Evidence map›Paper›PMID 19262960›Full record

Trial reportThe journal of nutrition, health & aging2009

New insights into clinical trial for Colostrinin in Alzheimer's disease.

P Szaniszlo, P German, G Hajas, D N Saenz, M Kruzel, I Boldogh

Open access · greenAbstract readClinical Trial, Phase IClinical Trial, Phase IIMulticenter Study
In one paragraph

Trial report in The journal of nutrition, health & aging, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 29% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Editorial: can we improve care for patients with dementia?The journal of nutrition, health & aging · 2011
    Article
  8. 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

6 authors at 3 institutions in 1 country.

P SzaniszloDepartment of Microbiology and Immunology, University of Texas Medical Branch at Galveston, Galveston, Texas 77555, USA.
P German
G Hajas
D N Saenz
M Kruzel
I Boldogh
Galveston College · USPharmaReview Corporation · USThe University of Texas Medical Branch at Galveston · US

Funding

Synthetic Organic Chemistry CoreP30ES006676 · NIEHS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI ELFERINK, CORNELIS JOHAN · 1995 to 2017
$21.7M
OXIDATIVE STRESS,REPAIR OF OXIDIZED GUANINES IN AGED CELLSP01AG021830 · NIA · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI PAPACONSTANTINOU, JOHN NMN · 2004 to 2010
$6.4M
NIA NIH HHS P01 AG021830NIEHS NIH HHS P30 ES006676
6 · The paper itself

Abstract

backgroundThe pathomechanism of Alzheimer's disease (AD) is multifactorial although the most popular hypotheses are centered on the effects of the misfolded, aggregated protein, amyloid beta (Abeta) and on Tau hyperphosphorylation.

objectivesDouble blinded clinical trials were planned to demonstrate the effect of Colostrinin (CLN) on instrumental daily activities of AD patients. The potential molecular mechanisms by which CLN mediates its effects were investigated by gene expression profiling.

methodsRNAs isolated from CLN-treated cells were analyzed by high-density oligonucleotide arrays. Network and pathway analyses were performed using the Ingenuity Pathway Analysis software.

resultsThe Full Sample Analysis at week 15 showed a stabilizing effect of CLN on cognitive function in ADAS-cog (p = 0.02) and on daily function in IADL (p = 0.02). The overall patient response was also in favor of CLN (p = 0.03). Patients graded as mild on entry also showed a superior response of ADAS-cog compared to more advanced cases (p = 0.01). Data derived from microarray network analysis show that CLN elicits highly complex and multiphasic changes in the cells' transcriptome. Importantly, transcriptomal analysis showed that CLN alters gene expression of molecular networks implicated in Abeta precursor protein synthesis, Tau phosphorylation and increased levels of enzymes that proteolitically eliminate Abeta. In addition, CLN enhanced the defense against oxidative stress and decreased expression of inflammatory chemokines and cytokines, thereby attenuating inflammatory processes that precede Alzheimer's and other neurological diseases.

conclusionTogether these data suggest that CLN has promising potential for clinical use in prevention and therapy of Alzheimer's and other age-associated central nervous system diseases.

Indexed as

Activities of Daily LivingAlzheimer DiseaseCells, CulturedCognitionDouble-Blind MethodGene ExpressionGene Expression ProfilingHumansIntercellular Signaling Peptides and ProteinsMiddle AgedNeuroprotective AgentsOligonucleotide Array Sequence AnalysisPeptidesSeverity of Illness IndexcolostrinineIntercellular Signaling Peptides and ProteinsNeuroprotective AgentsPeptides

Identifiers

PMID19262960
PMCPMC12876364
OpenAlexW2037994154

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.