Evidence map›Paper›PMID 27794478›Full record

ReviewDrug discovery today2017

Amyloid beta modulators and neuroprotection in Alzheimer's disease: a critical appraisal.

Chandra Sekhar Kuruva, P Hemachandra Reddy

Erratum issuedAbstract readReview
In one paragraph

Review in Drug discovery today, 2017. 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 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Review
  2. Article
  3. Korean Red Pine (Journal of microbiology and biotechnology · 2022
    Article
  4. Article
  5. Review
  6. Article
  7. The vexing complexity of the amyloidogenic pathway.Protein science : a publication of the Protein Society · 2019
    Review
  8. Alzheimer's disease: pathogenesis, diagnostics, and therapeutics.International journal of nanomedicine · 2019
    Review
  9. Reduction of Aβ Generation by Schisandrin B through Restraining Beta-Secretase 1 Transcription and Translation.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  10. Article
  11. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Chandra Sekhar KuruvaGarrison Institute on Aging, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, USA.
P Hemachandra ReddyGarrison Institute on Aging, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, USA; Department of Cell Biology & Biochemistry, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, USA; Department of Neuroscience & Pharmacology, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, USA; Department of Neurology, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, USA; Department of Speech, Language and Hearing Sciences, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, USA; Garrison Institute on Aging, South West Campus, Texas Tech University Health Sciences Center, 6630 S. Quaker Ste. E, MS 7495, Lubbock, TX 79413, USA. Electronic address: hemachandra.reddy@ttuhsc.edu.

Funding

Dynamin-Related Protein 1 and Mitochondrial Fragmentation in Alzheimer's DiseaseR01AG042178 · NIA · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI REDDY, P. HEMACHANDRA · 2012 to 2016
$2.0M
Voltage-Dependent Anion Channel and Neurodegeneration in Alzheimer's DiseaseR01AG047812 · NIA · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI REDDY, P. HEMACHANDRA · 2014 to 2018
$1.9M
NIA NIH HHS R01 AG042178NIA NIH HHS R01 AG047812
6 · The paper itself

Abstract

Multiple cellular changes have been identified as being involved in Alzheimer's disease (AD) pathogenesis, including mitochondrial damage, synaptic loss, amyloid beta (Aβ) production and/or accumulation, inflammatory responses, and phosphorylated tau formation and/or accumulation. Studies have established that Aβ-induced synaptic dysfunction is dependent on abnormal amyloid precursor protein (APP) processing caused by β- and γ-secretases, resulting in the generation of Aβ. The Aβ formed as a result of abnormal APP processing induces phosphorylated tau and activates glycogen synthase kinase-3β (GSK3β) and cyclin-dependent kinase-5 (CDK5). Here, we review the latest research on the development of Aβ modulators for neuroprotection in AD. We also review the use of molecular inhibitors as therapeutic targets in AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsHumansNeuroprotective AgentsAmyloid beta-PeptidesNeuroprotective Agents

Identifiers

PMID27794478
PMCPMC5344027

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.