Evidence map›Paper›PMID 28232023›Full record

ReviewPharmacology & therapeutics2017

Peptide regulation of cofilin activity in the CNS: A novel therapeutic approach for treatment of multiple neurological disorders.

Alisa E Shaw, James R Bamburg

Abstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.0field-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

34 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Reducing Cofilin dosage makes embryos resilient to heat stress.bioRxiv : the preprint server for biology · 2025
    Article
  5. Article
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  11. Review
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  17. Review
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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

2 authors at 1 institution in 1 country.

Alisa E ShawDepartment of Biochemistry and Molecular Biology, Molecular, Cellular and Integrative Neuroscience Program, Colorado State University, Fort Collins, CO 80523-1870, United States.
James R BamburgDepartment of Biochemistry and Molecular Biology, Molecular, Cellular and Integrative Neuroscience Program, Colorado State University, Fort Collins, CO 80523-1870, United States. Electronic address: James.Bamburg@colostate.edu.
Colorado State University · US

Funding

PrPC- and NOX-dependent signaling in dementiaR01AG049668 · NIA · COLORADO STATE UNIVERSITY · PI BAMBURG, JAMES R · 2015 to 2019
$1.5M
NIA NIH HHS R01 AG049668
6 · The paper itself

Abstract

Cofilin is a ubiquitous protein which cooperates with many other actin-binding proteins in regulating actin dynamics. Cofilin has essential functions in nervous system development including neuritogenesis, neurite elongation, growth cone pathfinding, dendritic spine formation, and the regulation of neurotransmission and spine function, components of synaptic plasticity essential for learning and memory. Cofilin's phosphoregulation is a downstream target of many transmembrane signaling processes, and its misregulation in neurons has been linked in rodent models to many different neurodegenerative and neurological disorders including Alzheimer disease (AD), aggression due to neonatal isolation, autism, manic/bipolar disorder, and sleep deprivation. Cognitive and behavioral deficits of these rodent models have been largely abrogated by modulation of cofilin activity using viral-mediated, genetic, and/or small molecule or peptide therapeutic approaches. Neuropathic pain in rats from sciatic nerve compression has also been reduced by modulating the cofilin pathway within neurons of the dorsal root ganglia. Neuroinflammation, which occurs following cerebral ischemia/reperfusion, but which also accompanies many other neurodegenerative syndromes, is markedly reduced by peptides targeting specific chemokine receptors, which also modulate cofilin activity. Thus, peptide therapeutics offer potential for cost-effective treatment of a wide variety of neurological disorders. Here we discuss some recent results from rodent models using therapeutic peptides with a surprising ability to cross the rodent blood brain barrier and alter cofilin activity in brain. We also offer suggestions as to how neuronal-specific cofilin regulation might be achieved.

Indexed as

AnimalsBrainCofilin 1HumansNervous System DiseasesPeptidesReactive Oxygen SpeciesCofilin 1PeptidesReactive Oxygen SpeciesCofilin phosphoregulationCognitive disordersDendritic spinesNeuropathic painPsychiatric disordersRodent modelsSleep deprivation

Identifiers

PMID28232023
PMCPMC5466456
OpenAlexW2591104912

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.