Evidence map›Paper›PMID 24746857›Full record

ReviewNeurobiology of disease2014

Alzheimer's and ABC transporters--new opportunities for diagnostics and treatment.

Jens Pahnke, Oliver Langer, Markus Krohn

Abstract readReview
In one paragraph

Review in Neurobiology of disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
–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

42 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Advancing 6-bromo-7-[EJNMMI radiopharmacy and chemistry · 2024
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Integrative metabolomics-genomics approach reveals key metabolic pathways and regulators of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022
    Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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.

Jens PahnkeNeurodegeneration Research Lab (NRL), Department of Neurology, University of Magdeburg, Leipziger Str. 44, Bldg. 64, 39120 Magdeburg, Germany; German Center for Neurodegenerative Diseases (DZNE) Magdeburg, Leipziger Str. 44, Bldg. 64, 39120 Magdeburg, Germany. Electronic address: jens.pahnke@web.de.
Oliver LangerHealth and Environment Department, AIT - Austrian Institute of Technology GmbH, 2444 Seibersdorf, Austria; Department of Clinical Pharmacology, Medical University of Vienna, Währinger-Gürtel 18-20, 1090 Vienna, Austria.
Markus KrohnNeurodegeneration Research Lab (NRL), Department of Neurology, University of Magdeburg, Leipziger Str. 44, Bldg. 64, 39120 Magdeburg, Germany.

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

Much has been said about the increasing number of demented patients and the main risk factor 'age'. Frustratingly, we do not know the precise pattern and all modulating factors that provoke the pathologic changes in the brains of affected elderly. We have to diagnose early to be able to stop the progression of diseases that irreversibly destroy brain substance. Familiar AD cases have mislead some researchers for almost 20 years, which has unfortunately narrowed the scientific understanding and has, thus, lead to insufficient funding of independent approaches. Therefore, basic researchers hardly have been able to develop causative treatments and clinicians still do not have access to prognostic and early diagnostic tools. During the recent years it became clear that insufficient Aβ export, physiologically facilitated by the ABC transporter superfamily at the brain's barriers, plays a fundamental role in disease initiation and progression. Furthermore, export mechanisms that are deficient in affected elderly are new targets for activation and, thus, treatment, but ideally also for prevention. In sporadic AD disturbed clearance of β-amyloid from the brain is so far the most important factor for its accumulation in the parenchyma and vessel walls. Here, we review findings about the contribution of ABC transporters and of the perivascular drainage/glymphatic system on β-amyloid clearance. We highlight their potential value for innovative early diagnostics using PET and describe recently described, effective ABC transporter-targeting agents as potential causative treatment for neurodegenerative proteopathies/dementias.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsATP-Binding Cassette TransportersBlood-Brain BarrierBrainChoroid PlexusHumansMicePositron-Emission TomographyAmyloid beta-PeptidesATP-Binding Cassette TransportersABCA7ABCB1ABCC1ABC transporterAlzheimer’s diseaseAmyloid-betaBBBBlood–brain barrierChoroid plexusGlymphatic systemNeurodegenerationPET

Identifiers

PMID24746857
PMCPMC4199932

What OpenQuestion holds

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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.