Evidence map›Paper›PMID 27213408›Full record

ReviewMarine drugs2016

Axonal Transport and Neurodegeneration: How Marine Drugs Can Be Used for the Development of Therapeutics.

Joseph A White, Rupkatha Banerjee, Shermali Gunawardena

Open access · goldAbstract readReview
In one paragraph

Review in Marine drugs, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Defects in Axonal Transport in Inherited Neuropathies.Journal of neuromuscular diseases · 2019
    Review
  9. Review
  10. 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

3 authors at 1 institution in 1 country.

Joseph A WhiteDepartment of Biological Sciences, The State University of New York at Buffalo, Buffalo, NY 14260, USA. jwhite2@buffalo.edu.
Rupkatha BanerjeeDepartment of Biological Sciences, The State University of New York at Buffalo, Buffalo, NY 14260, USA. rupkatha@buffalo.edu.
Shermali GunawardenaDepartment of Biological Sciences, The State University of New York at Buffalo, Buffalo, NY 14260, USA. sg99@buffalo.edu.
University at Buffalo, State University of New York · US

Funding

A synthetic vesicle to carry modifier compounds to axonal blocks induced by pathogenic polyQR03NS092024 · NINDS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI GUNAWARDENA, SHERMALI · 2015 to 2016
$156k
Dissecting the in vivo role of Huntingtin in Rab vesicle movement on microtubulesR03NS084386 · NINDS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI GUNAWARDENA, SHERMALI · 2013 to 2014
$155k
NINDS NIH HHS R03 NS084386NINDS NIH HHS R03 NS092024
6 · The paper itself

Abstract

Unlike virtually any other cells in the human body, neurons are tasked with the unique problem of transporting important factors from sites of synthesis at the cell bodies, across enormous distances, along narrow-caliber projections, to distally located nerve terminals in order to maintain cell viability. As a result, axonal transport is a highly regulated process whereby necessary cargoes of all types are packaged and shipped from one end of the neuron to the other. Interruptions in this finely tuned transport have been linked to many neurodegenerative disorders including Alzheimer's (AD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS) suggesting that this pathway is likely perturbed early in disease progression. Therefore, developing therapeutics targeted at modifying transport defects could potentially avert disease progression. In this review, we examine a variety of potential compounds identified from marine aquatic species that affect the axonal transport pathway. These compounds have been shown to function in microtubule (MT) assembly and maintenance, motor protein control, and in the regulation of protein degradation pathways, such as the autophagy-lysosome processes, which are defective in many degenerative diseases. Therefore, marine compounds have great potential in developing effective treatment strategies aimed at early defects which, over time, will restore transport and prevent cell death.

Indexed as

AnimalsAxonal TransportHumansMicrotubulesNeurodegenerative DiseasesOceans and SeasTubulin ModulatorsTubulin Modulatorsaxonal transportmolecular motor proteinsneurodegenerative diseases

Identifiers

PMID27213408
PMCPMC4882576
OpenAlexW2402504663

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.