Evidence map›Paper›PMID 24909306›Full record

ArticleDevelopmental neurobiology2014

Loss of Tau results in defects in photoreceptor development and progressive neuronal degeneration in Drosophila.

Bonnie J Bolkan, Doris Kretzschmar

Open access · greenAbstract read
In one paragraph

Article in Developmental neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

30 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. TBI and Tau Loss of Function Both Affect Naïve Ethanol Sensitivity inInternational journal of molecular sciences · 2024
    Article
  4. Article
  5. Towards early detection of neurodegenerative diseases: A gut feeling.Frontiers in cell and developmental biology · 2023
    Review
  6. Alzheimer's disease: an axonal injury disease?Frontiers in aging neuroscience · 2023
    Review
  7. Article
  8. Article
  9. Review
  10. Elongator promotes neuritogenesisFrontiers in cell and developmental biology · 2022
    Article
  11. Non-Rodent Genetic Animal Models for Studying Tauopathy: Review ofInternational journal of molecular sciences · 2021
    Review
  12. Article
  13. Retromer dysfunction at the nexus of tauopathies.Cell death and differentiation · 2021
    Review
  14. Article
  15. Article
  16. Article
  17. The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  18. Article
  19. Article
  20. 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.

Bonnie J BolkanOregon Institute of Occupational Health Sciences, Oregon Health & Science University, Portland, Oregon, 97239.
Doris Kretzschmar
Oregon Health & Science University · US

Funding

Ultrastructure and Single Particle Microscopy CoreP30NS061800 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI AICHER, SUE A · 2009 to 2020
$6.6M
SWS/NTE function in neurodegeneration and axonopathyR01NS047663 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI KRETZSCHMAR, DORIS · 2004 to 2013
$2.7M
Neuroscience of AgingT32AG023477 · NIA · OREGON HEALTH & SCIENCE UNIVERSITY · PI URBANSKI, HENRYK F · 2005 to 2015
$2.4M
Basic research training in embryonic developmentT32HD049309 · NICHD · OREGON HEALTH & SCIENCE UNIVERSITY · PI BARR-GILLESPIE, PETER GORDON · 2006 to 2010
$1.8M
NIA NIH HHS 5T32AG023477NIA NIH HHS T32 AG023477NICHD NIH HHS 5T32HD049309NICHD NIH HHS T32 HD049309NINDS NIH HHS P30 NS061800NINDS NIH HHS P30NS061800NINDS NIH HHS R01 NS047663
6 · The paper itself

Abstract

Accumulations of Tau, a microtubule-associated protein (MAP), into neurofibrillary tangles is a hallmark of Alzheimer's disease and other tauopathies. However, the mechanisms leading to this pathology are still unclear: the aggregates themselves could be toxic or the sequestration of Tau into tangles might prevent Tau from fulfilling its normal functions, thereby inducing a loss of function defect. Surprisingly, the consequences of losing normal Tau expression in vivo are still not well understood, in part due to the fact that Tau knockout mice show only subtle phenotypes, presumably due to the fact that mammals express several MAPs with partially overlapping functions. In contrast, flies express fewer MAP, with Tau being the only member of the Tau/MAP2/MAP4 family. Therefore, we used Drosophila to address the physiological consequences caused by the loss of Tau. Reducing the levels of fly Tau (dTau) ubiquitously resulted in developmental lethality, whereas deleting Tau specifically in neurons or the eye caused progressive neurodegeneration. Similarly, chromosomal mutations affecting dTau also caused progressive degeneration in both the eye and brain. Although photoreceptor cells initially developed normally in dTau knockdown animals, they subsequently degenerated during late pupal stages whereas weaker dTau alleles caused an age-dependent defect in rhabdomere structure. Expression of wild type human Tau partially rescued the neurodegenerative phenotype caused by the loss of endogenous dTau, suggesting that the functions of Tau proteins are functionally conserved from flies to humans.

Indexed as

Alternative SplicingAnimalsAnimals, Genetically ModifiedAxonsBrainDrosophilaDrosophila ProteinsGene Knockdown TechniquesHumansMicrotubulesMutationNerve DegenerationPhotoreceptor Cells, InvertebrateProtein IsoformsRetinal Degenerationtau ProteinsDrosophila ProteinsMAPT protein, humanProtein Isoformstau protein, Drosophilatau ProteinsDrosophilaeye developmentneurodegenerationtau

Identifiers

PMID24909306
PMCPMC4212004
OpenAlexW1932699762

What OpenQuestion holds

Textmetadata
LicenceTDM
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.