Evidence map›Paper›PMID 17047305›Full record

ArticleJournal of biomedicine & biotechnology2006

The creatine kinase/creatine connection to Alzheimer's disease: CK-inactivation, APP-CK complexes and focal creatine deposits.

Tanja S Bürklen, Uwe Schlattner, Ramin Homayouni, Kathleen Gough, Margaret Rak, Adriana Szeghalmi, Theo Wallimann

Open access · hybridAbstract read
In one paragraph

Article in Journal of biomedicine & biotechnology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

56 citing papers in PubMed, 119 citations in OpenAlex.

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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

7 authors at 4 institutions in 4 countries.

Tanja S BürklenInstitute of Cell Biology, ETH Zurich, Hönggerberg HPM, 8093 Zurich, Switzerland.
Uwe Schlattner
Ramin Homayouni
Kathleen Gough
Margaret Rak
Adriana Szeghalmi
Theo Wallimann
University of Manitoba · CAETH Zurich · CHInserm · FRUniversity of Tennessee Health Science Center · US

Funding

Arrowsmith Data Mining Techniques in Neuro-InformaticsR01LM007292 · NLM · UNIVERSITY OF ILLINOIS AT CHICAGO · PI SMALHEISER, NEIL R · 2001 to 2005
$3.2M
NLM NIH HHS R01 LM007292
6 · The paper itself

Abstract

Cytosolic brain-type creatine kinase (BB-CK), which is coexpressed with ubiquitous mitochondrial uMtCK, is significantly inactivated by oxidation, in Alzheimer's disease (AD) patients. Since CK has been shown to play a fundamental role in cellular energetics of the brain, any disturbance of this enzyme may exasperate the AD disease process. Mutations in amyloid precursor protein (APP) are associated with early onset AD and result in abnormal processing of APP, and accumulation of A beta peptide, the main constituent of amyloid plaques in AD brain. Recent data on a direct interaction between APP and the precursor of uMtCK support an emerging relationship between AD, cellular energy levels and mitochondrial function. In addition, recently discovered creatine (Cr) deposits in the brain of transgenic AD mice, as well as in the hippocampus from AD patients, indicate a direct link between perturbed energy state, Cr metabolism and AD. Here, we review the roles of Cr and Cr-related enzymes and consider the potential value of supplementation with Cr, a potent neuroprotective substance. As a hypothesis, we consider whether Cr, if given at an early time point of the disease, may prevent or delay the course of AD-related neurodegeneration.

Identifiers

PMID17047305
PMCPMC1510941
OpenAlexW2043604922

What OpenQuestion holds

Textmetadata
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.