Evidence map›Paper›PMID 32076757›Full record

ReviewDer Nervenarzt2020

[Gene-specific treatment approaches in Alzheimer's disease and other tauopathies].

E Feneberg, M Otto

Open access · hybridAbstract readReview
PubMed Publisher
In one paragraph

Review in Der Nervenarzt, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 55% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. 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

2 authors at 1 institution in 1 country.

E FenebergAbteilung für Neurologie, Universitäts- und Rehabilitationskliniken, Oberer Eselsberg 45, 89081, Ulm, Deutschland. emily.feneberg@ndcn.ox.ac.uk.
M OttoAbteilung für Neurologie, Universitäts- und Rehabilitationskliniken, Oberer Eselsberg 45, 89081, Ulm, Deutschland.
University and Rehabilitation Clinics Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathological hallmarks of Alzheimer's disease are aggregation and accumulation of amyloid-β and tau proteins. So far most interventional studies have focused on the removal of the toxic protein products, such as antibody-based immunotherapies targeted against amyloid-β and tau proteins; however, the development of gene therapies targeting gene products involved in the disease has opened up new therapeutic strategies to reduce the development of toxic protein aggregates by inhibiting the translation of pathological Alzheimer genes using antisense oligonucleotides (ASO). This has a timely influence on development of the disease. This article gives an overview of new advances in ASO-based treatment strategies for Alzheimer's disease.

Indexed as

Alzheimer DiseaseGenetic TherapyAmyloid beta-PeptidesHumansImmunotherapyOligonucleotides, Antisensetau ProteinsAmyloid beta-PeptidesOligonucleotides, Antisensetau ProteinsAmyloid betaAntibody therapyAntisense oligonucleotidesGene therapyTau

Identifiers

PMID32076757
OpenAlexW3006888002

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.