Evidence map›Paper›PMID 19263040›Full record

ArticlePsychopharmacology2009

Memory deficits and neurochemical changes induced by C-reactive protein in rats: implication in Alzheimer's disease.

Huan-Bing Lin, Xue-Mei Yang, Tie-Jun Li, Yu-Fang Cheng, Han-Ting Zhang, Jiang-Ping Xu

Abstract read
PubMed Publisher
In one paragraph

Article in Psychopharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
2.2field-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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. A Meta-Analysis of C-Reactive Protein in Patients With Alzheimer's Disease.American journal of Alzheimer's disease and other dementias · 2016
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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

6 authors at 3 institutions in 2 countries.

Huan-Bing LinDepartment of Pharmacology, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou, 510515, People's Republic of China.
Xue-Mei Yang
Tie-Jun Li
Yu-Fang Cheng
Han-Ting Zhang
Jiang-Ping Xu
Southern Medical University · CNSecond Military Medical University · CNWest Virginia University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationaleC-reactive protein (CRP), an acute phase protein that is released in response to inflammatory stimuli, is implicated in Alzheimer's disease (AD). However, the role of CRP in memory deficits associated with AD remains unclear.

objectiveExperiments were carried out to determine whether CRP impaired memory and altered neurochemical measures associated with AD.

methodsThe effects of intra-cerebroventricular administration of CRP or beta-amyloid peptide 25-35 (Abeta(25-35)) on memory performance were evaluated using rat Morris water-maze and step-through passive avoidance tests; the levels of inflammatory cytokines (interleukin-1beta (IL-1beta), IL-6, and tumor necrosis factor (TNF-alpha)), endogenous CRP, and markers of the endogenous production of Abeta, including amyloid precursor protein (APP), presenilins (PS-1 and PS-2), and beta-site of APP cleaving enzyme (BACE), were also determined in brain regions using real-time reverse transcriptase polymerase chain reaction (RT-PCR) and Western blotting analysis.

resultsTreatment with CRP (25.6 microg/rat) or Abeta(25-35) (10 microg/rat) 2 weeks ahead produced impairment of long-term memory in both animal tests. Real-time RT-PCR revealed increases in messenger RNA levels of APP, IL-1beta, IL-6, TNF-alpha, and CRP in the cerebral cortex and hippocampus and those of PS-1 and PS-2 in the cerebral cortex produced by treatment with CRP or Abeta(25-35). Immunoblotting analysis showed that while expression of APP was increased in both the cerebral cortex and the hippocampus, expression of IL-1beta, BACE, and TNF-alpha was increased only in the hippocampus.

conclusionsThe results suggest that CRP contributes to memory loss and early phase of pathogenesis of AD. CRP can be a novel target for therapeutic intervention of AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsAvoidance LearningBlotting, WesternCerebral CortexC-Reactive ProteinDisease Models, AnimalHippocampusInflammation MediatorsInjections, IntraventricularMaleMaze LearningMemory DisordersPeptide FragmentsAmyloid beta-Peptidesamyloid beta-protein (25-35)Amyloid beta-Protein PrecursorC-Reactive ProteinInflammation MediatorsPeptide FragmentsRNA

Identifiers

PMID19263040
OpenAlexW2148293753

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.