Evidence map›Paper›PMID 34896392›Full record

ReviewThe Journal of biological chemistry2022

Aptamers targeting amyloidogenic proteins and their emerging role in neurodegenerative diseases.

Kazuma Murakami, Naotaka Izuo, Gal Bitan

Open access · goldAbstract readReview
In one paragraph

Review in The Journal of biological chemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

21 citing papers in PubMed, 37 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

3 authors at 3 institutions in 2 countries.

Kazuma MurakamiDivision of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Kyoto, Japan. Electronic address: murakami.kazuma.4v@kyoto-u.ac.jp.
Naotaka IzuoLaboratory of Pharmaceutical Therapy and Neuropharmacology, Faculty of Pharmaceutical Sciences, University of Toyama, Toyama, Japan.
Gal BitanDepartment of Neurology, David Geffen School of Medicine, Brain Research Institute, and Molecular Biology Institute, University of California Los Angeles, Los Angeles, California, USA. Electronic address: gbitan@mednet.ucla.edu.
Kyoto University · JPUniversity of California, Los Angeles · USUniversity of Toyama · JP

Funding

Investigation of the Effect of Structural Modifications of Tau on Assembly State and SeedingRF1AG054000 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BITAN, GAL · 2017 to 2021
$2.1M
NIA NIH HHS RF1 AG054000
6 · The paper itself

Abstract

Aptamers are oligonucleotides selected from large pools of random sequences based on their affinity for bioactive molecules and are used in similar ways to antibodies. Aptamers provide several advantages over antibodies, including their small size, facile, large-scale chemical synthesis, high stability, and low immunogenicity. Amyloidogenic proteins, whose aggregation is relevant to neurodegenerative diseases, such as Alzheimer's, Parkinson's, and prion diseases, are among the most challenging targets for aptamer development due to their conformational instability and heterogeneity, the same characteristics that make drug development against amyloidogenic proteins difficult. Recently, chemical tethering of aptagens (equivalent to antigens) and advances in high-throughput sequencing-based analysis have been used to overcome some of these challenges. In addition, internalization technologies using fusion to cellular receptors and extracellular vesicles have facilitated central nervous system (CNS) aptamer delivery. In view of the development of these techniques and resources, here we review antiamyloid aptamers, highlighting preclinical application to CNS therapy.

Indexed as

Amyloidogenic ProteinsAptamers, NucleotideNeurodegenerative DiseasesPrion DiseasesAnimalsCentral Nervous SystemHumansSELEX Aptamer TechniqueAmyloidogenic ProteinsAptamers, Nucleotideoligonucleotide, RNA, DNA, amyloid, Alzheimer's disease, Parkinson's disease, prion, blood-brain barrier, oligomer, exosome

Identifiers

PMID34896392
PMCPMC8728582
OpenAlexW4200555036

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.