapeutics

Identifiers

PMID27531392
PMCPMC5296245

What OpenQuestion holds

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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.