Evidence map›Paper›PMID 27023508›Full record

ArticleMolecules (Basel, Switzerland)2016

Mechanistic Insight of Bivalent Compound 21MO as Potential Neuroprotectant for Alzheimer's Disease.

John M Saathoff, Kai Liu, Jeremy E Chojnacki, Liu He, Qun Chen, Edward J Lesnefsky, Shijun Zhang

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Special Issue: "Molecules against Alzheimer".Molecules (Basel, Switzerland) · 2016
    Article
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

7 authors at 1 institution in 1 country.

John M SaathoffDepartment of Medicinal Chemistry, Virginia Commonwealth University, Richmond, VA 23298, USA. saathoffjm@vcu.edu.
Kai LiuDepartment of Medicinal Chemistry, Virginia Commonwealth University, Richmond, VA 23298, USA. kliu4@vcu.edu.
Jeremy E ChojnackiDepartment of Medicinal Chemistry, Virginia Commonwealth University, Richmond, VA 23298, USA. chojnackij@vcu.edu.
Liu HeDepartment of Medicinal Chemistry, Virginia Commonwealth University, Richmond, VA 23298, USA. lhe3@vcu.edu.
Qun ChenDepartment of Medicine, Pauley Heart Center, Division of Cardiology, Virginia Commonwealth University, Richmond, VA 23298, USA. qchen8@vcu.edu.
Edward J LesnefskyDepartment of Medicine, Pauley Heart Center, Division of Cardiology, Virginia Commonwealth University, Richmond, VA 23298, USA. ejlesnefsky@vcu.edu.
Shijun ZhangDepartment of Medicinal Chemistry, Virginia Commonwealth University, Richmond, VA 23298, USA. szhang2@vcu.edu.
Virginia Commonwealth University · US

Funding

Center for Clinical and Translational ResearchUL1TR000058 · NCATS · VIRGINIA COMMONWEALTH UNIVERSITY · PI MOELLER, FREDERICK GERARD · 2012 to 2015
$12.5M
Novel bivalent multifunctional ligands towards Alzheimer's diseaseR01AG041161 · NIA · VIRGINIA COMMONWEALTH UNIVERSITY · PI ZHANG, SHIJUN · 2012 to 2016
$1.5M
Reduction of cardiac injury by targeting damaged mitochondria during reperfusionI01BX001355 · VA · VA VETERANS ADMINISTRATION HOSPITAL · PI LESNEFSKY, EDWARD J · 2012 to 2025
–
BLRD VA I01 BX001355NCATS NIH HHS UL1 TR000058NCATS NIH HHS UL1TR000058NIA NIH HHS R01 AG041161NIA NIH HHS R01AG041161
6 · The paper itself

Abstract

We have recently developed a bivalent strategy to provide novel compounds that potentially target multiple risk factors involved in the development of Alzheimer's disease (AD). Our previous studies employing a bivalent compound with a shorter spacer (17MN) implicated that this compound can localize into mitochondria and endoplasmic reticulum (ER), thus interfering with the change of mitochondria membrane potential (MMP) and Ca(2+) levels in MC65 cells upon removal of tetracycline (TC). In this report, we examined the effects by a bivalent compound with a longer spacer (21MO) in MC65 cells. Our results demonstrated that 21MO suppressed the change of MMP, possibly via interaction with the mitochondrial complex I in MC65 cells. Interestingly, 21MO did not show any effects on the Ca(2+) level upon TC removal in MC65 cells. Our previous studies suggested that the mobilization of Ca(2+) in MC65 cells, upon withdraw of TC, originated from ER, so the results implicated that 21MO may preferentially interact with mitochondria in MC65 cells under the current experimental conditions. Collectively, the results suggest that bivalent compounds with varied spacer length and cell membrane anchor moiety may exhibit neuroprotective activities via different mechanisms of action.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsCalciumCell LineCholesterolCurcuminEndoplasmic ReticulumHumansMembrane Potential, MitochondrialMitochondriaNeuronsNeuroprotective AgentsRisk Factors17MN compoundAmyloid beta-PeptidesCalciumCholesterolCurcuminNeuroprotective AgentsAlzheimer’s diseasebivalent compoundcalciummitochondriamultifunctionalneuroprotection

Identifiers

PMID27023508
PMCPMC4831581
OpenAlexW2306884556

What OpenQuestion holds

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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.