Evidence map›Paper›PMID 29641484›Full record

ReviewInternational journal of molecular sciences2018

An Overview on the Clinical Development of Tau-Based Therapeutics.

Miguel Medina

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
15.2field-weighted citation impact, top 1% 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

73 citing papers in PubMed, 150 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Organelle abnormalities in Alzheimer's disease.Organelle (Tucson, Ariz.) · 2025
    Article
  8. Review
  9. Resistance and Resilience to Alzheimer's Disease.Cold Spring Harbor perspectives in medicine · 2024
    Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Phosphorylated Tau in Alzheimer's Disease and Other Tauopathies.International journal of molecular sciences · 2022
    Review
  19. Article
  20. Review

13 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Miguel MedinaNetwork Center for Biomedical Research in Neurodegenerative Diseases (CIBERNED), Queen Sofia Foundation Alzheimer Center, CIEN Foundation, Carlos III Institute of Health, 28031 Madrid, Spain. mmedina@ciberned.es.ORCID 0000-0002-7016-5340
Biomedical Research Networking Center on Neurodegenerative Diseases · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tauopathies such as Alzheimer's disease (AD), frontotemporal lobar degeneration, or progressive supranuclear palsy constitute a group of brain disorders defined by neurodegeneration and the presence of tau aggregates in the affected brains regions. Tau is a microtubule-associated protein that accumulates in the cytosol under pathological conditions, steering the formation of aggregates or inclusions thought to be involved in the degeneration and neuronal death associated with these diseases. Despite a substantial and unmet medical need for novel, more effective disease-modifying therapies for the treatment of AD and tauopathies, the last couple of decades have seen numerous drug development undertakings primarily focused on β-amyloid, with disappointing results to date. On the other hand, tau-focused approaches have not received much attention until recently, notwithstanding that the presence of extensive tau pathology is fundamental for the disease and tau pathology shows a better correlation with impaired cognitive function than with amyloid pathology in AD patients. The last few years have brought us advances in our comprehension of tau biological functions beyond its well-established role as a microtubule-associated protein, unveiling novel physiological tau functions that may also be involved in pathogenesis and thus provide novel targets for therapeutic intervention. This review describes several emerging, encouraging therapeutic approaches aimed at tackling the underlying causes of tau pathology in AD and other tauopathies that have recently reached the clinical development stage.

Indexed as

AnimalsAntibodiesClinical Trials as TopicHumansImmunotherapyNeuroprotective AgentsProtein Processing, Post-TranslationalTauopathiestau ProteinsAntibodiesNeuroprotective Agentstau ProteinsaggregationAlzheimerdementiadrug developmentimmunotherapyneurodegenerationtautauopathiestherapy

Identifiers

PMID29641484
PMCPMC5979300
OpenAlexW2797727149

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.