Evidence map›Paper›PMID 24012632›Full record

ReviewMechanisms of ageing and development2013

Impaired mitochondrial energy production and ABC transporter function-A crucial interconnection in dementing proteopathies of the brain.

Jens Pahnke, Christina Fröhlich, Markus Krohn, Toni Schumacher, Kristin Paarmann

Abstract readReview
In one paragraph

Review in Mechanisms of ageing and development, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Measurement of cerebral ABCC1 transport activity in wild-type and APP/PS1-21 mice with positron emission tomography.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. ABCA1 agonist peptides for the treatment of disease.Current opinion in lipidology · 2016
    Review
  12. Molecular Targets of Cannabidiol in Neurological Disorders.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2015
    Review
  13. Perfusion single photon emission computed tomography in a mouse model of neurofibromatosis type 1: towards a biomarker of neurologic deficits.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2015
    Article
  14. Review
  15. Spinal cord pathology in chronic experimental Toxoplasma gondii infection.European journal of microbiology & immunology · 2014
    Article
  16. 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

5 authors.

Jens PahnkeNeurodegeneration Research Lab (NRL), Department of Neurology, University of Magdeburg, Leipziger Str. 44, H64, 39120 Magdeburg, Germany; German Center for Neurodegenerative Diseases (DZNE) Magdeburg, Leipziger Str. 44, H64, 39120 Magdeburg, Germany. Electronic address: jens.pahnke@gmail.com.
Christina Fröhlich
Markus Krohn
Toni Schumacher
Kristin Paarmann

Funding

YNPRC NHP CLINICAL MEDICINE RESIDENCY PROGRAM - SUPPLEMENTP51RR000165 · NCRR · EMORY UNIVERSITY · PI ALTMAN, JOHN DAVID · 1985 to 2011
$114.0M
NCRR NIH HHS P51 RR000165
6 · The paper itself

Abstract

Ageing is the main risk factor for the development of dementing neurodegenerative diseases (NDs) and it is accompanied by the accumulation of variations in mitochondrial DNA. The resulting tissue-specific alterations in ATP production and availability cause deteriorations of cerebral clearance mechanisms that are important for the removal of toxic peptides and its aggregates. ABC transporters were shown to be the most important exporter superfamily for toxic peptides, e.g. β-amyloid and α-synuclein. Their activity is highly dependent on the availability of ATP and forms a directed energy-exporter network, linking decreased mitochondrial function with highly impaired ABC transporter activity and disease progression. In this paper, we describe a network based on interactions between ageing, energy metabolism, regeneration, accumulation of toxic peptides and the development of proteopathies of the brain with a focus on Alzheimer's disease (AD). Additionally, we provide new experimental evidence for interactions within this network in regenerative processes in AD.

Indexed as

Agingalpha-SynucleinAlzheimer DiseaseAmyloid beta-PeptidesAnimalsATP-Binding Cassette TransportersBrainEnergy MetabolismHumansMicealpha-SynucleinAmyloid beta-PeptidesATP-Binding Cassette TransportersABCA1ABCA7ABCB1ABCC1ABC transportersAgeingAlzheimer's diseaseAqp4DementiaEnergy metabolismMitochondriaNeurodegenerationParkinson's disease

Identifiers

PMID24012632
PMCPMC3844141

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.