Evidence map›Paper›PMID 22484448›Full record

ReviewProgress in neurobiology2012

Axonal transport and neurodegenerative disease: can we see the elephant?

Lawrence S B Goldstein

Abstract readReview
In one paragraph

Review in Progress in neurobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
–field-weighted citation impact
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

37 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Zebrafish as a Model for the Study of LiveFrontiers in cell and developmental biology · 2019
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. A small-molecule activator of kinesin-1 drives remodeling of the microtubule network.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  17. Article
  18. Review
  19. Back to the tubule: microtubule dynamics in Parkinson's disease.Cellular and molecular life sciences : CMLS · 2017
    Review
  20. Tau Isoforms Imbalance Impairs the Axonal Transport of the Amyloid Precursor Protein in Human Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    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

1 author.

Lawrence S B GoldsteinDepartment of Cellular and Molecular Medicine and Department of Neurosciences, UCSD School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093-0695, USA. lgoldstein@ucsd.edu

Funding

Impairment of axonal transport by Amyloid precursor protein and amyloid Beta-protR01AG032180 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GOLDSTEIN, LAWRENCE S. · 2007 to 2011
$1.6M
Human Stem Cell Model of Niemann Pick Type CRC1NS068705 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GOLDSTEIN, LAWRENCE S. · 2010 to 2010
$1.0M
Pluripotent stem cell models of sporadic Alzheimer's DiseaseR21AG038849 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GOLDSTEIN, LAWRENCE S. · 2011 to 2012
$336k
Howard Hughes Medical InstituteNIA NIH HHS R01 AG032180NIA NIH HHS R21 AG038849NINDS NIH HHS RC1 NS068705
6 · The paper itself

Abstract

Although it is well established that axonal transport defects are part of the initiation or progression of some neurodegenerative diseases, the precise role of these defects in disease development is poorly understood. Thus, in this article, rather than enumerate the already well-reviewed evidence that there are transport deficits in disease, I will focus on a discussion of two crucial and unanswered questions about the possible role of axonal transport defects in HD and AD. (1) Are alterations in axonal transport caused by changes in the normal function of proteins mutated or altered in HD and AD and/or do such alterations in transport occur as a result of the formation of toxic aggregates of peptides or proteins? (2) Do alterations in axonal transport contribute to the causes of HD and AD or are they early, or late, secondary consequences of other cellular defects caused by disease-induction?

Indexed as

AnimalsAxonal TransportDisease ProgressionDyneinsHumansKinesinsNeurodegenerative DiseasesDyneinsKinesins

Identifiers

PMID22484448
PMCPMC3867006

What OpenQuestion holds

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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.