Evidence map›Paper›PMID 38073385›Full record

ArticleJournal of Alzheimer's disease : JAD2024

Treatment with 1, 10 Phenanthroline-5-Amine Reduced Amyloid Burden in a Mouse Model of Alzheimer's Disease.

Larry Schmued, Bryan Maloney, Calvert Schmued, Debomoy K Lahiri

Open access · bronzeAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 44% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

4 authors at 2 institutions in 1 country.

Larry SchmuedHisto-Chem Inc., White Hall, AR, USA.
Bryan MaloneyDepartment of Psychiatry, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA.
Calvert SchmuedHisto-Chem Inc., White Hall, AR, USA.
Debomoy K LahiriDepartment of Psychiatry, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA.
Indiana University School of MedicineThe White House · US

Funding

Research Education ComponentP30AG072976 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI ANDREW J SAYKIN · 2021 to 2026
$24.1M
Neurobiological Role of MicroRNA in Alzheimer'sR01AG051086 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI LAHIRI, DEBOMOY K · 2015 to 2019
$1.9M
Role of microRNA in regulating Fe, Amyloid, and Tau (FeAT) in Alzheimer's diseaseR56AG072810 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI LAHIRI, DEBOMOY K · 2021 to 2021
$630k
Brain protein alteration by vascular overexpressed miRNA (BravomiR)R21AG076202 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI LAHIRI, DEBOMOY K · 2022 to 2022
$435k
Testing a Novel Approach to Solve the On-target, Off-site Effects of Alzheimer's DrugsR21AG056007 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI LAHIRI, DEBOMOY K · 2019 to 2020
$435k
NIA NIH HHS P30 AG072976NIA NIH HHS R01 AG051086NIA NIH HHS R21 AG056007NIA NIH HHS R21 AG076202NIA NIH HHS R56 AG072810
6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is the most prevalent age-related dementia, and, despite numerous attempts to halt or reverse its devastating progression, no effective therapeutics have yet been confirmed clinically. However, one class of agents that has shown promise is certain metal chelators.

objectiveFor the novel assessment of the effect of oral administration of 1,10-phenanthroline-5-amine (PAA) on the severity of amyloid plaque load, we used a transgenic (Tg) mouse model with inserted human autosomally dominant (familial) AD genes: amyloid-β protein precursor (AβPP) and tau.

methodsAβPP/Tau transgenic mice that model AD were allotted into one of two groups. The control group received no treatment while the experimental group received PAA in their drinking water starting at 4 months of age. All animals were sacrificed at 1 year of age and their brains were stained with two different markers of amyloid plaques, Amylo-Glo+ and HQ-O.

resultsThe control animals exhibited numerous dense core plaques throughout the neo- and allo- cortical brain regions. The experimental group treated with PAA, however, showed 62% of the amyloid plaque burden seen in the control group.

conclusionsOral daily dosing with PAA will significantly reduce the amyloid plaque burden in transgenic mice that model AD. The underlying mechanism for this protection is not fully known; however, one proposed mechanism involves inhibiting the "metal-seeding" of Aβ.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsBrainDisease Models, AnimalHumansMiceMice, TransgenicPhenanthrolinesPlaque, AmyloidAmyloid beta-PeptidesAmyloid beta-Protein PrecursorPhenanthrolinesAgingAlzheimer’s diseaseamyloidmetal chelatorsmetalloproteinaseneurodegenerative disorders

Identifiers

PMID38073385
PMCPMC10789349
OpenAlexW4389475060

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.