Evidence map›Paper›PMID 28012891›Full record

ReviewNeurobiology of disease2017

Altered microtubule dynamics in neurodegenerative disease: Therapeutic potential of microtubule-stabilizing drugs.

Kurt R Brunden, Virginia M-Y Lee, Amos B Smith, John Q Trojanowski, Carlo Ballatore

Open access · greenAbstract readReview
In one paragraph

Review in Neurobiology of disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

56 citing papers in PubMed, 104 citations in OpenAlex.

  1. Review
  2. Article
  3. Patient-derived forebrain cortical organoids reveal biphasic tau-MAP6-microtubule axis dysfunction in tauopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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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

5 authors at 2 institutions in 1 country.

Kurt R BrundenCenter for Neurodegenerative Disease Research, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, United States. Electronic address: kbrunden@upenn.edu.
Virginia M-Y LeeCenter for Neurodegenerative Disease Research, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, United States.
Amos B SmithDepartment of Chemistry, School of Arts and Science, University of Pennsylvania, Philadelphia, PA 19104, United States.
John Q TrojanowskiCenter for Neurodegenerative Disease Research, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, United States.
Carlo BallatoreSkaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, La Jolla, CA 92093, United States.
University of Pennsylvania · USUniversity of California, San Diego · US

Funding

Transgenic Mouse Models of Tau PathologiesP01AG017586 · NIA · UNIVERSITY OF PENNSYLVANIA · PI LEE, VIRGINIA M · 2000 to 2021
$37.3M
UPenn ADCC Biomarker CoreP30AG010124 · NIA · UNIVERSITY OF PENNSYLVANIA · PI DETRE, JOHN A · 1991 to 2020
$35.1M
Orally-absorbed, small molecule microtubule-stabilizers for tauopathy treatmentR01AG044332 · NIA · UNIVERSITY OF PENNSYLVANIA · PI BALLATORE, CARLO, BRUNDEN, KURT R. · 2013 to 2017
$2.3M
Dictyostatin and related prodrugs as candidates for tauopathy treatmentR21NS087059 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI SMITH, AMOS B · 2014 to 2015
$800k
NIA NIH HHS P01 AG017586NIA NIH HHS P30 AG010124NIA NIH HHS R01 AG044332NINDS NIH HHS R21 NS087059
6 · The paper itself

Abstract

Many neurodegenerative diseases are characterized by deficiencies in neuronal axonal transport, a process in which cellular cargo is shuttled with the aid of molecular motors from the cell body to axonal termini and back along microtubules (MTs). Proper axonal transport is critical to the normal functioning of neurons, and impairments in this process could contribute to the neuronal damage and death that is characteristic of neurodegenerative disease. Although the causes of axonal transport abnormalities may vary among the various neurodegenerative conditions, in many cases it appears that the transport deficiencies result from a diminution of axonal MT stability. Here we review the evidence of MT abnormalities in a number of neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis and traumatic brain injury, and highlight the potential benefit of MT-stabilizing agents in improving axonal transport and nerve function in these diseases. Moreover, we discuss the challenges associated with the utilization of MT-stabilizing drugs as therapeutic candidates for neurodegenerative conditions.

Indexed as

AnimalsHumansMicrotubulesNeurodegenerative DiseasesTubulin ModulatorsTubulin ModulatorsAlzheimerAmyotrophic lateral sclerosisAxonsFrontotemporal lobar degenerationMicrotubulesNeurodegenerationParkinsonTransportTraumatic brain injury

Identifiers

PMID28012891
PMCPMC5481496
OpenAlexW2562065231

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.