Evidence map›Paper›PMID 34652482›Full record

ReviewDer Nervenarzt2021

[Neuroprotective treatment of tauopathies].

Gesine Respondek, Lea Krey, Meret Huber, Henning Pflugrad, Florian Wegner, Günter U Höglinger

Abstract readReview
PubMed Publisher
In one paragraph

Review in Der Nervenarzt, 2021. 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 45% 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, 2 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

6 authors at 1 institution in 1 country.

Gesine RespondekKlinik für Neurologie, Medizinische Hochschule Hannover (MHH), Carl-Neuberg-Str. 1, 30625, Hannover, Deutschland.
Lea KreyKlinik für Neurologie, Medizinische Hochschule Hannover (MHH), Carl-Neuberg-Str. 1, 30625, Hannover, Deutschland.
Meret HuberKlinik für Neurologie, Medizinische Hochschule Hannover (MHH), Carl-Neuberg-Str. 1, 30625, Hannover, Deutschland.
Henning PflugradKlinik für Neurologie, Medizinische Hochschule Hannover (MHH), Carl-Neuberg-Str. 1, 30625, Hannover, Deutschland.
Florian WegnerKlinik für Neurologie, Medizinische Hochschule Hannover (MHH), Carl-Neuberg-Str. 1, 30625, Hannover, Deutschland.
Günter U HöglingerKlinik für Neurologie, Medizinische Hochschule Hannover (MHH), Carl-Neuberg-Str. 1, 30625, Hannover, Deutschland. hoeglinger.guenter@mh-hannover.de.
Medizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tau pathology is now considered to be the main cause of a wide spectrum of neurodegenerative diseases, which are collectively referred to as tauopathies. These include primary tauopathies, in which tau plays the main role in the pathogenesis as well as secondary tauopathies, such as Alzheimer's disease, in which amyloid beta also plays a substantial role in the disease process in addition to the tau pathology. Primary tauopathies include progressive supranuclear palsy, corticobasal degeneration, Pick's disease and rare hereditary tauopathies, which are referred to as frontotemporal lobar degeneration with microtubule-associated protein tau (MAPT) mutation. Tauopathies differ from each other pathologically by the affected brain regions and cell types as well as by the biochemical characteristics of the aggregated tau protein. Various tau-centered neuroprotective treatment approaches are currently in preclinical and clinical development. They target different mechanisms, including the reduction of tau expression, inhibition of tau aggregation, dissolution of tau aggregates, improvement of cellular mechanisms to eliminate toxic tau species, stabilization of microtubules and prevention of intercellular tau spreading. This review article gives an overview of tauopathies and the current concepts for the development of disease-modifying treatment.

Indexed as

Alzheimer DiseaseCorticobasal DegenerationTauopathiesAmyloid beta-PeptidesHumanstau ProteinsAmyloid beta-Peptidestau ProteinsAlzheimer’s diseaseCausal treatmentCorticobasal degenerationMicrotubule-associated protein tauProgressive supranuclear palsy

Identifiers

PMID34652482
OpenAlexW3205363751

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.