Evidence map›Paper›PMID 25332075›Full record

ReviewMolecular genetics and genomics : MGG2015

The role of the retromer complex in aging-related neurodegeneration: a molecular and genomic review.

Christiane Reitz

Erratum issuedOpen access · greenAbstract readReview
In one paragraph

Review in Molecular genetics and genomics : MGG, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed, 39 citations in OpenAlex.

  1. Dissecting the genetic overlap between severe mental disorders and markers of cellular aging: Identification of pleiotropic genes and druggable targets.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article
  2. Protein expression/secretion boost by a novel unique 21-mer cis-regulatory motif (Exin21) via mRNA stabilization.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  3. Article
  4. Article
  5. Review
  6. Unveiling the cryo-EM structure of retromer.Biochemical Society transactions · 2020
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. The emerging role of retromer in neuroprotection.Current opinion in cell biology · 2017
    Review
  17. Article
  18. Article
  19. The Role of Retromer in Alzheimer's Disease.Molecular neurobiology · 2016
    Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Christiane ReitzThe Department of Neurology, The Department of Epidemiology, The Taub Institute for Research on Alzheimer's Disease and the Aging Brain, The Gertrude H. Sergievsky Center, Columbia University, 630 West 168th Street, New York, NY, 10032, USA, cr2101@cumc.columbia.edu.
Columbia University · US

Funding

Mapping Causative factors in the sortilin-related pathway in Alzheimer's DiseaseK23AG034550 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI REITZ, CHRISTIANE · 2009 to 2013
$479k
NIA NIH HHS K23 AG034550NIA NIH HHS K23AG034550
6 · The paper itself

Abstract

The retromer coat complex is a vital component of the intracellular trafficking mechanism sorting cargo from the endosomes to the trans-Golgi network or to the cell surface. In recent years, genes encoding components of the retromer coat complex and members of the vacuolar protein sorting 10 (Vps10) family of receptors, which play pleiotropic functions in protein trafficking and intracellular/intercellular signaling in neuronal and non-neuronal cells and are primary cargos of the retromer complex, have been implicated as genetic risk factors for sporadic and autosomal dominant forms of several neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease and frontotemporal lobar degeneration. In addition to their functions in protein trafficking, the members of the Vps10 receptor family (sortilin, SorL1, SorCS1, SorCS2, and SorCS3) modulate neurotrophic signaling pathways. Both sortilin and SorCS2 act as cell surface receptors to mediate acute responses to proneurotrophins. In addition, sortilin can modulate the intracellular response to brain-derived neurotrophic factor (BDNF) by direct control of BDNF levels and regulating anterograde trafficking of Trk receptors to the synapse. This review article summarizes the emerging data from this rapidly growing field of intracellular trafficking signaling in the pathogenesis of neurodegeneration.

Indexed as

AgingAnimalsGenetic Predisposition to DiseaseHumansMutationNeurodegenerative DiseasesPolymorphism, Single NucleotideProtein TransportReceptors, Cell SurfaceSignal TransductionVesicular Transport ProteinsReceptors, Cell SurfaceVesicular Transport Proteins

Identifiers

PMID25332075
PMCPMC4363161
OpenAlexW2031571139

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.