Evidence map›Paper›PMID 20218980›Full record

ArticleBritish journal of pharmacology2010

The metabolic enhancer piracetam ameliorates the impairment of mitochondrial function and neurite outgrowth induced by beta-amyloid peptide.

C Kurz, I Ungerer, U Lipka, S Kirr, T Schütt, A Eckert, K Leuner, W E Müller

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
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  4. Mechanisms associated with the dysregulation of mitochondrial function due to lead exposure and possible implications on the development of Alzheimer's disease.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2022
    Review
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  8. Hemp (ACS omega · 2018
    Article
  9. Review
  10. Mitochondrial Metabolism-Mediated Regulation of Adult Neurogenesis.Brain plasticity (Amsterdam, Netherlands) · 2017
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

C KurzDepartment of Pharmacology, Biocenter, University Frankfurt/M, Germany.
I Ungerer
U Lipka
S Kirr
T Schütt
A Eckert
K Leuner
W E Müller
Goethe University Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposebeta-Amyloid peptide (Abeta) is implicated in the pathogenesis of Alzheimer's disease by initiating a cascade of events from mitochondrial dysfunction to neuronal death. The metabolic enhancer piracetam has been shown to improve mitochondrial dysfunction following brain aging and experimentally induced oxidative stress. EXPERIMENTAL APPROACH: We used cell lines (PC12 and HEK cells) and murine dissociated brain cells. The protective effects of piracetam in vitro and ex vivo on Abeta-induced impairment of mitochondrial function (as mitochondrial membrane potential and ATP production), on secretion of soluble Abeta and on neurite outgrowth in PC12 cells were investigated. KEY

resultsPiracetam improves mitochondrial function of PC12 cells and acutely dissociated brain cells from young NMRI mice following exposure to extracellular Abeta(1-42). Similar protective effects against Abeta(1-42) were observed in dissociated brain cells from aged NMRI mice, or mice transgenic for mutant human amyloid precursor protein (APP) treated with piracetam for 14 days. Soluble Abeta load was markedly diminished in the brain of those animals after treatment with piracetam. Abeta production by HEK cells stably transfected with mutant human APP was elevated by oxidative stress and this was reduced by piracetam. Impairment of neuritogenesis is an important consequence of Abeta-induced mitochondrial dysfunction and Abeta-induced reduction of neurite growth in PC12 cells was substantially improved by piracetam. CONCLUSION AND IMPLICATIONS: Our findings strongly support the concept of improving mitochondrial function as an approach to ameliorate the detrimental effects of Abeta on brain function.

Indexed as

Adenosine TriphosphateAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsBrainCell LineHumansMembrane Potential, MitochondrialMiceNeuritesNeuroprotective AgentsOxidative StressPC12 CellsPeptide FragmentsPiracetamRatsAdenosine TriphosphateAmyloid beta-Peptidesamyloid beta-protein (1-42)Amyloid beta-Protein PrecursorNeuroprotective AgentsPeptide FragmentsPiracetam

Identifiers

PMID20218980
PMCPMC2874847
OpenAlexW1493486581

What OpenQuestion holds

Textmetadata
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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.