Evidence map›Paper›PMID 27335341›Full record

ArticleNanomedicine : nanotechnology, biology, and medicine2016

Small molecule NPT-440-1 inhibits ionic flux through Aβ

Alan L Gillman, Joon Lee, Srinivasan Ramachandran, Ricardo Capone, Tania Gonzalez, Wolf Wrasidlo, Eliezer Masliah, Ratnesh Lal

Open access · greenAbstract read
In one paragraph

Article in Nanomedicine : nanotechnology, biology, and medicine, 2016. 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 39% 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

8 authors at 1 institution in 1 country.

Alan L GillmanDepartment of Bioengineering, University of California, San Diego, La Jolla, CA, United States.
Joon LeeDepartment of Mechanical and Aerospace Engineering University of California, San Diego, La Jolla, CA, United States.
Srinivasan RamachandranDepartment of Bioengineering, University of California, San Diego, La Jolla, CA, United States; Department of Mechanical and Aerospace Engineering University of California, San Diego, La Jolla, CA, United States.
Ricardo CaponeDepartment of Neurosciences, University of California, San Diego, La Jolla, CA, United States.
Tania GonzalezDepartment of Neurosciences, University of California, San Diego, La Jolla, CA, United States.
Wolf WrasidloDepartment of Neurosciences, University of California, San Diego, La Jolla, CA, United States; Neuropore Therapies, Inc., San Diego, CA, United States.
Eliezer MasliahDepartment of Neurosciences, University of California, San Diego, La Jolla, CA, United States. Electronic address: emasliah@ucsd.edu.
Ratnesh LalDepartment of Bioengineering, University of California, San Diego, La Jolla, CA, United States; Materials Science and Engineering Program, University of California, San Diego, La Jolla, CA, United States; Department of Mechanical and Aerospace Engineering University of California, San Diego, La Jolla, CA, United States. Electronic address: rlal@eng.ucsd.edu.
University of California San Diego · US

Funding

VIRUS-INDUCED BRAIN PATHOLOGYP50AG005131 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GALASKO, DOUGLAS R · 1985 to 2018
$55.4M
B-Synuclein as a Treatment for Lewy Body DiseaseR01AG018440 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RISSMAN, ROBERT · 2001 to 2021
$5.2M
Project-002P30NS076411 · NINDS · SCINTILLON INSTITUTE FOR PHOTOBIOLOGY · PI LIPTON, STUART A · 2011 to 2016
$4.5M
Amyloid ion channels to design therapeutics for neurodegenerative diseasesR01AG028709 · NIA · UNIVERSITY OF CHICAGO · PI LAL, RATNESHWAR · 2006 to 2018
$3.6M
a-synuclein clearance strategies for the treatment of Lewy body disease.R37AG018440 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MASLIAH, ELIEZER · 2006 to 2014
$2.7M
NIA NIH HHS P50 AG005131NIA NIH HHS R01 AG018440NIA NIH HHS R01 AG028709NIA NIH HHS R37 AG018440NINDS NIH HHS P30 NS076411
6 · The paper itself

Abstract

Increased levels of soluble amyloid-beta (Aβ) oligomers are suspected to underlie Alzheimer's disease (AD) pathophysiology. These oligomers have been shown to form multi-subunit Aβ pores in bilayers and induce uncontrolled, neurotoxic, ion flux, particularly calcium ions, across cellular membranes that might underlie cognitive impairment in AD. Small molecule interventions that modulate pore activity could effectively prevent or ameliorate their toxic activity. Here we examined the efficacy of a small molecule, NPT-440-1, on modulating amyloid pore permeability. Co-incubation of B103 rat neuronal cells with NPT-440-1 and Aβ

Indexed as

Lipid BilayersAlzheimer DiseaseAmyloidAmyloid beta-PeptidesAnimalsPeptide FragmentsRatsAmyloidAmyloid beta-Peptidesamyloid beta-protein (1-42)Lipid BilayersPeptide FragmentsAlzheimer's diseaseAmyloid beta peptideAmyloid poreAtomic force microscopyBilayer electrophysiologyCalciumSmall molecule

Identifiers

PMID27335341
PMCPMC5116404
OpenAlexW2440988214

What OpenQuestion holds

Textmetadata
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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.