Evidence map›Paper›PMID 23420079›Full record

ReviewMolecular neurobiology2013

Molecular basis of etiological implications in Alzheimer's disease: focus on neuroinflammation.

Rituraj Niranjan

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
6.6field-weighted citation impact, top 3% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

  1. Pooled it
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  4. 3 Biotech · 2024
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  6. Review
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  8. Potential Use ofPlants (Basel, Switzerland) · 2022
    Review
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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

1 author at 1 institution in 1 country.

Rituraj NiranjanDivision of Gastroenterology and Liver Diseases, School of Medicine, Case Western Reserve University, 2109 Adelbert Rd., BRB 501, Cleveland, OH, 44106, USA, riturajniranjan@rediffmail.com.
Case Western Reserve University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Significant bodies of evidences have shown different mechanisms known to be the etiological cause of Alzheimer's disease (AD) involving amyloid-beta protein accumulation, chronic inflammatory reactions, oxidative stress, proteasome inhibition, and high-cholesterol level, but the presize etiology of AD still remains enigmatic. Recent studies indicate that these mechanisms seem to be interlinked, and neuroinflammation emerges as a major regulatory and commen factor in all these mechanisms. In amyloid-beta protein, induced neurodegenerative hypothesis of AD inflammatory cytokines IFN-γ, TNF-α, interleukin (IL)-1α plays an important role in the progression of the disease. In cholesterol induced hypothesis liver X receptor mediated IL-4 also plays a major role in the progression of neuroinflammation. Notably, Omi and HtrA2 proteases play very important functions in neuronal dysfunction, which may lead to neurodegeneration. Further at genetic level, alterations in the genes occur especially in APP, PSEN1, PSEN2, APO E(ε4), ADAM12, and SH3MD1 which mediate neurodegeneration. Additionaly, The role of SP-1, NF-κB, and BCAE-1 is critical in the regulation of neuroinflammation-associated disease pathogenesis. All together, in this review, we discus the importance of neuroinflammatory mediators and their mechanistic role in the process of AD neurodegeneration.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsCholesterolHumansInflammationNerve DegenerationNervous SystemAmyloid beta-PeptidesCholesterol

Identifiers

PMID23420079
OpenAlexW2087880903

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.