Evidence map›Paper›PMID 26768593›Full record

ArticleMolecular neurobiology2017

Pramlintide Antagonizes Beta Amyloid (Aβ)- and Human Amylin-Induced Depression of Hippocampal Long-Term Potentiation.

R Kimura, D MacTavish, J Yang, D Westaway, Jack H Jhamandas

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

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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

5 authors at 1 institution in 2 countries.

R KimuraFaculty of Engineering, Tokyo University of Science, Yamaguchi, Sanyo-onoda, Yamaguchi, Japan.
D MacTavishDepartment of Medicine (Neurology), University of Alberta, Edmonton, AB, T6G 2S2, Canada.
J YangDepartment of Medicine (Neurology), University of Alberta, Edmonton, AB, T6G 2S2, Canada.
D WestawayDepartment of Medicine (Neurology), University of Alberta, Edmonton, AB, T6G 2S2, Canada.
Jack H JhamandasDepartment of Medicine (Neurology), University of Alberta, Edmonton, AB, T6G 2S2, Canada. jack.jhamandas@ualberta.ca.
University of Alberta · CA

Funding

CIHR MOP 93601
6 · The paper itself

Abstract

Accumulation of amyloid-β peptide (Aβ) is a pathological hallmark of Alzheimer's disease (AD). We have previously demonstrated that electrophysiological and neurotoxic effects of Aβ and human amylin are expressed via the amylin receptor. Recently, pramlintide, a synthetic analog of amylin, has been reported to improve cognitive function in transgenic AD mouse models. In this study, we examined the effects of pramlintide on Aβ

Indexed as

Amino Acid SequenceAmyloid beta-PeptidesAnimalsFemaleHippocampusHumansIslet Amyloid PolypeptideLong-Term PotentiationMaleMiceMice, 129 StrainMice, TransgenicOrgan Culture TechniquesPeptide FragmentsAmyloid beta-Peptidesamyloid beta-protein (1-42)Islet Amyloid PolypeptidePeptide FragmentspramlintideAlzheimer’s diseaseAmylin receptorAmyloidDiabetesHippocampusLTPSynaptic plasticity

Identifiers

PMID26768593
OpenAlexW2233064811

What OpenQuestion holds

Textmetadata
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.